PREVENTING COVID: SUSCEPTIBILITY AND AMELIORATION


A weird medicopolitical kludge - the resistance against resisting insulin resistance - covid and adipocytes - prophylaxis must be a problem - psychiatric diagnoses are mad - more trouble in the covid stadium - sleep apnea and the Town Smell - a permanent change - 39 out of 40 conditions worse - better dead than off your head? - covid cell fusion - you can't drink it better - cannabis and vaccine injury - trip yourself better.

By April 2020 it was already clear that

"Similar to other respiratory pathogens, SARS-CoV2 is transmitted through respiratory droplets, with potential for aerosol and contact spread. It uses receptor-mediated entry into the human host via angiotensin-converting enzyme II (ACE2) that is expressed in lung tissue, as well as oral and nasal mucosa, kidney, testes, and the gastrointestinal tract. Modulation of ACE2 levels in these gateway tissues may prove a plausible strategy for decreasing disease susceptibility. Cannabis sativa, especially one high in the anti-inflammatory cannabinoid cannabidiol (CBD), has been proposed to modulate gene expression and inflammation and harbour anti-cancer and anti-inflammatory properties. Working under the Health Canada research license, we have developed over 800 new Cannabis sativa lines and extracts and hypothesized that high-CBD C. sativa extracts may be used to modulate ACE2 expression in COVID-19 target tissues. Screening C. sativa extracts using artificial human 3D models of oral, airway, and intestinal tissues, we identified 13 high CBD C. sativa extracts that modulate ACE2 gene expression and ACE2 protein levels. Our initial data suggest that some C. sativa extract down-regulate serine protease TMPRSS2, another critical protein required for SARS-CoV2 entry into host cells."

And Wang et al considered that:

"Given the current dire and rapidly evolving epidemiological situation, every possible therapeutic opportunity and avenue must be considered."

And yet, despite this dire need for easy to use preventives, this research had already steered away from others - on purely emotional grounds: the dire need to avoid any medicine which might make people feel good, and the need to look "respectable".

And that is why Wang et al's paper is about CBD extracts and not cannabis or THC.

The ratios for the red lines in their Table 1 average 1 part THC to 22.8 parts CBD.

The ratios for the black lines average 17.56.

The ratios in the red lines were found to inhibit ACE2 expression.

Can we conclude from these ratios that THC is of no value in reducing ACE2 expression?

No, because the authors have chosen low THC:CBD ratios to begin with (the highest is 1:1). But you could equally well have a ratio of 30:1.

The question whether THC is helpful or even superior is cast aside, as it becomes clear that the priority is not medical assistance, but a legal distinction born before Covid-19 was even a blueprint on a laboratory technician's computer screen. Namely:

"Most importantly, seven active lines have less than 0.3% of total THC and
therefore can be classified as CBD Hemp in Canada and USA, allowing for easier implementation."

It has been assumed a priori that it is better to die than get high, when catching SARS.

And yet, as Wang et al eventually get around to mentioning:

"...cannabis has over 100 phytocannabinoids, of which the main ones are delta-9- tetrahydrocannabinol (Δ⁹-THC) and cannabidiol (CBD). Beyond these main cannabinoids, cannabis possesses many minor cannabinoids, as well as numerous terpenes. The latter are responsible for variations in scent and may act synergistically with cannabinoids, with the potential to strongly enhance cannabinoid effects. Terpenes and minor cannabinoids are responsible for the ‘entourage’ effect, whereby whole plant extracts have more pronounced biological effects than individual cannabinoids. In the future, it would be important to identify the cannabinoids and terpenes responsible for the observed effects, albeit, based on the entourage effects, one could predict that whole flower extracts may be more potent than single compounds."

And although they are at pains to state that:

"Application was intended to model medical delivery, such as local mouth wash applications, encapsulated extracts and dosed oils, and inhalers or nebulizers, and therefore these results cannot be extrapolated to the effects of cannabis smoking. Moreover, in light of recent findings that tobacco smoking increases ACE2 levels and exacerbates clinical outcomes of COVID-19, the effects of cannabis smoking on the levels of ACE2 expression should be carefully investigated."
https://www.preprints.org/manuscript/202004.0315/v1 [4817]

Mohammed et al (2020) soon found that

"THC caused induction of Myeloid-Derived Suppressor Cells (MDSCs). THC acted through CB2 receptor as pharmacological inhibitor of CB2 receptors blocked the anti-inflammatory effects. THC-treated mice showed significant alterations in the expression of miRNA (miRs) in the lung-infiltrated mononuclear cells (MNCs). Specifically, THC caused downregulation of let7a-5p which targeted SOCS1 and downregulation of miR-34-5p which caused increased expression of FoxP3, NOS1, and CSF1R. Together, these data suggested that THC-mediated alterations in miR expression in the lungs may play a critical role in the induction of immunosuppressive Tregs and MDSCs as well as suppression of cytokine storm leading to attenuation of SEB-mediated lung injury."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7308536/ [1543]
 
Using Mendelian randomization to elucidate causal factors in Covid risks, Jabalameli and Zhang (2022) found:

"Our study showed that two classes of medications, including vasodilators and statin (used for cardiac diseases) are causally related to the risk of COVID-19 hospitalization (Table 1). The impact of vasodilators on the risk of hospitalization was almost negligible (up to 1% increase), but statin showed a stronger effect on the risk of hospitalization (OREgger = 1.06, PEgger = 3.46E-56). The positive genetic correlation of both medication classes with COVID-19 hospitalization (vasodilators: rg = 0.17, statin: rg = 0.24) confirms the previously reported higher baseline prevalence cardiovascular conditions among hospitalized patients (Wang B. et al., 2020). Neither of the two classes of medication showed a significant causality relationship with COVID-19 respiratory failure. We also detected a significant negative causal effect for diuretics and medication class acting on the renin-angiotensin system (RAAS) with the risk of COVID-19 reparatory failure. Since both medication classes are primarily prescribed for patients with hypertensive disease, this negative causal effect further underlines the importance of ACE inhibitors in controlling COVID-19 severe illness (diuretics: ORIVW = 0.47, PIVW = 2.66E-15; RAAS: ORIVW = 0.36, PIVW = 1.87E-17).

"We detected evidence for a (negative) causal effect of cannabis abuse with COVID-19 hospitalization (Hospitalization: ORIVW = 0.77, PIVW = 1.18E-08, Table 1). There is no clear mechanistic evidence linking cannabis use disorder (CUD) to COVID-19 symptoms, but we hypothesize that this negative causal effect is exerted through immunomodulatory pathways related to cannabinoid receptors. We found this observation interesting since Wang et al. also observed a protective association for lifetime CUD and COVID-19 (OR = 0.85, p = 0.006)."
https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2022.1070428/full [4827]

The Defendant did not wait for these investigations, or the many investigations into the mechanisms which followed, as everyone with a cold knows when to smoke cannabis and when not to. The Defendant reports a survivor bias, and was able to still be around by 2022 when Nguyen et al reported that "Cannabidiol inhibits SARS-CoV-2 replication through induction of the host ER stress and innate immune responses" - acting by

"...up-regulating the host IRE1α ribonuclease endoplasmic reticulum (ER) stress response and interferon signaling pathways."

Moreover, and as the Defendant can confirm from his own case history:

"As reported, SARS-CoV-2 infection suppresses the interferon signaling pathway (Fig. 7A and fig. S17). Many genes in the pathway such as interferon-stimulated gene 15 (ISG15), interferon induced protein with tetratricopeptide repeats 1 (IFIT1), IFIT3, suppressor of cytokine signaling 1 (SOCS1), and 2’-5’-oligoadenylate synthetase 1 (OAS1), an interferon-induced gene that leads to activation of RNase L and RNA degradation, were moderately up-regulated by CBD alone but highly induced by CBD in the presence of the virus (Fig. 7A...and figs. S18 and S19). These latter results are consistent with the possibility that CBD sufficiently lowers the effective viral titer to enable normal host activation of the interferon pathway. At the same time, CBD effectively reversed viral induction of cytokines that can lead to the deadly cytokine storm at later stages of infection (Fig. 7BO)."
https://www.science.org/doi/full/10.1126/sciadv.abi6110?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org [4818]

In "Persistent immune dysregulation and metabolic alterations following SARS-CoV-2 infection" Lage et al (2025) did not find a significant difference in genetic age between Covid and non-Covid histories. However...

"Significant differences in the gene methylation patterns, however, were found between the group with prior COVID-19 and naïve controls (Figure 10A). Figure 10B and Supplemental Table 2 highlight the most differentially methylated CpGs and their respective genes. Among them, several genes associated with various intracellular processes were found to be highly methylated in those with prior COVID-19 as compared to naïve controls (Figure 10B). Those include genes involved in cellular metabolism such as PCED1A, GLB1L, and IGFBP as well as anti-inflammatory immune responses (ZC3H8). The SLC12A family of genes which play a functional role in the pathophysiology of hypertension and cardiovascular disease and VPS16, which encodes a protein involved in vesicle trafficking, are also of particular interest, since changes in these genes have been associated with neurodevelopmental diseases and dementia."

...

"We identified prominent post-acute metabolic dysfunction that may contribute to adverse outcomes from COVID-19. For example, our analysis using Elastinet regression models identified that dysregulation in lipid mediators of inflammation provided the greatest differentiation between the Long COVID and fully recovered groups. AA and 11–12-DiHETrE, found to be increased post-COVID, play a crucial role in inflammatory and allergic reactions, and have been implicated in the pathogenesis of many chronic inflammatory diseases. In contrast, AEA and DHEA, which are derived from AA and omega-3 fatty acids [ω−3 FAs], respectively, and associated with beneficial cardiovascular, neurological and anti-inflammatory effects, were lower in those with prior COVID-19 compared to naïve controls. Collectively these observations suggest that treatments targeting lipid pathways, such as omega-3 supplementation or agents like metformin which have been shown to prevent LC, could provide benefit as they have been found to positively impact AA metabolism."
https://pmc.ncbi.nlm.nih.gov/articles/PMC12047922/ [5256]
https://pmc.ncbi.nlm.nih.gov/articles/PMC5544256/ [5257]

Among those who claim we would rather die than get high is Tanja Bagar, a microbiologist with a PhD in biomedicine and a Slovenian Woman Of The Year. As she quite rightly says:

"More and more research shows that the induction or recruitment of beige or brite adipocytes, together with the activation of BAT, could be protective against obesity. BAT activity has the potential to significantly influence body weight, glucose, and lipid metabolism. It is involved in dissipating energy as heat, due to a special protein called UCP1 on the inner mitochondria membrane. Brown adipocytes seem to be responsible for large heat production, significantly higher than in other organs, thereby enhancing body energy expenditure. Several activators have been associated with WAT browning, like cold exposure, exercise, thyroid hormones, catecholamines, capsaicin etc. The conversion of WAT in beige adipose tissue is a potential new therapeutic target for obesity.

"Adipose tissues express both cannabinoid receptors, and their activation significantly influences the metabolic activity of adipose cells. Blockade of the CB1 receptor was shown to induce the differentiation of white adipocytes towards a thermogenic brown cell phenotype, which is highly beneficial when we want to reduce adipose tissue. The effects of the CB2 receptor on obesity are poorly characterized, but we do know it is strongly involved in energy homeostasis."

After explaining the pre-eminent role of CB1R in browning, the paragraph trundles on to focus on the more mysterious CB2.

"It was shown that the activation of CB2 induces heat generation with consequent energy expenditure in adipose tissue and that chronic stimulation of CB2 attenuates body weight gain."

So CB1 is completely ignored, to fit the legal and perhaps perceived public opinion. Remember, the public has never been asked or voted about banning itself from using cannabis.

In this schema, then, the connection between a phytocannabinoid-based lifestyle and the favourable outcome to be expected therefrom is assumed to be broken.

It is broken in favour of the proprietary drug market with what is, by Dr Bagar's own admission, the "highly beneficial" mechanism of browning.

Indeed it is axiomatic that both CB1 and CB2 receptors existed in the lissom phytogenic cannabis users described in the literature. And on the basis of this mixture of selected medical truths, law, business, and mixed up reasoning:

"Therefore, CB2 seems like a promising target in obesity, as it should facilitate the anti-obesity effects without exerting central psychotropic activity."

In her Conclusion, ignoring the well-known fact that cannabis is a medicine so awesome that most people take it just for the side-effects, Dr Bagar returns to the difficulties of finding something that is just like weed but isn't weed.

"Obesity-related co-morbidity is increasing. It comes at a high cost for society and it has a negative impact on a patient's lifestyle. Recent findings in the field of white adipose tissue browning (WAT to BAT transformation) have pointed out the potential role of this phenomenon in obesity treatment. BAT activity has been associated with the improvement of metabolic profile in adults. The activation of CB2 in enhancing browning and transforming chemical energy into thermic energy could be an important piece of the puzzle.

"Targeting of CB1 is also important, but we must bear in mind the experiences with Rimonabant, a CB1 receptor antagonist that appeared to be a promising anti-obesity drug during clinical trials, but also exhibited immense psychiatric side effects and had to be taken off the market. The discontinuation of clinical trials related to FAAH inhibitors because of serious adverse events has also shown that meddling with this vital, fundamental protective system needs to be done very judiciously. Here, once again, phytocannabinoids and also other ligands, the cannabinoid receptors from the plant world, show immense potential."

In some strange world, it is as if cannabis, the inspiration for all this knowledge, doesn't already exist.
https://www.fundacion-canna.es/en/role-endocannabinoid-system-and-selected-phytocannabinoids-metabolism [2757]

In "Effect of oral cannabis administration on the fat depots of obese and streptozotocin-induced diabetic rats" (2022) Ramlugon et al state:

"The prevalence of obesity and insulin-resistance is on the rise, globally. Cannabis have [sic] been shown to have anti-diabetic/obesity properties, however, the effect mediated at various fat depots remains to be clarified. The aim of this study was to (1) investigate the anti-diabetic property of an oral cannabis administration in an obese and streptozotocin-induced diabetic rat model and (2) to determine and compare the effect mediated at the peritoneal and intramuscular fat level. Cannabis concentration of 1.25 mg/kg body weight (relative to THC content) was effective in reversing insulin-resistance in the rat model, unlike the other higher cannabinoid concentrations. At the peritoneal fat level, gene expression of fat beigeing markers, namely Cidea and UCP1, were significantly increased compared to the untreated control."
https://onlinelibrary.wiley.com/doi/full/10.1002/ptr.7694 [2758]

"Fibrin drives thromboinflammation and neuropathology in COVID-19" say Ryu et al (2024).
https://www.nature.com/articles/s41586-024-07873-4 [3616]

The Court must consider the role of coagulopathy in diabetes, cardio, and Covid, and the roles of the relevant Benedictions in each.

According to Akassoglou et al in "Pioneering discovery and therapeutics at the brain-vascular-immune interface" (2024):

"Genetic loss-of-function and pharmacological studies identified that among blood proteins, fibrin is necessary and sufficient for neurotoxic microglia polarization, while its blockade preserves homeostatic microglia in several animal models of neurological diseases, such as MS, AD, TBI, and COVID-19 neuropathology (Figure 2B).


https://www.cell.com/cell/fulltext/S0092-8674(24)01037-7 [3614]

In a longitudinal study of 5115 black and white men and women enrolled in 1985-1986, and followed up for over 25 years, Alshaarawy et al (2019) found that

"Overall, cannabis users have lower levels of fibrinogen and CRP compared to never users."


https://pmc.ncbi.nlm.nih.gov/articles/PMC6883146/pdf/nihms-1530428.pdf [3615]

A similar but less reliable cross-sectional study of 5636 subjects by Okafor (2020) found similar results. Once again the results were less impressive for the part-timers than the more dedicated user, suggesting higher levels of these markers were NECUD-associated.


https://www.sciencedirect.com/science/article/pii/S2666354620300740

A microscopic image of a blood clot showing fibrin fibres:



For "Laboratory and Clinical Manifestations of COVID-19 Coagulopathy" we refer to Farkouh et al (2022).

The COVID-19 coagulopathy is characterized by laboratory abnormalities including increased levels of fibrinogen and D-dimer, and mild prolongation of prothrombin time or activated partial thromboplastin time, sometimes with mild thrombocytopenia. Some patients hospitalized due to COVID-19 may develop a coagulopathic state that meets the International Society on Thrombosis and Haemostasis definition for disseminated intravascular coagulation (DIC). In a cohort from Wuhan, 16 of 183 hospitalized patients developed DIC, which was associated with worse prognosis (all but 1 of these patients died during the hospitalization). Elevated D-dimer alone at hospital admission is also associated with worse prognosis, including elevated risks for bleeding, thrombosis, critical illness, and death.
https://www.sciencedirect.com/science/article/pii/S0735109722000079?via%3Dihub [4568]

The covid-19 epidemic measures were declared March 12 then again on October 19 2020.

The risk/benefit calculation for cannabis has been shifted in its favour by Slovenianness, i.e. alcoholism, and covid. Drinking makes people fat.

Fat and alcoholic Slovenian people are at greater risk of hospitalisation and death.

Now it seems Covid attacks fat cells directly.
https://www.newsbreak.com/news/2456107168804/the-coronavirus-attacks-fat-tissue-scientists-find?pd=05OJxYQR&lang=en_US&s=i2 [810]

"This latter possibility, that SARS-CoV-2 could directly infect adipose tissue, was originally hypothesized based on expression of RNA for angiotensin-converting enzyme-2 (ACE2), the SARS-CoV-2 entry receptor, in adipose tissue samples. Supporting this idea, several groups recently reported detection of SARS-CoV-2 RNA in adipose tissue from 28 of 59 COVID-19 autopsy cases, infection of human adipocytes in vitro, and infection of adipose tissue in the hamster model of SARS-CoV-2 infection. SARS-CoV-2 infection of adipose tissue could induce inflammation and alter adipose tissue function, potentially contributing to disease pathogenesis. For instance, virus infection can impact adipogenesis and could increase adipose tissue hypertrophy and hyperplasia, in turn serving as a fuel for further infection. One recent study demonstrates that COVID-19 is associated with diminished adiponectin expression in vivo, suggesting alterations of adipose tissue function. This same study also shows that in vivo infection of hamsters and in vitro infection of murine adipocytes leads to decreased adiponectin expression in adipocytes, yet it is unclear if infection is the direct cause of this change in humans because SARS-CoV-2 infection of human adipocytes in vitro did not change adiponectin expression. Adipocytes can also play a role in inflammation, secreting chemokines such as monocyte chemoattractant protein-1 (MCP-1), which can fuel macrophage infiltration and activation. Virus infection of peri-organ fat could even contribute to organ damage through inflammation and downstream processes such as extracellular matrix deposition and fibrosis, impaired cellular function, and hypercoagulability. Many questions remain unanswered, including which adipose tissue cells are infected, whether they can serve as a reservoir for continued virus production, and how infection changes inflammatory and functional profile of adipose tissue cells."

And their findings in brief:

"In particular, obesity increases the risk of severe COVID-19, yet clear mechanisms driving this association remain unknown. Here, we report that SARS-CoV-2 infects human adipose tissue, targeting both mature adipocytes and a subset of adipose tissue macrophages, leading to immune activation and the secretion of inflammatory factors associated with severe COVID-19."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9529056/ [4569]

align="middle"

Here's a diagram from the American Heart Association journal Circulation showing the pathways linking lower socioeconomic status, poorer diet, reduced activity and race or ethnic factors with obesity and excess ectoptic fat.

Among them reduced forced expiration volume, reduced forced vital capacity and an increase in diabetes. More on these in the COPD and lung capacity, and HNSCC sections. 

The covid-19 epidemic measures were declared March 12 then again on October 19 2020.

Cannabis helps you stay slim. This is not only a matter of metabolism. The Defence asserts that cannabis people are more particular about their diet than drunk people.

Cannabinoids are potent anti-inflammatory agents and they exert their effects through induction of apoptosis, inhibition of cell proliferation, suppression of cytokine production and induction of T-regulatory cells.

Nature reports a 17.5% greater risk of covid for people who are not lifelong problem cannabis users.

Here's a diagram from the American Heart Association journal Circulation showing the pathways linking lower socioeconomic status, poorer diet, reduced activity and race or ethnic factors with obesity and excess ectoptic fat.

Among them reduced forced expiration volume, reduced forced vital capacity and an increase in diabetes. More on these in the COPD and lung capacity, and HNSCC sections.

These are empirical metrics. But are the SUDs real diagnoses? No.

Was it really necessary to have an x-axis up to 14? Yes: only in this way could the positive effect of "cannabis use disorder" be played down to fit the expectation that prohibition places upon the authors.

The Prosecution's problem, says this Defence, is the dogma that anything to do with cannabis has to be a problem, regardless of the scientific truth. Here we see the lengths to which authors are prepared to prostrate themselves before the religion of prohibition however absurd the claim.
https://www.nature.com/articles/s41380-020-00880-7 [218]

Some problems with Wang et al's analysis:

Skewed sample: "Recently diagnosed" = victimhood may be in their legal interest.

Selective truth: the 7.7X likelihood in drunks eluded your headline.

Biased language: "substance use disorder" is psychobabble. Most substance use is perfectly in order. A psychiatric diagnosis is not a disease. Psychology Today addresses this psychobabble problem and the difficulties it causes, in a 19 March 2024 article:

"Confusion arises because medical diagnoses often point to etiology—underlying biological causes. This is why 'chest pain' is not a disease, it is a symptom. Atherosclerosis, myocarditis, and pneumonia are diseases. They are underlying biological conditions that can cause chest pain.

"Psychiatric diagnoses are categorically different because they are merely descriptive, not explanatory. It's not that we don't know their causes yet. It's that DSM diagnoses cannot speak to causes, now or ever. The DSM was not designed to speak to causes, only describe effects."
https://www.psychologytoday.com/us/blog/psychologically-minded/201907/a-psychiatric-diagnosis-is-not-a-disease [4634]

Chuck Ruby PhD, Executive Director of the International Society for Ethical Psychology and Psychiatry, and a retired Lieutenant Colonel who served 20 years in the United States Air Force and who specialises in criminal, counterintelligence, counterespionage investigations, and investigative psychology elaborates on the arc of psychiatry for madinamerica.com:

"In the latter half of the 19th century, medicine’s growing interest in 'mental disease' was impacted by yet another new science, but one that focused on the mind – psychology. This merger of medical and psychological thinking would eventually spawn the emergence of psychiatry and the clinical versions of psychology, counseling, and social work, which I will simply refer to in combination as psychiatry. The impact of psychological science on medicine was underscored by the 1892 name change of psychiatry’s forerunner professional organization to the American Medico-Psychological Association.

"However, despite its origin in the Scientific Revolution, psychiatry drifted away from this empirical foundation for two reasons. First, the subjectivity of mind prevented objective observation and measurement of it, while its individualized nature interfered with the development of general scientific laws applying to all people. Second, and relatedly, medicine’s physiological dysfunction-correction model that had been in use long before psychology’s impact was felt was poorly suited for understanding suffering that had no underlying dysfunction to correct. These two problems derailed psychiatry from continuing its intended path as an empirically based medical specialty of mind, placing it on a new path toward becoming an authoritarian moral ideology that hearkened back to earlier centuries’ religious ideology."

The "diagnoses" - including all the "substance use disorders" are a mythical and self-serving construct:

"As every psychiatric professional knows, mental illness diagnoses are not based on hypothesizing and testing. Instead, they are derived from an increasing array of DSM checklists of common experiences and behaviors, misleadingly called symptoms, that are a priori assumed to be dysfunctional. But these diagnoses are not medical decisions based on dysfunction; instead, they are bureaucratic decisions about which DSM categories the person best fits. To highlight the non-scientific and non-medical nature of the diagnoses, they result from the political wrangling of appointed members of DSM committees that meet periodically to issue new editions. Still, despite this moral and bureaucratic foundation, the DSM continues to claim that mental illness reflects “dysfunction in the psychological, biological, or developmental processes underlying mental functioning” without ever providing robust theory or evidence of such a dysfunction."

He concludes:

"Notwithstanding the momentous effects of its emergence, psychiatry would abandon this empirical journey very early on in its development. In its eagerness to join the Scientific Revolution, it failed to keep the immaterial and private nature of mind in focus, and it overlooked the misapplication of its physiological dysfunction-correction model to the non-physiological mind. The only thing left for it to do was to make judgments about the appropriateness of people’s experiences and behaviors, and to attempt enforcement of appropriate ones. As such, psychiatry morphed into a moral ideology, returning us back to the days when a sacred religion ruled over people’s lives."
https://www.madinamerica.com/2025/03/psychiatry-medical-science-of-mind-or-moral-ideology/ [4836]

Dr. Sami Timimi is a consultant in child and adolescent psychiatry, Director of medical education at Lincolnshire Partnership NHS Foundation Trust, and a visiting professor of child psychiatry at the University of Lincoln.

"Timimi is skeptical of the benefits of psychiatric diagnosis, seen as primarily cultural constructions, and has critiqued the medicalisation of the various problems subsumed under the categories of ADHD and Autism (the latter co-authored with people with the diagnosis). He has described global mental health initiatives as a form of neo-liberalism."

He writes:

"Psychiatric diagnoses are not valid or useful. The use of psychiatric diagnosis increases stigma, does not aid treatment decisions and is associated with worsening long-term prognosis for mental health problems…formal psychiatric diagnostic systems such as the mental health section of the International Classification of Diseases Tenth Edition (ICD-10) and Diagnostic Statistical Manual Fifth Edition (DSM 5) should be abolished…."

“Prevention has proved elusive, with mental health diagnoses becoming more not less common. The diagnoses listed in the major psychiatric diagnostic manuals have not yet been linked with any sort of physical test or other biological marker and so, unlike the rest of medicine, psychiatric diagnoses do not have pathophysiological correlates and no independent data is available to the diagnostician to support their subjective assessment of diagnosis.”
https://en.wikipedia.org/wiki/Sami_Timimi [4733]

Psychiatric labels don't describe reality. They create it.

Kajanoja and Valtonen examined the presentation of psychiatric diagnoses and found a depressing prevalence of circular reasoning:

"Most psychiatric diagnoses are descriptive: They describe states of mental distress and dysfunction but do not in themselves contain causal explanations. Nonetheless, diagnoses in psychiatry are commonly talked about as if they are concrete entities that explain the symptoms they describe. In this study, we examined whether health organizations themselves contribute to this logical fallacy. We searched for popular websites managed by leading mental health organizations, and evaluated whether they discussed the diagnosis of depression accurately as a description, or inaccurately as a cause for depressive symptoms. We found that the majority of websites presented depression as a cause, instead of a description of symptoms. We discuss the potential harmful consequences of inaccurately presenting descriptive psychiatric diagnoses as causes."
https://karger.com/psp/article-abstract/doi/10.1159/000538458/909052/A-Descriptive-Diagnosis-or-a-Causal-Explanation?redirectedFrom=fulltext [3125]

Psychiatric diagnoses are of their time and follow fashions. With its steady quota of spousal murder-suicides Slovenia is no stranger to the experience of "limerence" - lovesickness, infatuation and romantic excess, with elements of melancholy, unfulfilled desire and obsessive-compulsivity. And yet today, limerence is not a trendy professional explanation that can be used in court.

"Lovesickness has been pathologized in previous centuries, but is not currently in the ICD-10, ICPC or DSM-5. There is also a debate over the moral implications of using modern drugs for this, and there are currently no drugs which are a realistic candidate."
https://en.wikipedia.org/wiki/Limerence [3275]

Psychiatric diagnoses are heteronormative. According to Metzl et al in "Conflations of Marital Status and Sanity: Implicit Heterosexist Bias in Psychiatric Diagnosis in Physician-Dictated Charts at a Midwestern Medical Center" (2016):

"Of equal relevance for this paper, links between normative gender roles and normative mental health also appeared as central components of late twentieth-century American medical and popular rhetoric surrounding prescription psychopharmaceuticals. For instance, Valium and other minor tranquilizers became widely known as 'mother’s little helpers' during the same era that psychiatry expunged homosexuality from the DSM. Doctors in the 1960s and 1970s prescribed tranquilizers to help women care for their husbands, play with their children, and cope with the pressures of white, middle class housewifery. One oft-cited ad from the Archives of General Psychiatry from the early 1970s showed a woman named Jan whose inability or refusal to attract a man by the age of 35 led her to seek psychiatric treatment.

"Starting in the late 1980s, rhetoric surrounding serotonin uptake inhibitor (SSRI) antidepressants promoted the notion that psychoactive drugs restored productive white maternity. Pharmaceutical advertisements featured white women whose successful pharmacotherapy was marked by wedding rings and children, or that quoted happy women who claimed, 'I got my playfulness back' while playing with infants. The SSRI era also saw the expansion of gender normativizing scripts about men and masculinity, though to a lesser extent than those that linked psychiatric treatment with women’s gender roles. These and other representations reinforce critiques of depression as a stereotypically white illness in the U.S. whose construction potentially excludes, silences, or effaces the 'suffering' or 'shame' of women of color."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918875/ [3588]

Syme and Hagen of Washington State University in Vancouver, writing in the American Journal of Biological Anthropology in 2019, think the whole topic of "disorders" needs an overhaul:

"Understanding the complex, multi-level mechanisms that underlie mental disorders, and cognition and behavior more generally, cannot be achieved by focusing only on the lowest mechanistic levels (e.g., molecules, neurotransmitters) (Sapolsky, 2018). Nor can we rely solely on the descriptive symptom-based approach to mental disorders epitomized by the DSM.

"We sketched a provisional evolutionary scheme that categorizes a group of relatively rare disorders, such as autism and schizophrenia, as disorders of development that involve dysfunctions of cognitive adaptations related to sociality and defenses against socioecological threats. These are highly heritable and probably caused, in large part, by genetic variants. There is a second group of disorders, such as Alzheimer's, that appear late in life and are probably explained by senescence. A third group of disorders, such as ADHD some eating disorders, might be explained by mismatches between modern and ancestral environments.

"A final group of disorders, such as anxiety, depression, and PTSD, have low heritability, are caused by adversity, and involve symptoms that seem to be adaptive responses to adversity. Because they are relatively common throughout adult life, they account for a substantial fraction of disease burden attributable to mental illness. These might not be disorders at all, however, but instead aversive yet adaptive responses to adversity. If so, this has several important implications. First, these conditions would largely indicate social problems, not medical ones, and therefore call for social, not medical, solutions. Research and social policy on these “disorders” should shift from altering brain chemistry to avoiding and mitigating adversity and resolving conflicts. Second, treatment would still be valuable, but could not ignore circumstances. A broken bone is a biological dysfunction, for example, but the physical pain it causes is not. Therefore, it would be unethical to provide pain medication without also setting the broken bone. Similarly, it would be unethical to suppress the psychic pain without addressing the source of adversity. Third, effective psychotropic medication that suppressed these emotions and behaviors would provide substantial benefits to those who are inconvenienced by them, raising the troubling specter of chemical forms of social control, which, at least in some cases, might already be occurring with the use of stimulants and other medications to treat ADHD."
https://onlinelibrary.wiley.com/doi/full/10.1002/ajpa.23965 [3648]

Selective truths meet perceived risk: the 7.7X likelihood of Covid in drunks eludes the headlines.

The Defendant asserts the population's legal right to these effects. The public have voted with their feet, and like the Ugandan chimps have found their own preventitive, ameliorative, and curative plants.

Without caring what the prohibitionists think, 354,845 Slovenians have essentially decided the risks of not being permitted cannabis - from feeling a bit pooped to dying from Covid - outweigh the alleged benefits of prohibition. To classify this number of people as mentally ill recalls the crusade against "feeble-mindedness" of the early 20th century.

In case it's necessary to state the obvious, the Defendant asserts the population's legal right to anti-Covid effects.

Ptuj Police treat all crime equally and so their ideal would be to take cannabis away from everyone equally.

Out of 1,366,751 tested cases in Slovenia, 9,914 died.
https://en.wikipedia.org/wiki/COVID-19_pandemic_death_rates_by_country [6003]

1,366,751 is nearly 138 times more than 9,914.

So your mortality odds were (and are) 137 to 1.

But for older cases the difference was huge. According to the CDC, as 27 April 2021 the reported case fatality ratios were 0.015%, 0.15%, 2.3%, and 17% for the age groups 0–17, 18–49, 50–74, and 75 or over, respectively.
https://www.cdc.gov/covid/php/surveillance/index.html [6004]

So the Defendant was in the 2.3% group in 2020, 7.39 times the all-age rate, with odds of dying of 42.5 to 1.

Now what if a hit man and a hit woman decided to do what they were told and were paying their bills by doing hits?

And what if they were paid to target a particular type of individual, but maybe their gun was bent or they were just too drunk to shoot straight, and they were only able to successfully complete their mission once in every 250 attempts...would you think that was too insignificant a problem to investigate?

And would it matter, in fact, if their 1 unlucky victim out of 250 murder attempts was dead after one day, or one month, or a year?

In fact the death rate 2.3%, from the 17.5% increase of cases you were attempting to procure, is 0.4025% of all the cases.

Thus the actual rate is 1 in 248.44 not 250.

How can we apply this to the Slovenian cases? We do not know how many of the 9,914 dead were lifetime cannabis users. But we can be sure that the Defendant was impeded in his lifetime use by the intervention of Mr T and his employers in September 2020.

They increased the Defendant's risk of infection by 17.5%. The risk of death in his age group was 2.3%. 0.4025% of a murder does not sound like much. But of course it is 100% of a murder for the victim.

To apply this to the 9,914 is not a straightforward sum. We are forced to trawl the known but varying estimates of usage among the population, which lie between 5.4% (use in the last 12 months) [5995] and the 66.71% supporters of "medical use" in the 2024 referendum.

We can therefore only guess that the impact of the hit man and her's intervention on mortality is a positive integer, since no one is claiming the usage in the population is 0%.

0.4025% of 1,366,751 is 5,501 cases, representing the maximum achievable hit rate if the Police are 100% successful in their aim.

Were the interdiction rate only 1% their hit rate would be 55.

Importantly for the judicial economy, the responsibility would be nobody's - because the perpetrators are merely somewhat educated middle class persons whose job in the prosecutors' office depends on following, not leading, thought on the hit man problem.

They were just trying to pay their bills and renovate their houses by covering their ears. If pushed, they would say that if that were true, other middle class people trying to pay their bills by practising medicine would have mentioned it.

Yet unless the referendum was unrepresentative of these folks, a large proportion would themselves take "drugs". They would all say they were against "drugs". All would hide behind a word.

Of course they are free to argue their innocence, and in the attempted murders also, as they are habituated to the idea that there can be no good things about bad things and there is no profit in such nuances or facts which only provoke thought - inimical to their continued ride on the drug war gravy train.

And to avoid any accusation of bias, this all applies equally to the Defendants' lawyers as well. Nothing can be proved against them, because they are the ones that did it. They are all accessories to this unknown positive integer number of murders, which we know must be true due to the levels of significance obtained.

With these ~55 insoluble murders per 1% of successful interdiction in mind, the Defence presents two possible routes by which cannabis ameliorates infection: directly by alleviating the cytokine storm, and indirectly via the attenuation in the population of opiate and alcohol addiction.

While the Prosecution can prove without difficulty that the ZPPPD predated Covid and that its authors and General Smuts could not possibly have known what we know now, the Court will observe that the true timeline is more nuanced.

Firstly, the cytokine storm's baptism postdates the presently-constituted Slovenia, initially appearing in connection with bone marrow transplant ejection in 1993. But it was SARS-1 (2003) which sealed its connection to coronavirus infection, followed by MERS-Cov (2012). By 2004 the signatures of the storm were well known.

Secondly, studies on cannabinoids dampening excessive immune responses and cytokine production began in the mid-to-late 1970s — roughly 15-20 years before the term "cytokine storm" was coined. It was called "immune suppression" or "immunomodulation" rather than cytokine storm specifically.

And thirdly, cannabis users but not never-users have known forever when it is time to smoke a cold or case of influenza better, an activity studiously ignored by the professions. The Defendant has known for 50 years.

Here we show the risks of not being permitted cannabis outweigh the benefits of prohibition for the bourgeoisie. Covid measures, after all, supposedly applied to everyone.

Death is not a matter in which the bourgeoisie can hold the population to ransom, require everyone to obtain a specific diagnosis or digital certificate, or oblige them to acquire survival materials from a particular place or in a particular way.

The Executive is merely wrong, to deny access to known health benefits. Only individual wussiness saves them.

CBD induces interferon expression and upregulates its antiviral signaling pathway. A cohort of human patients previously taking CBD had significantly lower SARSCoV-2 infection incidence of up to an order of magnitude relative to matched pairs or the general population.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7987002/ [219]

When asked in a virtual interview if the potential for NT-VRL inhalation to be used as a preventative for coronavirus infections suggests that smoking or vaping cannabis could have a similar effect, Eybna CEO and co-founder Nadav Eyal notes that it "is important to be careful to not jump to conclusions of this kind."

Of course he does. To which the Defendant says, you're too late. He admits, grudgingly, that if a clinical trial of the compound as a preventative for coronavirus infections is successful, "due to the fact that NT-VRL terpenes are also found in cannabis strains, it can be estimated that cannabis evaporation will also have some effectiveness."'
https://www.forbes.com/sites/ajherrington/2021/04/14/compounds-in-cannabis-show-promise-as-a-treatment-for-coronavirus-infections/ [220]

The importance of ignoring some old wives' tales and preventing infection is emphasised by Dr Divid Putrino, Director of Rehabilitation Innovation for the Mount Sinai Health System, and a Professor in the Department of Rehabilitation and Human Performance at the Icahn School of Medicine at Mount Sinai:

"We need to be very, very firm with our messaging that there is no such thing as a mild SARS-CoV-2 infection. There is no such thing as a SARS-CoV-2 infection that does NOT have prolonged consequences. Until we can fully understand the long-term effects of COVID and who is susceptible and who is not, the only thing that we can do to protect ourselves, our families, our immune systems in the long term is to avoid infection...

"Even mild COVID infections seem to affect the way that your natural killer cells attack infections. It seems to affect the way that our T-cells attack infections and protect us from infections. So, I think one of the notions that we actually need to challenge is that for the longest time we've told people that if you get an illness and you recover, it just makes you stronger. What we're seeing over and over again is that's not the case with COVID. Every time you get a COVID infection, your immune system seems to suffer. It's kind of like a boxer, every fight takes a little bit more out of them. And they're not getting stronger with every fight, they're not getting stronger with every hit that they take. Every single time there's an increased chance that something bad is going to happen to the immune system and I think that this influx of illness that we're seeing is related to that."
https://www.youtube.com/watch?v=heT5myyBkNA [3157]

A long Covid definition:



https://www.nationalacademies.org/our-work/examining-the-working-definition-for-long-covid [3158]

Data from Canada shows the risk of long Covid goes up with each new Covid infection:

"The potential impact of re-infections on the risk of developing or exacerbating pre-existing long-term symptoms is important considering the endemic nature of COVID-19. However, studies providing evidence of increased risk are limited in number and generalizability....Canadians reporting two known or suspected COVID-19 infections (25.4%) were 1.7 times more likely to report prolonged symptoms than those reporting only one known or suspected infection (14.6%), and those with 3 or more infections (37.9%) 2.6 times more likely."


https://www150.statcan.gc.ca/n1/pub/75-006-x/2023001/article/00015-eng.htm [3231]

Repeat infections and other brain traumas have effects greater than the sum of their parts:

"'Neuroimmune "priming" is an effect by which subsequent immune challenges – such as several infections in a row – can cause increasingly profound and protracted neuroinflammation,' said PolyBio co-founder and neuroimmunologist Dr. Michael VanElzakker. 'This means that multiple inflammatory challenges can add up to be greater than the sum of their parts. While this group used LPS which is the part of bacteria that drives inflammation, the phenomenon of priming also relates to other, non-infectious inflammatory challenges such as a concussion.'"
https://polybio.org/multiple-hit-model-shows-that-covid-protein-potentiates-subsequent-infection-related-neuroinflammation-and-other-physiological-problems/ [4955]

Federowski and Sutton (2023) encountered "Autonomic dysfunction and postural orthostatic tachycardia syndrome in post-acute COVID-19 syndrome", finding POTS in 30% of patients.

[pots 4956]
https://www.nature.com/articles/s41569-023-00842-w [4956]

Asymptomatic long covid falls outside the definition of long covid, with a range of effects in heart, brain, endocrine system, endothelial cells and blood vessels, and the immune system:

[longer covid 3211]
https://www.degruyter.com/document/doi/10.1515/mr-2024-0030/html [3211]

A large 2024 study of long covid in children found the following symptoms:

[long covid 3594]
https://www.medscape.com/viewarticle/long-covid-rates-kids-revised-upward-what-know-2024a1000hzi?form=fpf [3594]

Almulla et al (2025) in a meta-analysis of 44 studies encompassing 8,114 participants
(3,353 LC patients and 4,761 controls) found:

"LC patients exhibited significant elevations in Castelli Risk Indexes 1 (standardized mean difference, SMD = 0.199; 95% confidence intervals, CI: 0.087;0.312) and 2 (SMD = 0.202; 95% CI: 0.087;0.318). Atherogenic ratios, including triglyceride (TG)/high-density lipoprotein (HDL) (SMD = 0.294; 95% CI: 0.155;0.433), (TG + low-density lipoprotein, LDL + very low-density lipoprotein, VLDL)/(HDL + apolipoprotein, ApoA) (SMD = 0.264; 95% CI: 0.145;0.383), and ApoB/ApoA (SMD = 0.515; 95% CI: 0.233;0.796), were also significantly elevated. Additionally, LC patients demonstrated increased levels of LDL, total cholesterol, triglycerides, and ApoB, alongside reduced HDL and ApoA levels. Results were free from publication bias.

"Conclusion: LC is associated with a pro atherogenic lipid profile, marked by increased atherogenic components and decreased protective lipid biomarkers. These findings highlight a potential heightened risk for cardiovascular complications in LC patients, warranting further clinical and mechanistic investigations."
https://www.medrxiv.org/content/medrxiv/early/2025/01/06/2025.01.06.25320068.full.pdf [3876]

How long is long? The data is still coming in. From Peluso et al, "Tissue-based T cell activation and viral RNA persist for up to 2 years after SARS-CoV-2 infection" (2024):

"We performed whole-body positron emission tomography imaging in a well-characterized cohort of 24 participants at time points ranging from 27 to 910 days after acute SARS-CoV-2 infection using the radiopharmaceutical agent [18F]F-AraG, a selective tracer that allows for anatomical quantitation of activated T lymphocytes. Tracer uptake in the postacute COVID-19 group, which included those with and without continuing symptoms, was higher compared with prepandemic controls in many regions, including the brain stem, spinal cord, bone marrow, nasopharyngeal and hilar lymphoid tissue, cardiopulmonary tissues, and gut wall. T cell activation in the spinal cord and gut wall was associated with the presence of LC symptoms. In addition, tracer uptake in lung tissue was higher in those with persistent pulmonary symptoms specifically. Increased T cell activation in these tissues was also observed in many individuals without LC. Given the high [18F]F-AraG uptake detected in the gut, we obtained colorectal tissue for in situ hybridization of SARS-CoV-2 RNA and immunohistochemical studies in a subset of five participants with LC symptoms. We identified intracellular SARS-CoV-2 single-stranded spike protein–encoding RNA in rectosigmoid lamina propria tissue in all five participants and double-stranded spike protein–encoding RNA in three participants up to 676 days after initial COVID-19, suggesting that tissue viral persistence could be associated with long-term immunologic perturbations."
https://www.science.org/doi/10.1126/scitranslmed.adk3295 [3226]

Lage et al (2025) had a mean follow-up median of 4.1 months in "Persistent immune dysregulation and metabolic alterations following SARS-CoV-2 infection":

"Compared to the naïve controls, those with prior COVID-19 demonstrated profound metabolic and immune alterations at the proteomic, cellular, and epigenetic level. Specifically, there was an enrichment in immature monocytes with sustained inflammasome activation and oxidative stress, elevated arachidonic acid levels, decreased tryptophan, and variation in the frequency and phenotype of peripheral T-cells. Those with LC had increased CD8 T-cell senescence and a distinct transcriptional profile within CD4 and CD8 T-cells and monocytes by single cell RNA sequencing."

They recount:

"Inflammasomes, formed in the cytosol in response to pathogen- or damage-associated molecular patterns (PAMPs/DAMPs), activate pro-caspase-1, which processes IL-1β and IL-18 into their active forms and coordinates their secretion. Oxidative stress mediators, such as reactive oxygen species (ROS) and toxic lipid peroxides, also trigger inflammasomes, creating a feedback loop that promotes a systemic hyperinflammatory state. This hyperinflammation leads to tissue damage and is being explored as a target for host-directed therapies to reduce/mitigate COVID-19 complications.

"T-cells are also crucial in regulating COVID-19 pathogenesis, and disruptions in the adaptive immune system can affect acute responses to the virus. Delayed T-cell responses, caused by an uncoordinated innate and adaptive response, and sustained CD8 T-cell dysfunction have been linked to severe COVID-19. Prolonged inflammation and T-cell activation, marked by exhaustion indicators like PD-1 and TIM-3, also predict worse outcomes during acute COVID-19. Beyond the acute phase, improper adaptive immune responses contribute to LC, characterized by systemic inflammation, immune dysregulation, and abnormal CD4 and CD8 T-cell behavior. T-cell exhaustion and immunosenescence have also been linked with LC. For example, a pilot study in individuals recovering from COVID-19 found a connection between CD57 expression, a marker of cellular senescence and extensive proliferative history, on CD8 T-cells and the persistence of symptoms three months following SARS-CoV-2 infection, but this has not been further evaluated."

[Phenotypic changes in circulating monocyte subsets post-COVID-19 5093]

Among several findings...

"Gene set enrichment analysis (GSEA) identified distinct biological processes enriched in the T-cell compartment of LC indicating sustained activation. In CD4 T-cells, 12 pathways were significantly enriched in LC compared to RC (Figure 8A), including gene sets related to chromatin organization and immune response; specifically, multiple pathways related to immune activation including complement, humoral immunity, and signaling pathway activation. GSEA identified 21 pathways enriched in CD8 T-cells from LC individuals (Figure 8B), including pathways related to adhesion and chemotaxis, further supporting sustained activation in this subset. Apoptotic cell clearance was also significantly enriched in CD8 T-cells of those with LC, which may reflect an ongoing response to cellular turnover and tissue damage. Interestingly, within the monocyte compartment, numerous pathways were downregulated in LC compared to full recovery, including endocytosis, response to external stimuli, regulation of inflammatory responses, cytokine-mediated signaling pathway and myeloid activation (Figure 8C). This confirms a profoundly altered myeloid profile in LC."

[inflammasome activity and oxidative stress in monocytes from participants with and without prior COVID-19 5093]

A summary:

Persistent Immune Activation. Researchers found long-lasting elevation of pro-inflammatory cytokines in LC patients, including:
IL-6
TNF-α
IL-1β

These markers were still elevated 8 months after infection, indicating ongoing immune activation.

T Cell Exhaustion and Dysregulation:
The study identified dysfunctional T cell responses:
Reduced naïve T cells
Increased exhausted memory T cells
Altered regulatory T cell function

This may contribute to lingering symptoms and impaired immune recovery.

Metabolic Disruption:
Long COVID individuals showed major shifts in metabolites, including:
Decreased amino acids (glutamine, glycine).

Disrupted lipid metabolism:
Elevated kynurenine, a marker of chronic inflammation and fatigue.
https://pmc.ncbi.nlm.nih.gov/articles/PMC12047922/ [5093]

Ernst et al (2023) examined 54 subjects for "Neuronal and Glial Metabolite Abnormalities in Participants With Persistent Neuropsychiatric Symptoms After COVID-19: A Brain Proton Magnetic Resonance Spectroscopy Study":

"When compared with controls, the post–COVID-19 group had lower total N-acetyl compounds (tNAA; ACC-GM: −5.0%, P = .015; FWM: –4.4%, P = .13), FWM glutamate + glutamine (–9.5%, P = .001), and ACC-GM myo-inositol (−6.2%, P = .024). Additionally, only hospitalized patients post–COVID-19 showed age-related increases in myo-inositol, choline compounds, and total creatine (interaction P = .029 to <.001). Across all participants, lower FWM tNAA and higher ACC-GM myo-inositol predicted poorer performance on several cognitive measures (P = .001–.009), while lower ACC-GM tNAA predicted lower endurance on the 2-minute walk (P = .005)."

The University of Maryland team reported:

"Autopsy studies of patients and nonhuman primates with COVID-19 show prominent neuroinflammation and activated microglia. A mouse model evaluated acute and long COVID-19 seven weeks after infection and found persistent microglial activation, white matter (WM) myelin loss, and elevated cerebral spinal fluid (CSF) cytokines and chemokines. Additionally, patients with acute COVID-19 showed elevated plasma glial fibrillary acidic protein (GFAp; glial activation marker) and neurofilament light chain protein (NfL; neuronal damage marker). In recovered patients with COVID-19, plasma GFAp or NfL levels remained elevated at 4 months but normalized by 7 months.

Since glial and neuronal metabolites can be assessed noninvasively with proton magnetic resonance spectroscopy (1H-MRS), we used 1H-MRS to evaluate possible neuronal and glial metabolite abnormalities in patients with post–acute COVID-19 who had persistent neuropsychiatric symptoms. Neuronal injury or loss is associated with reduced neuronal metabolites: total N-acetyl-compounds (tNAA; N-acetylaspartate + N-acetylaspartyl-glutamate) and glutamate + glutamine (Glu + Gln). Neuroinflammation is typically shown by elevated glial marker myo-inositol (mI) and often concomitantly elevated choline compounds (Cho) and total creatine (tCr), due to their higher concentrations in glia than neurons. Multiple 1H-MRS studies not only showed age-related increases in glial metabolites but delineated neuronal injury and neuroinflammation in various viral infections, including HIV, John Cunningham virus, hepatitis C virus, Epstein-Barr virus, and cytomegalovirus. These metabolite abnormalities in patients with HIV or hepatitis C virus often predicted disease severity and correlated with clinical variables."

Brain metabolite levels associated with long Covid predicted cognitive, motor performance, and pain levels. Lower metabolite levels persisted long term, "suggesting that neuronal injury or loss and glial abnormalities are either irreversible or still present", and varied by Covid-9 severity. The authors discuss iron dyshomeostasis–mediated oxidative damage, and quoting Peluso et al and Needham et al (both 2022) consider longitudinal evidence showing that:

"Four months after COVID-19 diagnosis, elevated NfL was present only in those with moderate to severe COVID-19, while higher GFAp was observed in patients who had long COVID-19 with persistent neurologic symptoms."
https://academic.oup.com/jid/article/228/11/1559/7237266?login=false [5748]

In "Exploring the Relationship Between Cannabis Use And COVID-19 Outcomes" from Wei et al at Northwell Health, New York (2024):

"National Inpatient Sample Database was used to sample individuals admitted with the diagnosis of COVID-19. Patients were divided into two groups based on cannabis use. Baseline demographics and comorbidities were collected using ICD-10 codes. Patients with missing data or age under 18 were excluded. Propensity matching using R was performed to match cannabis users to non-cannabis users 1:1 on age, race, gender, and 17 other comorbidities. The primary outcome was severe COVID-19 infection, defined as a composite of acute respiratory failure, intubation, acute respiratory distress syndrome (ARDS), or severe sepsis with multiorgan failure. Results: Out of 322,214 patients included in the study, 2,603 were cannabis users. Cannabis users were younger and had higher prevalence of tobacco use. On initial analysis, cannabis users had significantly lower rates of severe COVID-19 infection, intubation, ARDS, acute respiratory failure, severe sepsis with multiorgan failure, mortality, and shorter length of hospital stay. After 1:1 matching, cannabis use was associated with lower rates of severe COVID-19 infection, intubation, ARDS, acute respiratory failure, severe sepsis with multiorgan failure, mortality, and shorter length of hospital stay. Conclusion: Cannabis users had better outcomes and mortality compared with non-users. The beneficial effect of cannabis use may be attributed to its immunomodulatory effects."
https://pubmed.ncbi.nlm.nih.gov/39194156/ [4758]

In their massive 2024 multicenter retrospective observational cohort analysis of adults (≥ 18 years-old) Igwe and Alaribe analysed a staggering 1.7 million COVID-19-related hospitalisations, revealing a stark contrast: only 1.56% of cannabis users were hospitalised, compared to 6.29% of non-users.

That's a difference of 4730 human lives in our hypothetical stadium of 100,000 law-abiding citizens.

"There were 1,698,560 Covid-19-related hospitalizations which were associated with higher mortality (13.44% vs 2.53%, p ≤ 0.001) and worse secondary outcomes generally. Among all-cause hospitalizations, 1.56% of CU and 6.29% of N-CU were hospitalized with Covid-19 (p ≤ 0.001). ACU [active cannabis use] was associated with lower odds of MV [mechanical ventilation] and acute pulmonary embolism, PE, and death among the Covid-19 population. On PSM [propensity score matching], ACU(N(unweighted) = 2,382) was associated with 83.97% lower odds of death compared to others(N(unweighted) = 282,085) (2.77% vs 3.95%, respectively; aOR:0.16, [0.10–0.25], p ≤ 0.001)."

Active cannabis users showed significantly lower rates of needing medical ventilation, developing lung blood clots, and succumbing to COVID-19.

Applying the aOR of 0.16 to Ptuj's active cannabis users, who are so stupid because they don't believe the NIJZ or similar "authorities", we can easily calculate an expected (100/16*100)-100 = 525% increased mortality rate in those whose cannabis is stolen by the Police or Mr Teodorović and his friends, if they are unable to replace it. For definition of active use see the Methods.

This calculation could similarly be applied to the patients of any particular clinic or doctor that refused to prescribe this successful preventative for them.

"Of note, the mortality rate among Covid-19-Ob-DM [obesity with complicated diabetes] was significantly lower for CU (N = 640) compared to N-CU (N = 145,390) (6.25% vs 15.99%, p ≤ 0.001)."

By performing the calculation (15.99/6.25*100)-100 we can therefore see that Ptuj Police taking away cannabis from Ob-DM users increases their chances of mortality in these circumstances by 155.84%. [4567]

Wei et al (2025) emphasise the importance of the peroxisomes in alleviating viral lung injury in "Macrophage peroxisomes guide alveolar regeneration and limit SARS-CoV-2 tissue sequelae":

"Severe COVID-19 significantly remodeled the peroxisome compartment, reducing the number of peroxisomes in mouse lung macrophages, as revealed by bioinformatic and immunofluorescence analyses. We found that increased interferon signaling, especially IFNγ signaling, inhibited peroxisome biogenesis and promoted peroxisome degradation through pexophagy (autophagy of peroxisomes) in macrophages. Mouse models with selective depletion of macrophage peroxisomes demonstrated that peroxisomes were essential for resolving inflammation and promoting alveolar regeneration after severe viral injury. Mechanistically, peroxisomes exhibited cell type–specific modulation of lipid metabolism, enhancing mitochondrial health and supporting macrophage repair programs for the self-renewal of alveolar type 2 (AT2) cells. Macrophage peroxisome dysfunction, however, led to increased inflammasome activation and excessive IL-1β release by means of the Gasdermin D pore. Persistent IL-1β production subsequently caused the accumulation of dysplastic KRT8 transitional epithelial progenitors in the lung, driving chronic tissue pathology and fibrotic remodeling following acute SARS-CoV-2 infection. Chronic peroxisome impairment was observed in the lungs from human patients with PASC pulmonary fibrosis and relevant mouse models. Notably, in our mouse models, pharmacological enhancement of peroxisome biogenesis using sodium 4-phenylbutyrate (4-PBA) restored peroxisome function in macrophages, mitigated lung inflammation and fibrosis, and enhanced alveolar regeneration after viral infection."
https://www.science.org/doi/10.1126/science.adq2509 [4822]

Although marijuana's potency against the cytokine storm via PPAR-γ seems to have been lost on Ciavarella et al at the University of Bologna, they are able to remind us that besides the man-made pharmacological interventions such as TZDs,

"...also nutritional ligands of PPAR-γ, like curcuma, lemongrass, and pomegranate, possess anti-inflammatory properties through PPAR-γ activation."
https://www.mdpi.com/1420-3049/25/9/2076/htm [939]

So with the enactment of the ZPPPD Slovenia invented a deadly anti-nutrition law, reducing the number of compounds available over the counter to address this need. Does Slovenia want to ban these other Asiatic compounds? Why not?

If you don't want the public to think that prohibition is all a plot by big pharma, don't go around depriving them of a plausible treatment in the midst of a respiratory virus pandemic.

In January 2022, van Breemen et al at Linus Pauling and the Oregon Health and Science Institute reporting findings of Wang Q et al of the CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences that:

"Recently, the crystal structure of the C-terminal domain of the SARS-CoV-2 spike protein in complex with the human ACE2 receptor was solved. The key interactions involve residues along the spike protein C-terminal domain interface that contribute to a network of hydrogen bonding and salt-bridge interactions with the ACE2 receptor. The residues on the spike protein involved in the binding to ACE2 include A475, N487, E484, Y453, K417, G446, Y449, G496, Q498, T500, G502, Y489, and F486. The interaction of the virus with the ACE2 receptor is mainly contributed by the polar interactions resulting from hydrophilic residues on the surface of the spike protein C-terminal domain."

They go on to explain:

"In the AutoDock Vina docking program, the ligand docking in the active site is based on algorithms that take into consideration the steric, hydrophobic bonding, and hydrogen bonding interactions between the ligand and active site residues. The best predicted binding conformation should have the lowest free energy of binding (kcal/mol). CBGA gave the lowest free energy of binding (−6.7 kcal/mol) to an allosteric site, with a root-mean-square deviation of 24.3 from the orthosteric site. On the other hand, THCA-A and CBDA had slightly higher energies of binding at −6.5 and −6.3 kcal/mol, respectively. Overall, the MagMASS data show that CBGA binds to the spike protein S1 subunit strongly in cannabinoid mixtures, suggesting that it binds allosterically and does not compete for binding with orthosteric cannabinoid ligands.

"Variants of the SARS-CoV-2 virus such as B.1.1.7 and B.1.351 include amino acids in the spike protein S1 subunit that interact with the ACE2 receptor. For example, the N501Y mutation was identified by bioinformatics analysis of data derived by metagenomics sequencing of samples obtained from a patient with persistent SARS-CoV-2 infection. Other highly infectious variants identified that include mutation of the active site residues include N501T, K417, and E484 K (Figure 44). With the rapid mutations occurring, a novel inhibitor capable of binding to an orthosteric site would be of great interest in the intervention of SARS-CoV-2 variants characterized by active site mutations.

"Our infection inhibition assay results clearly indicate that CBDA and CBGA are both able to block cell entry by SARS-CoV-2. The concentrations needed to block infection by 50% of viruses is high but might be clinically achievable."
https://pubs.acs.org/doi/10.1021/acs.jnatprod.1c00946 [1117]

In an interview for Patients for Medical Cannabis Dr Richard van Breemen favours oral prophylactic administration over smoking, one reason being heat degradation of the constituents he considers useful.

"In answer to one of my grant reviews, we have established the principle that small molecules CAN prevent viral infection. So that, I believe, is an important sort of basic science discovery. Secondly, we found compounds in hemp that have, at least in cell culture with live virus, the ability to stop cells from being infected. I would love to see a follow up study where we start developing what the oral dose ought to be. How can we maintain how many doses per day and what level do we need to help prevent viral infection or transmission? And I think we have a product that should be safe to use eventually. I can envision hemp extracts being used to help people stay healthy and help stop them getting sick from COVID."
https://patients4medicalmarijuana.wordpress.com/2022/01/15/qa-with-scientist-who-discovered-cannabis-can-prevent-covid-19/ [2742]

And to take one example of a spike protein mutation:

"E484K is called an escape mutation because it helps the virus slip past the body's immune defences. Ravindra Gupta at the University of Cambridge and colleagues have confirmed that the new B.1.1.7 plus E484K variant substantially increases the amount of serum antibody needed to prevent infection of cells."
https://www.bmj.com/content/372/bmj.n359 [1121]

The N501Y and K417N mutations, meanwhile, enhance the transmissibility of the virus.
https://www.news-medical.net/news/20220317/Novel-screening-method-detects-new-N501T-SARS-CoV-2-variant.aspx [1122]

In other words, NECUD from any cause including illegality presents a real risk of increased susceptibility to Covid infection. The Court will recall that in 1995 it was established by Taura et al that CBD and THC are formed by decarboxylation of the acidic forms of these molecules (CBDA and THCA), the form in which they are originally synthesized in the plant. CBDA and THCA are separately generated by enzymatic reactions from their common precursor, CBGA.
https://pubs.acs.org/doi/pdf/10.1021/ja00143a024 [1118]

We have a diagram of that:

[cbga cbda 1119]

The alert seeker after truth will enquire, what then is the quantitative relationship between these molecules from different points in the pathway in the final product? For such insights the Defence refers him to an analysis of different strains available through the New Jersey Medical Marijuana Program which reported in 1999 that:

"...the overwhelmingly [sic] majority of strains contain only trace (< 1%) CBDA but high THCA concentration; a handful are balanced in CBDA and THCA content; and a very few strains have a high concentration of CBDA and minimal THCA (< 1%). In those strains that contain more than 1% of both THCA and CBDA, those two substances are present in comparable quantities. The concentration of CBGA is higher in those strains that have the highest THCA concentration, though there are strains that have high THCA (> 20%) with CBGA concentrations at the low end of the range (< 0.5%). In the high CBD strains, the concentration of CBGA is positively correlated with CBDA, but the CBGA concentrations are several fold less in CBD-dominant strains than in THC-dominant strains: the highest measured CBGA concentration in a CBD-dominant strain is only at the average value of CBGA concentration in THC-dominant strains. The most-recently tested strains are overwhelmingly of the THC-dominant type."

And they concluded:

"Though some high CBD strains are available in the New Jersey medical marijuana program, the vast majority of strains that have been tested are the THC-dominant strains which contain less than 1% CBDA. The data available from the State does not include any information on how well the different strains sell, but it can be inferred from the trend in strain types tested that the demand in the New Jersey medical market is for THC-dominant strains."
https://jcannabisresearch.biomedcentral.com/articles/10.1186/s42238-019-0011-z [1119]

There is all the information needed to show that high THC cannabis also contains a higher amount of CBGA and therefore a greater reduction of Covid infection susceptibility. And "the concentration of CBGA is positively correlated with CBDA".

The statistics show that long term cannabis users have immunised themselves against Covid.

Finally, and leaving aside the benefits of THC per se, what is the legal justification for preferring to not die, via the use of CBGA and CBDA, contained in cannabis along with psychoactive substances? There is no licence for CBGA or CBDA as therapeutic compounds in Slovenia, therefore the only way to get them would be via CBD products, which as we saw are likely to be lower in CBGA, or via THC-containing products. With an effective dose only partially within reach, it is a simple choice between NECUD and mild NECUD.

For reckless, suicidal Slovenians terrified about how others will denigrate them, the only dilemma remaining is the very difficult decision whether to get high or die. What each chooses for themself may differ from what they choose for others, of course.

As a potential SARS or ARDS patient the Defendant has no difficulty in assessing that the evidence demonstrates that restriction of availability on the grounds of psychoactivity is actually an anti-health measure in this field.

Had the Defendant been born in 1925 he would be 100 and still waiting for the medico-legal system to discover its way back to normality. As it is the Defendant has only been waiting since 1973.

 "Cannabis consumption is associated with lower COVID-19 severity among hospitalized patients: a retrospective cohort analysis" is the title of an August 2022 paper by UCLA researchers Carolyn M Shover and colleagues.
 
"Of 1831 patients admitted with COVID-19, 69 patients reported active cannabis use (4% of the cohort). Active users were younger (44 years vs. 62 years, p < 0.001), less often diabetic (23.2% vs 37.2%, p < 0.021), and more frequently active tobacco smokers (20.3% vs. 4.1%, p < 0.001) compared to non-users. Notably, active users had lower levels of inflammatory markers upon admission than non-users—CRP (C-reactive protein) (3.7 mg/L vs 7.6 mg/L, p < 0.001), ferritin (282 μg/L vs 622 μg/L, p < 0.001), D-dimer (468 ng/mL vs 1140 ng/mL, p = 0.017), and procalcitonin (0.10 ng/mL vs 0.15 ng/mL, p = 0.001). Based on univariate analysis, cannabis users had significantly better outcomes compared to non-users as reflected in lower NIH scores (5.1 vs 6.0, p < 0.001), shorter hospitalization (4 days vs 6 days, p < 0.001), lower ICU admission rates (12% vs 31%, p < 0.001), and less need for mechanical ventilation (6% vs 17%, p = 0.027). Using propensity matching, differences in overall survival were not statistically significant between cannabis users and non-users, nevertheless ICU admission was 12 percentage points lower (p = 0.018) and intubation rates were 6 percentage points lower (p = 0.017) in cannabis users."
 
Covariants considered in the study included diabetes mellitus, cardiac disease, chronic kidney disease, chronic lung disease, and liver disease reported at time of admission.
https://jcannabisresearch.biomedcentral.com/articles/10.1186/s42238-022-00152-x [1519]
 
In "Serum IgG4 level predicts COVID-19 related mortality" Della-Torre et al spell it out:
 
"At baseline, IgG1, IgG2, IgG3, IgG4 subclasses were elevated in 8 (6%), 6 (5%), 6 (5%), and 13 (10%) patients, respectively. Thirty patients (23%) died at 30-days follow-up. As shown in Table 1 and Fig. 1A, age, C-reactive protein (CRP), interleukin (IL)-6 serum IgG4 level, IgG4/IgG ratio, and IgG4/IgG1 ratio were significantly higher in non-survivors, while the PaO2/FiO2 ratio was significantly lower in survivors. Receiving operating curves (ROC) curves of statistically significant variables were created to predict mortality at 30 days. The AUC for age, serum IgG4, IgG4/IgG and IgG4/IgG1 ratio was 0.78 (95%CI 0.69-0.97), 0.63 (95%CI 0.51-0.75), 0.66 (95%CI 0.55-0.76), and 0.65 (95%CI 0.53-0.77), respectively (p<0.05 for all the analyses). At logistic regression analysis, all variables were significantly associated with a poor outcome but only age, CRP, and the IgG4/IgG1 ratio represented independent predictors of 30-days mortality at multivariate analysis (Table 1). Specifically, a concentration of serum IgG4 > 700 mg/dl and an IgG4/IgG1 ratio > 0.05 were associated with a significantly increased mortality at 30-days (Fig. 1B). Of note, a significantly positive correlation was found between serum IgG4 and IL-6 level, an established predictor of COVID-19 related mortality (Fig. 1C)."

[igg crp 5014]
https://www.ejinme.com/article/S0953-6205(21)00312-5/fulltext [5014]

About the NIH COVID-19 severity score, it is a modified version of the earlier National Early Warning Score 2 (NEWS2). NEWS2 is a diagnostic system used on hospital admission for patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6542226/ [1520]

It is

"...a scale which...classifies disease severity from 1 (not hospitalized, no limitations) to 8 (death)...Secondary outcomes included need for supplemental oxygen, ICU admission, mechanical ventilation (including duration thereof), length of hospitalization and in-hospital death."

The parameters of the COVID-19 severity score are shown in Figure 1 at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7832368/ [1521]

[covid 19 severity score 1521]

In "Exploring the relationship between marijuana smoking and covid-19 outcomes" published in Chest Journal in 2023, Siddiqui et al showed that

"Out of 322,214 patients included in the study, 2,603 were marijuana users. Marijuana users were younger and had higher prevalence of tobacco use. However, other comorbidities including obstructive sleep apnea, obesity, hypertension, and diabetes mellitus were more prevalent in marijuana non-users. On univariate analysis, marijuana users had significantly lower rates of intubation (6.8% vs 12%), acute respiratory distress syndrome (ARDS) (2.1% vs 6%), acute respiratory failure (25% vs 52.9%) and severe sepsis with multiorgan failure (5.8% vs 12%). They also had lower in-hospital cardiac arrest (1.2% vs 2.7%) and mortality (2.9% vs 13.5%). After 1:1 matching, marijuana users had lower rates of intubation (OR: 0.64 [0.51-0.81]; p<0.01), ARDS (OR: 0.39 [0.26-0.58]; p<0.01), acute respiratory failure (OR: 0.53 [0.47-0.61]; p<0.01), severe sepsis with multiorgan failure (OR: 0.68 [0.52-0.89]; p<0.01) and lower mortality (OR: 0.48 [0.33-0.69]; p<0.01)

"CONCLUSIONS: Marijuana smokers had better outcomes and mortality compared to non-users. The beneficial effect of marijuana use may be attributed to its potential to inhibit viral entry into cells and prevent the release of proinflammatory cytokines, thus mitigating cytokine release syndrome."
https://journal.chestnet.org/article/S0012-3692(23)02201-8/fulltext#%20 [3079]

Sleep apnea is mentioned here. It can be fatal with or without Covid, as shown by Lavie et al in the European Respiratory Journal in 2005:

"The crude all-cause mortality rate was 5.55/1,000 patient-yrs, and increased with RDI (p<0.009 for trend; table 2⇓). The highest mortality rate (11.47/1,000 patients-yrs) was observed in the obese group (BMI ≥31.0) with RDI >40. Regression analysis revealed a significant linear increase in crude mortality in males at their recommended weight (test for trend p<0.02), and for the obese (p<0.05). A borderline significant linear trend was found for the overweight (p<0.08)."
https://erj.ersjournals.com/content/25/3/514 [4592]

In the largest study to date "Obstructive Sleep Apnea Patients in the Minnesota Medical Cannabis Program" (2025) - apnea was added to Minnesota's list of qualifying conditions in 2018 - reported after five years:

[apnea thc cbd ratios 5006]

Patients who experienced >=30% symptom improvement and retained that degree if imporovement for at least four months amounted to 36.7% for anxiety, 44.2% for  appetite lack, 39.8% for depression, 39.4% for disturbed sleep, 33.5% for fatigue, 44.8% for nausea, 23.1% for pain, and 53% for vomiting (Table 4.1).
https://mn.gov/ocm/assets/Obstructive_Sleep_Apnea_Report_2025_tcm1202-683956.pdf [5006]
 
With or without Covid, what do the comorbidities of sleep apnea have to do with Ptuj's Town Smell? According to Alrahbeni et al (2024) exposure to persistently high levels of air pollution can cause systemic inflammation or inflammation throughout the body, and oxidative stress, potentially leading to or worsening upper airway dysfunction during sleep:

"The systematic review included twelve studies, four of which were analyzed in the meta-analysis. The meta-analysis revealed diverse results on the association of PM2.5 and NO2 with OSA [obstructive sleep apnea] risk. PM2.5 exposure showed a pooled OR of 0.987 (95% CI: 0.836 to 1.138), indicating no substantial overall impact on OSA risk. Conversely, NO2 exposure was linked to a pooled OR of 1.095 (95% CI: 0.920 to 1.270), a non-significant increase in risk. Many studies found a relationship between air pollution exposure and elevated Apnea-Hypopnea Index (AHI) levels, indicating a relationship between air pollution and OSA severity."
https://www.sciencedirect.com/science/article/pii/S0161813X24000366 [4591]

Ptuj does of course have traffic and therefore some NO2. However, many specific pollutants sui generis to rendering emissions and which we expect would be found in the Town Smell during any secret public health investigations of this air are not considered by these studies.

[new smell]

It might appear from a cursory investigation that rendering emissions have nothing to do with NO2, however about 10% of rendered products is nitrogen, as shown in this table from the North American Renderers' Association. The aim is to capture this in the form of protein, in which respect the Defendant is sure the factory is mostly successful.

[nra no2 4592]

VOCs are associated with sleep apnea. In two different models, only one out of thirteen VOCs had a positive effect on trouble sleeping, while in one model only one out of fifteen VOCs had a beneficial association with short sleep duration (SSD), and zero out of fifteen in Model 2. See Table 2 of "Association between Exposure to Volatile Organic Compounds and the Prevalence of Sleep Problems in US Adults" by Sun et al (2024).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10976002/ [4593]

According to ApneaMed:

"A study conducted by researchers at the University of Illinois in 2002 discovered that medical marijuana improved the breathing patterns in rats with sleep apnea. Following this study, there was a human trial done in 2013 to look at how humans reacted to medical marijuana as a treatment for sleep apnea and found an improvement in the reduction of sleep apnea symptoms. Although these studies are still in the early stages, researchers believe there is promising evidence that medical marijuana can alleviate sleep apnea symptoms in patients with mild to moderate conditions.

"Following these promising study results of fewer episodes of shallow breathing and apneas throughout the night, the Minnesota Department of Health approved medical cannabis to treat sleep apnea in 2017."

However the American Academy of Sleep Medicine holds back on supporting its use for apnea because it is hung up on standardisation, formulae and a bias towards synthetic cannabinoids.
https://www.apneamed.org/blogs/info/sleep-apnea-and-medical-marijuana [4594]

Slovenia of course is not bound by the American Academy of Sleep Medicine. Nor is the approval of an inferior artificial product over a natural one of much interest to breathers of air.

Preventing wider access to marijuana per the provisions of the ZPPPD would increase the risk of death involving sleep apnea contrary to ECHR Article 2.

As an indicator of prohibition's slovenly approach to the medical consequences, the Police do not enquire whether any Defendants or witnesses against them had apnea before taking their cannabis away for reasons they have not stated.

Therefore the Police have implemented a medical intervention without an examination, diagnosis, rationale, or follow-up by taking cannabis away, with potentially fatal consequences. And not by this route alone.

Nobody is suggesting breathing VOCs is helpful in any way in any health condition, of which sleep apnea is but one example. Just to emphasise how legally obtuse this everyday situation is, residents have no power to compel the Town Smell to cease infilitrating their nostrils. Yet it is against the law for them to sell each other a useful, or at least harmless, treatment.

As it appears from the evidence that air pollution is associated with OSA, which can be fatal, while cannabis is associated with improved sleep and less sleep apnea, which cannot be fatal, and whereas cannabis prohibition is associated with death, imprisonment, impoverishment and other unhealthy outcomes, and whereas Slovenian authorities have not shown a negative outcome from cannabis in apnea, the Defence contends that the savvy person in the zone of the Ptuj aroma, assuming they wish to maximise their survival chances, will close their windows and use marijuana to reduce oxidative stress and inflammation in their upper airway.

In the Lancet, in two groups previously hospitalized for Covid were followed up at 1 year by the PHOSP-COVID Collaborative Group (2022):

"After adjustment for age, BMI, and comorbidity count, 13 proteins were significantly increased in participants in the very severe recovery cluster compared with those in the mild cluster (appendix p 33; figure 3). These proteins were trefoil factor 2 (TFF2), transforming growth factor α (TGFA), lysosomal associated membrane protein 3 (LAMP3), CD83 molecule (CD83), galectin-9 (LGALS9), urokinase plasminogen activator surface receptor (PLAUR), interleukin-6 (IL-6), erythropoietin (EPO), FMS-related receptor tyrosine kinase 3 ligand (FLT3LG), agrin (AGRN), secretoglobin family 3A member 2 (SCGB3A2), follistatin (FST), and C-type lectin domain family 4 member D (CLEC4D; appendix p 33). Additionally, IL-6 and CD70 molecule were significantly increased in the moderate with cognitive impairment cluster compared with the mild cluster (appendix p 34)."
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(22)00127-8/fulltext [4545]

More on Covid and the interferon response:
https://www.nature.com/articles/s41586-024-07575-x [3197]

Kammerer et al (2024) found autoimmune-triggering DNA in Covid vaccines used in Germany.

"We demonstrated that transfection of the human cell line HEK293 with four different BNT162b2 lots results in the production of spike proteins over several days, which are released into the cell supernatant via exosomes. We detected residual plasmid-DNA in all vials at concentrations far exceeding the allowed EMA limit of 0.33 ng dsDNA per 1 mg RNA. We identified all plasmid genes as well as the two copies of the SV40 promoter/enhancer element. The DNA was shown to enter and persist in the cells."
https://publichealthpolicyjournal.com/biontech-rna-based-covid-19-injections-contain-large-amounts-of-residual-dna-including-an-sv40-promoter-enhancer-sequence/ [3752]

Where we are at in our relationship with respiratory infections, air pollution, cytokines and cannabis is not merely a matter of illnesses come and gone. It is a permanent change of biologic status.

In contrast with influenza A virus, "SARS-CoV-2 infection in hamsters and humans results in lasting and unique systemic perturbations after recovery", say Frere et al (2022):

"Results demonstrated that SARS-CoV-2 exceeded IAV in its capacity to cause permanent injury to the lung and kidney and uniquely affected the olfactory bulb (OB) and olfactory epithelium (OE). Despite a lack of detectable infectious virus, the OB and OE demonstrated myeloid and T cell activation, proinflammatory cytokine production, and an interferon response that correlated with behavioral changes extending a month after viral clearance. These sustained transcriptional changes could also be corroborated from tissue isolated from individuals who recovered from COVID-19. These data highlight a molecular mechanism for persistent COVID-19 symptomology..."

and

"Given that long COVID may also involve neurological and neuro-psychiatric symptomology, we next assessed the consequences of SARS-CoV-2 infection on the nervous system. For these studies, we transcriptionally profiled several areas of the nervous system from 3 and 31 dpi [days post infection] cohorts. More specifically, the areas surveyed included the olfactory bulbs (OBs), medial prefrontal cortex (mPFC), striatum, thalamus, cerebellum, and trigeminal ganglion (tissues collected as depicted in Fig. 4A). These areas were chosen either because of their previously documented positivity for SARS-CoV-2 transcripts in human patients (OB and trigeminal ganglion) or because of their functional  importance in sensory, motor, cognitive, or affective processes—all of which have been noted to be altered in subsets of patients with long COVID. Matched tissues from hamsters infected with IAV were also collected for comparison. After tissue processing, brain regions from 3 dpi were surveyed for the presence of viral RNA. As expected, in hamsters infected with IAV, no viral RNA could be detected from the surveyed neural tissue that aligned to the IAV genome (fig. S4A). In contrast, within the SARS-CoV-2–infected hamster cohort, viral reads were readily detectable in the nervous system in a subset of animals, consistent with the findings of others. In one hamster, SARS-CoV-2 reads were detectable in all surveyed regions of the nervous system (Fig. 4B)."
https://www.science.org/doi/epdf/10.1126/scitranslmed.abq3059 [4561]

Confirming the increase in astrogliosis in Covid, which cannabis counteracts [1543, 4542], "SARS-CoV2 infection triggers inflammatory conditions and astrogliosis-related gene expression in long-term human cortical organoids" say Colinet et al (2025):

"SARS-CoV2, severe acute respiratory syndrome coronavirus 2, is frequently associated with neurological manifestations. Despite the presence of mild to severe CNS-related symptoms in a cohort of patients, there is no consensus whether the virus can infect directly brain tissue or if the symptoms in patients are a consequence of peripheral infectivity of the virus. Here, we use long-term human stem cell-derived cortical organoids to assess SARS-CoV2 infectivity of brain cells and unravel the cell-type tropism and its downstream pathological effects. Our results show consistent and reproducible low levels of SARS-CoV2 infection of astrocytes, deep projection neurons, upper callosal neurons and inhibitory neurons in 6 months human cortical organoids. Interestingly, astrocytes showed the highest infection rate among all infected cell populations that led to changes in their morphology and upregulation of SERPINA3, CD44 and S100A10 astrogliosis markers. Further, transcriptomic analysis revealed overall changes in expression of genes related to cell metabolism, astrogliosis and, inflammation and further, upregulation of cell survival pathways. Thus, local and minor infectivity of SARS-CoV2 in the brain may induce widespread adverse effects and lead to resilience of dysregulated neurons and astrocytes within an inflammatory environment."
https://academic.oup.com/stmcls/advance-article/doi/10.1093/stmcls/sxaf010/8086416?login=false [4846]

According to Parks and Smith (2020):

"The SARS-CoV-2 genome encodes approximately 25 proteins that are needed by the virus to infect humans and to replicate."
https://www.nejm.org/doi/pdf/10.1056/NEJMcibr2007042?articleTools=true [4722]

Aswad et al (2022) found "High-CBD Extract (CBD-X) Downregulates Cytokine Storm Systemically and Locally in Inflamed Lungs":

"Our investigation revealed that CBD-X extract impaired T-cell migration induced by the chemoattractant SDF1. In addition, the phosphorylation levels of T cell receptor (TCR) signaling proteins Lck and Zap70 were significantly reduced, demonstrating an inhibitory effect on the early events downstream to TCR activation. In a lung inflamed mouse model, we observed a reduction in leukocytes including neutrophil migration to the lungs and decreased levels of IL-1β, MCP-1, IL-6 and TNFα, in response to the administration of the high-CBD extract."
https://www.frontiersin.org/articles/10.3389/fimmu.2022.875546/pdf [3974]

Which is just as well, as according to "Gastrointestinal Barrier Disruption in Post-COVID Syndrome Fatigue Patients" from Rohrhofer et al (2025):

"Epithelial barrier damage leads to alarmin release and inflammation, as epithelial cells secrete proinflammatory cytokines. To detect signs of chronic low-grade inflammation in PCS Fatigue patients, the pro-inflammatory and intestinal barrier integrity-related cytokines IFN-γ, TNF-α, IL-6, IL-1-β, IL-8, and IL-33 were measured in serum samples. A significant elevation in IL-6 levels and a reduction in serum TNF-α and IL-1-β levels were observed in PCS Fatigue patients (Figure 2A–C)."
https://onlinelibrary.wiley.com/doi/10.1111/all.16593 [5038]

Besides its influence as a comorbidity up to a Covid diagnosis, the presence of extra new diagnoses of diabetes following the infection has also been quantified.

In a large cohort 2023 study Tesch et al found "Incident autoimmune diseases in association with a SARS-CoV-2 infection", with new 3-15 month diagnoses up by as much as 55% for Celiac Disease, 42% for rheumatoid arthritis, 25% for diabetes type 1, 24% for primary biliary cirrhosis, 17% for psoriasis, and other autoimmune conditions as shown in their Table 2.

Only 1 out of 40 categories tested showed an incidence rate ratio (IRR) below 1.

[autoimmune after covid 3103]

Greatest risk by group was to the under-18s. The risk of new autoimmune for outpatients was higher than the 80+ group.

[autoimmune after covid young and outpatients 3103]

"In total, 641,704 patients with COVID-19 were included. Comparing the incidence rates in the COVID-19 (IR=15.05, 95% CI: 14.69-15.42) and matched control groups (IR=10.55, 95% CI: 10.25-10.86), we found a 42.63% higher likelihood of acquiring autoimmunity for patients who had suffered from COVID-19. This estimate was similar for common autoimmune diseases, such as Hashimoto thyroiditis, rheumatoid arthritis, or Sjögren syndrome. The highest IRR was observed for autoimmune disease of the vasculitis group. Patients with a more severe course of COVID-19 were at a greater risk for incident autoimmune diseases."

The follow-up period ended prior to widespread vaccine availability, and in 2023:

"According to current knowledge, autoimmunity following viral infection may be triggered by mechanisms such as epitope spreading, bystander activation, molecular mimicry, and cryptic epitopes. SARS-CoV-2 shares characteristics of other viruses associated with the development of autoimmunity. Acosta-Ampudia and Anaya summarized these hypotheses as follows. 1. Superantigen activity: The S protein of SARS-CoV-2 contains sequence and structure motifs similar to those of a bacterial superantigen and can bind directly to the T-cell receptor. 2. Molecular mimicry: Accumulating evidence demonstrates that the virus has structural similarity to host-derived components. 3. Neutrophil extracellular trap (NET) formation. 4. Type I interferon (IFN) response. 5. 'Overt immunity' which describes the appearance of multiple autoantibodies and diverse autoimmune diseases that are significantly associated with SARS-CoV-2. These mechanisms are in line with several serological studies demonstrating the onset of IgG autoantibodies or emergence of self-reactive B cells as a response to SARS-CoV-2."
https://www.medrxiv.org/content/medrxiv/early/2023/01/26/2023.01.25.23285014.full.pdf [3103]

Sarah Russo writes:

"Cannabis and other adaptogenic herbs are known to be immune modulating. They act as a regulating tool: they can bring an over or under-reacting immune system back into balance. However, the difference between 'immune modulating' and 'immune boosting' can be tricky to decipher. It is generally felt that someone with autoimmunity would not want to take anything which boosts the immune system, but this is a point of contention among practitioners.

"According to Kevin Spelman, faculty member in Botanical Medicine at National University of Natural Medicine, the definition of immune modulatory is the biphasic effect of an herbal medicine. 'Immunomodulatory herbs offer a very beneficial strategy to treat autoimmune conditions. The category of immunomodulation rests on biphasic activity. If someone's immune response is overly vigilant, there would be a down regulation of immune response. If someone's immune response is 'deficient' there would be an increase of immune activity.' Spelman explained that a patient's therapeutic response is dependent on how their individual molecular environment is behaving."
https://www.fundacion-canna.es/en/molecular-mimicry-role-cannabis-healing-autoimmune-disease [5015]

In "SARS-CoV-2 Infection and New-Onset Type 2 Diabetes Among Pediatric Patients, 2020 to 2022" by Miller et al at Case Western Reserve University School of Medicine, Cleveland, Ohio (2024) specifically looked at this in children aged 10-19 with no prior T2D diagnosis. The paper also summarises similar increases in the overall population including adults:

"Infection with SARS-CoV-2 is associated with a wide range of subsequent chronic illness in patients, including diabetes. Among adults, a meta-analysis considering data from December 2019 through October 20223 found an overall 66% higher risk of new-onset diabetes after SARS-CoV-2 infection; a second meta-analysis found that 12 of 14 studies found a significantly increased risk, ranging from 11% to 276%, for new-onset diabetes after SARS-CoV-2 infection. Several studies indicate that this risk is greater in male patients and in those with more severe SARS-CoV-2 infection. While most studies included adults, the Centers for Disease Control and Prevention (CDC) reported an increased incidence of diabetes after COVID-19 among patients younger than 18 years based on health claims data but without distinguishing type 1 (T1D) from type 2 (T2D) diabetes. Subsequent studies, including a large study using electronic health records (EHRs), found an association between SARS-CoV-2 infection and risk of subsequent new-onset T1D in children. Another report documented increases in other disorders in children following COVID-19, especially autoimmune complications, such as post–COVID-19 conditions, multisystem inflammatory syndrome, or myocarditis. One study found that new cases of T2D, which may or may not have an autoimmune component, increased by 77.2% in the first year of the pandemic compared with the mean of the previous 2 years of the pandemic. However, the reported research on the incidence of T2D in children following SARS-CoV-2 infection is sparse, and most studies include only small study populations."

Their results for children only:

"The main study population included 613 602 patients, consisting of 306 801 with COVID-19 (mean [SD] age at index, 14.9 [2.9] years; 52.8% female) and 306 801 with other respiratory infections (ORIs) but no documented COVID-19 (mean [SD] age at index, 14.9 [2.9] years; 52.6% female) after propensity score matching. Risk of a new diagnosis of T2D was significantly increased from day of infection to 1, 3, and 6 months after COVID-19 diagnosis compared with the matched cohort with ORIs (RR at 1 month, 1.55 [95% CI, 1.28-1.89]; RR at 3 months: 1.48 [95% CI, 1.24-1.76]; RR at 6 months: 1.58 [95% CI, 1.35-1.85]). Similar results were found in the subpopulation classified as having overweight or obesity (RR at 1 month: 2.07 [95% CI, 1.12-3.83]; RR at 3 months: 2.00 [95% CI, 1.15-3.47]; RR at 6 months: 2.27 [95% CI, 1.38-3.75]) and the hospitalized subpopulation (RR at 1 month: 3.10 [95% CI, 2.04-4.71]; RR at 3 months: 2.74 [95% CI, 1.90-3.96]; RR at 6 months: 2.62 [95% CI, 1.87-3.66]). Similar elevation in risk was found at 3 and 6 months when excluding patients diagnosed during the interval from the index date to 1 month after infection."
https://jamanetwork.com/journals/jamanetworkopen/articlepdf/2824731/miller_2024_oi_241138_1727892281.84651.pdf [3597]

Increases in Type 1 diabetes in children after Covid have also been shown by Vlad et al in Romania (2021) and Unsworth et al (2020) in the UK.
https://doi.org/10.3390/medicina57090973 [3599]
https://www.mdpi.com/1648-9144/57/9/973 [3600]

Yang et al at Weill Cornell Medicine, used human pluripotent stem cell (hPSC)-derived vascularized macrophage-islet (VMI) organoids to uncover the mechanism by which SARS-CoV-2 induces new cases of diabetes, and worsens complications in people who already have it. The team found that viral exposure activates immune cells that in turn destroy beta (β) cells, the pancreatic cells that produce insulin. Their highlights:

"Proinflammatory macrophages are enriched in COVID-19 pancreatic autopsy samples

"Virus exposure causes proinflammatory macrophage activation and β cell pyroptosis

"Construction of hPSC-derived vascularized macrophage-islet organoids

"Proinflammatory macrophages induce β cell pyroptosis through TNFSF12 signal"
https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(24)00293-5 [3598]

The Court will recall that evidence showing "Inhibition by delta-9-tetrahydrocannabinol of tumor necrosis factor alpha production by mouse and human macrophages" goes back to 1992 [4064].

In "Genetically supported targets and drug repurposing for brain aging: A systematic study in the UK Biobank" from Yi et al:

"By integrating Mendelian Randomization (MR) and colocalization analysis on eQTL and pQTL data, we prioritized seven genetically supported druggable genes, including MAPT, TNFSF12, GZMB, SIRPB1, GNLY, NMB, and C1RL, as promising targets for brain aging, as measured by Brain age gap (BAG), the deviation between estimated brain age and chronological age:

In detail:

"Following MR analysis on pQTLs, we observed that six proteins, granulysin (coded by GNLY, beta = 0.08, SE = 0.023, FDR-corrected P = 0.0030), granzyme B (coded by GZMB, beta = −0.097, SE = 0.028, FDR-corrected P = 0.0039), MPIP2 (coded by CDC25B, beta = 0.24, SE = 0.083, FDR-corrected P = 0.041), ERK-1 (coded by MAPK3, beta = −0.34, SE = 0.10, FDR-corrected P = 0.013), CN37 (coded by CNP, beta = −0.54, SE = 0.19, FDR-corrected P = 0.041), and TNF12, exhibited a significant causal effect on BAG. Notably, TNF12, coded by TNFSF12, showed consistently significant causal effects on BAG in both INTERVAL study and the deCODE studies (beta = −0.25, SE = 0.085, FDR-corrected P = 0.013 in INTERVAL and beta = −0.28, SE = 0.058, FDR-corrected P = 0.0001; Fig. 4. Furthermore, 14 proteins (gene symbols: MAPT, TNFSF12, GZMB, SIRPB1, GNLY, NMB, C1RL, TG, RRM1, CA4, NPPA, CAPNS1, A2ML1, and CD163) displayed strong evidence of colocalization. Among them, C1RL and SIRPB1 demonstrated significance in the colocalization analysis using both the deCODE and INTRVAL pQTLs.

"Prioritized druggable genes with strong genetic evidence for BAG
Of the 64 druggable genes identified, 37 genes have been supported by at least two pieces of evidence in the MR and colocalization analysis, using the results of BAG GWAS, blood/brain tissue eQTL, and plasma pQTL. Among these, we have further prioritized seven druggable genes that exhibit at least three pieces of evidence, namely, MAPT, TNFSF12, GZMB, SIRPB1, GNLY, NMB, and C1RL. It is noteworthy that MAPT and TNFSF12 are Tier 1 druggable genes, respectively. This strong evidence in the MR and colocalization analysis with xQTLs suggests that they may serve as promising candidate targets for brain aging."
https://www.science.org/doi/10.1126/sciadv.adr3757 [4856]

Therefore downregulation of TNF-α via TNFSF12 has benefits for the brain age gap regardless of Covid.

Similarly

"CCL5 and other proteins showing age-dependent increases in circulation were reduced by senotherapeutic agents." [3840]

And according to Raborn et al (2009) "The Cannabinoid Delta-9-tetrahydrocannabinol Mediates Inhibition of Macrophage Chemotaxis to RANTES/CCL5 through the CB2 Receptor"
https://pmc.ncbi.nlm.nih.gov/articles/PMC2677557/ [4860]

...making THC one such agent, as

"The expression of GNLY is positively and causally associated with BAG at both transcript and proteomic levels, and granulysin (encoded by GNLY) is colocalized with BAG (PPH4 = 1). Granulysin is an antimicrobial and proinflammatory peptide in the granules of human cytotoxic T lymphocytes and natural killer cells and could activate expression of C-C Motif Chemokine Ligand 5 (CCL5) [aka RANTES], Monocyte chemoattractant protein-1 (MCP-1), IL-10, IL-1β, IL-6, and IFN-α (interferon-α)." [4856]

"Combined anti CXC receptors 1 and 2 therapy is a promising anti-inflammatory treatment for respiratory diseases by reducing neutrophil migration and activation" say Planaguma et al (2015).
https://pubmed.ncbi.nlm.nih.gov/26271598/ [4857]

While Yu et al (2016) report that in acute colitis induced in female Balb/c mice by administration of 5% dextran sodium sulfate (DSS) "Immunoneutralization of CCL5 but not CXCL4 reduces tissue damage, CXC chemokine expression, and neutrophil recruitment in DSS-treated animals."
https://pubmed.ncbi.nlm.nih.gov/26089223/ [4858]

"The aberrant chemotaxis of leukocytes and lymphocytes also contribute to inflammatory diseases such as atherosclerosis, asthma, and arthritis."

and

"CCL5 plays an important role in various human disorders, such as atherosclerosis, COVID-19, SARS, atopic dermatitis, asthma, glomerulonephritis, alcohol liver disease, acute liver failure and viral hepatitis."
https://en.wikipedia.org/wiki/CCL5 [4859]

Therefore THC inhibition of overabundant chemotaxis via CCL5 is also protective against these conditions.

"The earliest research on pyroptosis can be traced back to 1986."

[pyroptosis timeline 3577]
https://www.nature.com/articles/s41392-021-00507-5 [3577]

"Cannabinoids as Key Regulators of Inflammasome Signaling: A Current Perspective" Suryavanshi et al (2021) lists inflammasome disorders along with known cannabinoid effects in their Table 1:

"The ongoing COVID-19 outbreak is a global pandemic caused by a novel coronavirus named 'severe acute respiratory syndrome coronavirus 2' (SARS-CoV-2). The angiotensin-converting enzyme 2 (ACE2), a metallopeptidase, is a known functional receptor for coronaviruses, and their surface spike glycoproteins (S) bind physically to ACE2. A high expression of ACE2 is correlated to innate and acquired immune response, cytokine secretion, and enhanced inflammatory response in COVID-19 patients. A clinical study in Wuhan pointed out that the levels of IL-1β, IL-10, and IL-8 were significantly higher in critically ill patients with SARS-CoV-2 infection, indicating a cytokine-mediated inflammatory response. Recently, it was established that the SARS-CoV open reading frame (ORF)-8b activates the NLRP3 inflammasome affecting innate immunity and SARS-CoV viroporin 3a protein independently activates NLRP3 inflammasome in macrophages isolated from adult mice. Very recently published reviews strongly suggest that SARS-CoV-2 could directly activate NLRP3 inflammasome and NLRP3 activation could be a potential drug target in the treatment of COVID-19. In our laboratory, we established several novel high-CBD C. sativa extracts that significantly inhibited the expression of ACE2, entry point of the SARS-CoV-2. The reason for choosing high-CBD cannabis extracts was to avoid psychoactive side-effects of Δ9-THC and to avoid CB1 agonism-mediated pathologic changes observed in the pulmonary tissues. Therefore, with the established evidence suggesting the role of cannabinoids as key regulators of inflammasome signaling, the vital cannabinoid moieties (CBD and THC) might be beneficial in alleviating the inflammatory aspects of COVID-19 by blocking inflammasome signaling."

They explain that:

"TLR-induced priming is often required to activate and assemble the inflammasome. Once formed and activated at the cellular level, canonical inflammasomes activate caspase-1 by autoproteolysis, resulting in proteolytic maturation of IL-1β and IL-18, which in turn leads to respective cell death by pyroptosis. Non-canonical inflammasome activation by bacterial pathogens leads to caspase-11 activation and the subsequent hyper-activation of innate immunity in mice. Nevertheless, IL-1β and IL-18 are crucial pro-inflammatory cytokines implicated in a variety of human disorders, such as aging, lung cancer, cardiovascular diseases, gout, etc. Besides pyroptosis, inflammasomes may be involved in eicosanoid synthesis, phagosome maturation, glycolysis, lipid metabolism, and autophagy in a cytokine- and pyroptosis-independent manner."
https://pmc.ncbi.nlm.nih.gov/articles/PMC7876066/ [5039]

Suryavanshi et al (2022) add that:

"Our results revealed that CBD and, for the first time, THC significantly inhibited NLRP3 inflammasome activation following LPS + ATP stimulation, leading to a reduction in the levels of IL-1β in THP-1 macrophages and HBECs. CBD attenuated the phosphorylation of nuclear factor-κB (NF-κB), and both cannabinoids inhibited the generation of oxidative stress post-LPS. Our multiplex ELISA data revealed that CBD and THC significantly diminished the levels of IL-6, IL-8, and tumor necrosis factor-α (TNF-α) after LPS treatment in THP-1 macrophages and HBECs. In addition, the phosphorylation of STAT3 was significantly downregulated by CBD and THC in THP-1 macrophages and HBECs, which was in turn attributed to the reduced phosphorylation of tyrosine kinase-2 (TYK2) by CBD and THC after LPS stimulation in these cells. Overall, CBD and THC were found to be effective in alleviating the LPS-induced cytokine storm in human macrophages and primary HBECs, at least via modulation of NLRP3 inflammasome and STAT3 signaling pathways."
https://pmc.ncbi.nlm.nih.gov/articles/PMC9103143/ [4997]

Jiaswal et al (2024) warn of the oncogenic potential of Covid via the NLRP3 inflammasome, explaining how

"The virus encodes several proteins that alter key signaling pathways associated with cancer hallmarks. Unlike classical oncogenic viruses, which transform cells through viral oncogenes or by activating host oncogenes, SARS-CoV-2 appears to promote tumorigenesis by inhibiting tumor suppressor genes and pathways while activating survival, proliferation, and inflammation-associated signaling cascades. Bioinformatic analyses and experimental studies have identified numerous interactions between SARS-CoV-2 proteins and cellular components involved in cancer-related processes."

[activation of NLRP3 inflammasomes by the N protein of sars-covid-19 5465]
https://www.researchgate.net/publication/384355306_Oncogenic_potential_of_SARS-CoV-2-targeting_hallmarks_of_cancer_pathways/link/66f556c7869f1104c6b53ba8/download?_tp=eyJjb250ZXh0Ijp7ImZpcnN0UGFnZSI6Il9kaXJlY3QiLCJwYWdlIjoicHVibGljYXRpb24iLCJwcmV2aW91c1BhZ2UiOiJfZGlyZWN0In19 [5465]
 
In the International Journal of Molecular Sciences Noemi Cárdenas-Rodríguez (2024) et al describe the "Possible Role of Cannabis in the Management of Neuroinflammation in Patients with Post-COVID Condition":

[long covid 3136]

"Figure 3. (a). Potential anti-inflammatory and antioxidant effects of cannabis compounds in COVID-19 and post-COVID condition (PCC). CBD (cannabidiol) alone, and in combination with CBG (cannabigerol) and THC (Delta-9-tetrahydrocannabinol), exhibits similar potential antiviral, anti-inflammatory, and antioxidant properties in the context of COVID-19. These effects could benefit patients with PCC. (A) Undamaged blood–brain barrier. (B) Neuroinflammation in PCC. (b) Interaction of Cannabinoids CBD, CBG, and THC with CNS cells and their impact on modulating inflammation and oxidative stress in the post-COVID condition. This figure demonstrates how cannabidiol (CBD), cannabigerol (CBG), and tetrahydrocannabinol (THC) engage with neurons, astrocytes, and microglia within the central nervous system (CNS) during the post-COVID condition to influence the production of pro-inflammatory cytokines and oxidative stress markers. By activating cannabinoid receptor types 1 (CB1) and 2 (CB2), CBD, CBG, and THC reduce the secretion of pro-inflammatory agents such as tumor necrosis factor-alpha (TNFα), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), phosphorylation of STAT3, phosphorylation of tyrosine kinase-2 (TYK2), interleukin-8 (IL-8), interleukin-17 (IL-17), and interferon-gamma (IFNγ), as well as myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS), nitrogen dioxide (NO2), prostaglandin E2 (PGE2), and reactive oxygen species (ROS), thus fostering a neuroprotective environment. The vertical black arrows indicate the dynamics of production for various elements: a downward orientation reflects a decrease in the production of the elements specified next to such an arrow, whereas an upward orientation indicates an increase. On the other hand, the green arrows highlight the specific effect of each phytocannabinoid upon interacting with its corresponding receptor."
https://www.mdpi.com/1422-0067/25/7/3805 [3136]

From "How Covid-19 affects the brain" Boldrini et al (2021):

[covid brain 3809]

"A, SARS-CoV-2 invades endothelial cells via transmembrane angiotensin-converting enzyme 2 (ACE2) receptor, enabled by transmembrane protease, serine 2 (TMPRSS2). B, Cytokine elevation and microglia activation result in increased kynurenine, quinolinic acid, and glutamate, and neurotransmitter depletion. C, Coagulation cascade and elevation of von Willebrand factor (vWF) lead to thrombotic events. D, Altered neurotransmission, excitotoxicity by increased glutamate, and hypoxic injury contribute to neuronal dysfunction and loss. E, Neuropsychiatric symptoms differ depending on the Brodmann area involved. IL indicates interleukin; NMDA, N-methyl-d-aspartate; TNF, tumor necrosis factor."
https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2778090 [3809]

"Posthospitalization COVID-19 cognitive deficits at 1 year are global and associated with elevated brain injury markers and gray matter volume reduction" from Wood et al (2024) found elevated inflammatory markers known to be lowered by cannabinoids.

"Median (IQR) 384 (155–574) days after COVID-19, median (IQR) serum neurofilament light chain (NfL, a marker of axonal injury), and glial fibrillary acidic protein (GFAP; a marker of astrocyte injury) were significantly raised in patients who had had COVID-19 compared with healthy controls (healthy control versus COVID: NfL 5.46 (3.66–10.5) versus 12.4 (9.2–18.0) pg ml−1 (U = 2,151, estimate (CI) = 5.84 (4.09 to 7.54), effect size = 0.41, P < 0.001) and GFAP 42.4 (33.3–69.6) versus 94.3 (65.6–128.2) pg ml−1 (U = 1,824, estimate (CI) = 43.4 (31.2 to 56.8), effect size = 0.46, P < 0.001)). NfL and GFAP were further raised in those with neurological complications (COVID versus NeuroCOVID: NfL 12.4 (9.2–18.0) versus 15.2 (10.5–21.7) pg ml−1 (U = 10,234, estimate (CI) = 2.64 (4.33 to 1.07), effect size = 0.18, P = 0.001) and GFAP 94.3 (65.6–128.2) versus 105.4 (79.9–154.8) pg ml−1 (U = 11,246, estimate (CI) = 12.3 (23.6 to 0.685), effect size = 0.12, P = 0.039)) (Fig. 3a). Tau was raised exclusively in those with neurological complications (COVID versus NeuroCOVID: 0.69 (0.40–1.22) versus 1.32 (0.57–1.98) pg ml−1 (U = 8,854, estimate (CI) = 0.452 (0.260 to 0.661), effect size = 0.27, P < 0.001))."
https://www.nature.com/articles/s41591-024-03309-8 [3717]

...while "Post-COVID cognitive deficits at one year are global and associated with elevated brain injury markers and grey matter volume reduction: national prospective study" (2023) the researchers "assayed NfL, ubiquitin carboxy-terminal hydrolase L1, tau and GFAP":

"Cognitive deficits were global, associated with elevated brain injury markers and reduced anterior cingulate cortex volume 1 year after COVID-19. Severity of the initial infective insult, postacute psychiatric symptoms and a history of encephalopathy were associated with the greatest deficits. There was strong concordance between subjective and objective cognitive deficits. Longitudinal follow-up in 106 patients demonstrated a trend toward recovery. Together, these findings support the hypothesis that brain injury in moderate to severe COVID-19 may be immune-mediated, and should guide the development of therapeutic strategies."
https://www.researchgate.net/publication/377196179_Post-COVID_cognitive_deficits_at_one_year_are_global_and_associated_with_elevated_brain_injury_markers_and_grey_matter_volume_reduction_national_prospective_study/fulltext/65994dae0bb2c7472b364844/Post-COVID-cognitive-deficits-at-one-year-are-global-and-associated-with-elevated-brain-injury-markers-and-grey-matter-volume-reduction-national-prospective-study.pdf?_tp=eyJjb250ZXh0Ijp7ImZpcnN0UGFnZSI6InB1YmxpY2F0aW9uIiwicGFnZSI6InB1YmxpY2F0aW9uIn19 [3718]

The fluoridated "authors Professor Matthew Broome and Dr Thomas Jackson, from the University of Birmingham commented: 'Post-COVID cognitive deficits seen in this study were equivalent to 20 years of normal ageing, but we should remember that these were patients hospitalised with COVID. The results shouldn’t be too widely generalised to all people with lived experience of COVID.

"'However, the scale of deficit in all the cognitive skills tested, and links to brain injury in the brain scans and blood tests, provide the clearest evidence to date that COVID can have significant impacts on brain and mind health long after recovery from respiratory problems.'”
https://www.birmingham.ac.uk/news/2024/covid-hospitalisation-leads-to-loss-of-brain-function-study [3719]

Corrigan et al (2024) report accelerated cortical thinning in 160 subjects aged 11 to 20.

"We assessed the impact of the COVID-19 pandemic lockdowns on adolescent brain structure with a focus on sex differences. We collected MRI structural data longitudinally from adolescents prior to and after the pandemic lockdowns. The pre-COVID data were used to create a normative model of cortical thickness change with age during typical adolescent development. Cortical thickness values in the post-COVID data were compared to this normative model. The analysis revealed accelerated cortical thinning in the post-COVID brain, which was more widespread throughout the brain and greater in magnitude in females than in males. When measured in terms of equivalent years of development, the mean acceleration was found to be 4.2 y in females and 1.4 y in males. Accelerated brain maturation as a result of chronic stress or adversity during development has been well documented. These findings suggest that the lifestyle disruptions associated with the COVID-19 pandemic lockdowns caused changes in brain biology and had a more severe impact on the female than the male brain."
https://www.pnas.org/doi/10.1073/pnas.2403200121 [3582]

Cortical thickness is presented in more detail in the Brain Volumes section. Cannabis use has been associated with volume increases, whereas alcohol has been associated with volume reduction but "recreational cannabis use has been associated with volume in
creases"

"cannabis findings in GM average to a null effect" [2834]

Meanwhile, according to The Economist on 24 April 2024 describes how a girl diagnosed with "spending too much time on TikTok" actually had Paediatric Autoimmune-Neuropsychiatric Disorders Associated with Streptococcus (PANDAS), a post-streptococcal infection syndrome which presents a range of symptoms including movement disorders (chorea, tics, dystonia, and Parkinsonism), psychiatric disorders (particularly emotional disorders), and associated sleep disorders. If Strep A is identified antibiotics may be prescribed, to the further detriment of the gut microbiome.

"It is increasingly clear that inflammatory disorders and metabolic conditions can also have sizeable effects on mental health, though psychiatrists rarely look for them. All this is symptomatic of large problems in psychiatry."
https://www.economist.com/science-and-technology/2024/04/24/many-mental-health-conditions-have-bodily-triggers [3104]

Das et al (2024):

"Since the majority of lung tissue contains cannabinoid receptors, cannabis can be an effective medical tool for treating COVID-19 as well as pulmonary infections. Notably, CB2 and CB1 receptors play a major role in immune system modulation and anti-inflammatory activities. In this review, we put forth the idea that cannabis might be helpful in treating pulmonary contagion brought on by viral integration, such as that caused by SARS-CoV-2, haemophilus influenza type b, Streptococcus pneumoniae, influenza virus, and respiratory syncytial virus. Also, a detailed overview of CB receptors, intricate mechanisms, is highlighted connecting link with COVID-19 viral structural modifications along with molecular basis of CB receptors in diminishing viral load in pulmonary disorders supported through evident literature studies."
https://www.degruyter.com/document/doi/10.1515/jbcpp-2023-0030/html [4566]

June 2024 and Classen et al report that "Cannabigerol and Cannabicyclol Block SARS-CoV-2 Cell Fusion":

"Selected cannabinoids such as cannabigerol, cannabicyclol, cannabichromene, and cannabicitran from Cannabis sativa and synthetic homologues of cannabigerol and cannabicyclol were evaluated for effects on the cell viability of Vero cells (CC50 of cannabigerol and cannabicyclol 40 resp. 38 µM) and reduced virus entry of vesicular stomatitis pseudotyped viruses with surface-expressed SARS-CoV-2 spike protein at 20 µM. In addition to a reduction of pseudotyped virus entry, a titer reduction assay on Vero cells after preincubation of Wuhan SARS-CoV-2 significantly confirmed antiviral activity. Investigations on the molecular targets addressed by cannabigerol and cannabicyclol indicated that both compounds are inhibitors of SARS-CoV-2 spike protein-mediated membrane fusion, as could be shown by a virus-free reporter fusion inhibition assay (EC50 for cannabigerol 5.5 µM and for cannabicyclol 10.8 µM) and by monitoring syncytia formation in Vero reporter cells. Selectivity indices were calculated as 7.4 for cannabigerol and 3.5 for cannabicyclol. Systematic semisynthetic alterations of cannabigerol and cannabicyclol indicated that the side chains of both compounds do not contribute to the observed anti-membrane fusion activity."
https://pubmed.ncbi.nlm.nih.gov/38885660/ [3153]

Pitakbut and Kayser (2025) tested "Anti-Infective Screening of Selected Nine Cannabinoids Against Clostridium perfringens and Influenza A (H5N1) Neuraminidases, and SARS-CoV-2 Main Protease and Spike Protein Interactions, using

"...THC, CBD, CBC, CBE, CBF, CBG, CBL, CBN, and CBT against Clostridium perfringens and Influenza A (H5N1) neuraminidases and SARS-CoV-2 main protease and spike protein–human ACE2 interaction using a standard in vitro biochemical enzyme-binding assay. As a result, to the authors’ knowledge, this study is the first to demonstrate the most promising effect of CBG over others in its class against C. perfringens and influenza A (H5N1) neuraminidases and SARS-CoV-2 main protease and spike protein–human ACE2 interaction. In comparison to CBG, CBD and THC were the second and third most promising candidates. Meanwhile, the other derivatives, such as CBC, CBE, CBF, CBL, CBN, and CBT, showed at least one anti-infective effect."

In the heat map, "Asterisk (*) represents a calculation based on a result obtained from a screening study, while the other calculates based on IC50 values compared to a positive control or standard drug."

[heat map cann covid 4854]

Cannabinoids have a broader spectrum of action than standard prescriptions:

"Interestingly, the human digestive and respiratory systems are protected by mucin (Figure 10A,B). To initiate pathogenesis in the human digestive tract, bacteria like C. perfringens release a neuraminidase enzyme to destroy mucin and start colonization, as shown in Figure 10A. On the other hand, in the respiratory system, the influenza A virus uses neuraminidase in the late stage of viral replication, detaching newly reproduced viral cells from the human cellular hosts (Figure 10B). Therefore, inhibiting viral neuraminidase does not prevent viral colonization but diminishes viral reproduction, allowing the human immune response to eliminate the viruses more effectively. Even though both enzymes exhibit a similar biochemical function, the protein sequences between bacteria and viruses are significantly different (only 16% similarity, Supplementary File). This structural diversity contributes to the lack of effectiveness of a viral neuraminidase inhibitor drug like zanamivir against bacterial neuraminidase. Yet, THC, CBG, and CBN were able to inhibit both enzymatic activities in an in vitro setup. Our preliminary result here hints at the potential of these cannabinoids for further investigation and development. Since no current drug in the clinic targets bacterial and viral neuraminidase, developing a new inhibitor to inhibit both enzymes can be beneficial."
https://www.mdpi.com/1467-3045/47/3/185 [4854]

Sommariva et al (2024)

"...analyzed the molecular events occurring in the MCF7, MDA-MB-231 and HCC1937 breast cancer cell lines, representative of the luminal A, basal B/claudin-low and basal A subtypes, respectively, upon SARS-CoV-2 infection."

And:

"Considering the different expression patterns in our cellular models, we first investigated the involvement of ACE2 and NRP1 in SARS-CoV-2 entry by silencing experiments. In MCF7 cells, silencing of either ACE2 or NRP1 reduced the viral load, suggesting that these two receptors play important roles in mediating SARS-CoV-2 entry in this cell line. However, viral infection did not seem to be particularly affected by reduced levels of the ACE2 and NRP1 proteins in the MDA-MB-231 and HCC1937 cell lines. These dissimilar behaviors may be explained by the presence of alternative receptors that can facilitate SARS-CoV-2 entry into cells as well as its propagation through a cell-to-cell transmission mechanism."
https://www.nature.com/articles/s41598-024-63804-3 [5012]

We have seen cannabinoids increase interleukin-10. In "The multifaceted nature of IL-10: regulation, role in immunological homeostasis and its relevance to cancer, COVID-19 and post-COVID conditions" Carlini et al (2023) report that:

"Circulating interleukin 10 (IL-10) binds as a homodimer to tetrameric IL-10 receptor (IL-10R) complex and induce the downstream activation of Janus kinase 1 (Jak1) and tyrosine kinase 2 (Tyk2) and the subsequent phosphorylation of signal transducer and activator of transcription 3 (STAT3). Phospho-STAT3 (p-STAT3) homodimers translocate into the nucleus, where they directly bind to specific sequences and regulate the transcription of its target genes, including anti-inflammatory genes and ACE2. Upregulating ACE2, IL-10 can help to restore RAAS balance, with a reduction of ACE/Ang II/AT1R axis and an increase of ACE2/Ang-(1–7)/MasR axis, resulting in beneficial effects on COVID-19 and post-COVID-19 symptoms. We have previously reported that, in lung-derived and endothelial cell lines, IL-10 administration increased the expression level of SARS-CoV-2 receptor, ACE2 a potent anti-inflammatory molecule ( Figure 2 )."
https://pmc.ncbi.nlm.nih.gov/articles/PMC10287165/ [5013]

According to "High-Acuity Alcohol-Related Complications During the COVID-19 Pandemic", a study based on US national insurance claims data from March 2017 to September 2021, in which researchers compared prepandemic rates of serious alcohol-related problems to rates seen during pandemic months. A secondary outcome was the subset of episodes of alcohol-related liver disease (ALD).

Relevance: Other Defence evidence shows the ameliorative effects of cannabis via alcohol substitution, in the alcoholic liver, alcohol dysbiosis, alcohol withdrawal, prevention of and recovery from SARS-Covid, and the usefulness against addiction, including alcohol addiction, of psychedelics.

"Rates of high-acuity alcohol-related complications were statistically higher than expected in 4 of 18 pandemic months after March 2020 (range of absolute and relative increases: 0.4-0.8 episodes per 100 000 people and 8.3%-19.4%, respectively). Women aged 40 to 64 years experienced statistically significant increases in 10 of 18 pandemic months (range of absolute and relative increases: 1.3-2.1 episodes per 100 000 people and 33.3%-56.0%, respectively). In this same population, rates of complication episodes due to alcohol-related liver disease increased above expected in 16 of 18 pandemic months (range of absolute and relative increases: 0.8-2.1 episodes per 100 000 people and 34.1%-94.7%, respectively)."

[covid alco 4562]
https://jamanetwork.com/journals/jama-health-forum/articlepdf/2817439/shuey_2024_br_240001_1712168394.52718.pdf [4562]

Says fat America, in the form of the CDC, with a 30-365 day follow-up until the first of 26 incident conditions or October 31 2021:

"COVID-19 survivors have twice the risk for developing pulmonary embolism or respiratory conditions; one in five COVID-19 survivors aged 18–64 years and one in four survivors aged ≥65 years experienced at least one incident condition that might be attributable to previous COVID-19."

[long covid risk ratios 4548]
https://www.cdc.gov/mmwr/volumes/71/wr/pdfs/mm7121e1-H.pdf [4548]

To assess the prevalence and persistence of cognitive impairment in long covid  "Changes in memory and cognition during the SARS-CoV-2 human challenge study" by Trender et al (2024) was published in The Lancet.

Thirty-four young, healthy, seronegative volunteers were inoculated with Wildtype SARS-CoV-2 under prospectively controlled conditions. Volunteers completed daily physiological measurements and computerised cognitive tasks during quarantine and follow-up at 30, 90, 180, 270, and 360 days. Linear modelling examined differences between ‘infected’ and ‘inoculated but uninfected’ individuals. The main cognitive endpoint was the baseline corrected global cognitive composite score across the battery of tasks administered to the volunteers. Exploratory cognitive endpoints included baseline corrected scores from individual tasks. The study was registered on ClinicalTrials.gov with the identifier NCT04865237 and took place between March 2021 and July 2022.

"Findings
Eighteen volunteers developed infection by qPCR criteria of sustained viral load, one without symptoms and the remainder with mild illness. Infected volunteers showed statistically lower baseline-corrected global composite cognitive scores than uninfected volunteers, both acutely and during follow up (mean difference over all time points = −0.8631, 95% CI = −1.3613, −0.3766) with significant main effect of group in repeated measures ANOVA (F (1,34) = 7.58, p = 0.009). Sensitivity analysis replicated this cross-group difference after controlling for community upper respiratory tract infection, task-learning, remdesivir treatment, baseline reference and model structure. Memory and executive function tasks showed the largest between-group differences. No volunteers reported persistent subjective cognitive symptoms.

"Interpretation
These results support larger cross sectional findings indicating that mild Wildtype SARS-CoV-2 infection can be followed by small changes in cognition and memory that persist for at least a year. The mechanistic basis and clinical implications of these small changes remain unclear."
https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(24)00421-8/fulltext [3561]

According to Leon et al:

"COVID-19 typically produces olfactory loss, and comparisons of MRI scans from individuals both pre-infection and post-infection have revealed neural deterioration that resembles a decade of aging in the cognitive brain regions that receive olfactory-system projections, along with damage to those areas involved in olfaction (Kollndorfer et al., 2015; Segura et al., 2013). Kay (2022) made the case that COVID-19 infections that produce olfactory loss may foster the cognitive loss that is seen in Alzheimer's disease. In fact, Wang et al. (2022) did a retrospective study of 6,245,282 older adults and showed that people with COVID-19 were at significantly increased risk for new diagnosis of Alzheimer's disease within 360 days after the initial COVID-19 diagnosis. Rahmati et al. (2023) went on to do a meta-analysis of twelve studies tracking over 33 million individuals who either had contracted COVID-19 or did not contract the virus. The pooled analyses showed a significant association between COVID-19 infection and subsequent increased risk for new-onset Alzheimer's disease. Given the remarkable number of physiological systems that were affected by the disease (Nasserie et al., 2021), there is no reason to believe that the olfactory loss was the sole factor in increasing the risk of Alzheimer's, but it may be that the loss of olfaction contributed to the degradation of regions in the brain integral to normal memory functioning, as mentioned previously (Kovalová et al., 2024).

Their work supports the neuroprotective benefits of replacing an unpleasant odour, e.g. Ptuj, with smells the respiring individual finds pleasant, e.g. cannabis:

"1.3 Efficacy of olfactory enrichment
1.3.1 Olfactory enrichment improves symptoms of cognitive impairment
Shi et al. (2023) reviewed a number of studies examining the effects of exposure to essential oils and found a wide range of benefits to the brain and behavior. The benefits included normalizing neurotransmitter levels, decreasing inflammatory factors, decreasing oxidation, increasing neuroprotective factors, improving memory, decreasing neuronal loss, and suppressing beta amyloid levels.

"1.3.2 Olfactory enrichment results in memory benefits for healthy adults
From a preventive perspective, about 20 studies have now been performed showing that increasing olfactory stimulation can improve memory (Vance et al., 2024).

"For example, olfactory enrichment improves cognition in older adults. Birte-Antina et al. (2018) provided olfactory enrichment with 4 essential-oil odorants twice a day for 5 months, while controls solved daily Sudoku puzzles. The olfactory-enriched group had a significant improvement of olfactory function, improved verbal function, and decreased depression symptoms. Oleszkiewicz et al. (2022) exposed 68 older adults either to 9 odorants twice a day or to no new odorants for 3–6 months, and found the enriched olfactory experience produced improvements in cognitive abilities, dementia status, and olfactory function relative to controls. Specifically, the Montreal Cognitive Assessment revealed a significant improvement in the olfactory-enriched group relative to controls, and the AD8 Dementia Screening Interview showed that enriched participants had no increase in dementia symptoms over the trial period, while control participants had an increase in symptoms.

"Increased complexity of olfactory enrichment also improves dementia symptoms. Cha et al. (2022) exposed 34 older adults with dementia to 40 odorants twice a day for 15 days. The control group consisting of 31 individuals with dementia received no such stimulation. There were no initial differences between groups, and all had a Mini-Mental Status Examination score of at least 10. The results were remarkable, as the olfactory-enriched group showed highly significant improvements in memory, olfactory identification, depression symptoms, attention, and language skills. Olfactory-enriched individuals improved their olfactory identification, while controls did not. The Verbal Fluency Test also showed significant improvements for the enriched group relative to the controls. Similarly, the Boston Naming Test revealed a significant improvement in the enriched subjects relative to controls. The Word-List Memory Test, the Word-List Recall Test, the Word List Recognition Test, and the Geriatric Depression Scale all improved in the enriched group relative to controls.

"Lin and Li (2022) exposed older adults with mild-to-moderate dementia to 15 essential oils/essences twice a week for 30-min sessions over a 12-week randomized clinical trial. Participants in the olfactory enrichment group also were asked to relate each scent to a matching photo of the scent source. The olfactory enrichment group showed significant cognitive improvement on the Loewenstein Occupational Therapy Cognitive Assessment-Geriatric test. In addition, olfactory enrichment prevented the increase in plasma beta amyloid seen in the control group.

"In an effort to minimize burden and increase compliance, we tested the idea that we could get enhanced neural and cognitive outcomes after even minimal olfactory enrichment at night (Woo et al., 2023). The limitations of the available diffusion devices at the time forced us to use this minimal level of olfactory enrichment. Therefore, we gave olfactory enrichment or control exposures to older adults (60–85 years old) for 2 h every night for 6 months, using a single odorant each night, rotating through seven scents a week (Woo et al., 2023). There were statistically significant differences between enriched and control older adults in their cognitive ability using the Rey Auditory Verbal Learning Test, with enriched individuals scoring 226% better than controls. We also found a statistically significant change in mean diffusivity in the uncinate fasciculus of the enriched group compared to controls." [3641]

[sledilnik cases to 2 april 2023]

Slovenia has 1,349,424 recovered cases as of 14 April 2024 [845], and up to 2 April 2023 172,560 cases over 65, dead and alive [364]. Unfortunately Sledilnik doesn't show the survivors by age, as far as can be seen. 10,083 died altogether, so the total survivors 65 or over cannot be less than 172,560 - 10,083 i.e. 162,477. One in four would be 40,619.

Does Slovenia have the facilities to monitor and treat these 26 conditions in 40,619 patients, ignoring the 121,858 under 65?

Evidence attesting to the influence of cannabis on, inter alia, IL-6 [1909], astrocytes [2621], mechanical ventilation, C-reactive protein (CRP), ferritin, D-dimer, procalcitonin and mortality [1845,4567,2006] along with the 26 conditions listed in [4548] therefore supports the Article 2 challenge with respect to post-Covid cognitive quality of recovery.

While it is not possble to guarantee a positive effect in any individual, the evidence for the Benedictions show it to be improbable that taking cannabis away would be, overall, a health-enhancing step in a population. The Prosecution has not shown any such thing.

Rather the patient population has been only additionally insulted by the actions of the Police and Prosecution, who in the midst of the pamdemic have distrained a means of preventing, controlling, and ameliorating the after-effects of SARS-Covid-19.

The consequences are not statistics, but actual people including the dead 10,083 Slovenian residents, the majority of whom, we assume, went law-abidingly to their graves.

Among the survivors, a second, less obvious pandemic continues. Trimarco et al (2024)

"...conducted a 6-year longitudinal study to examine the broader effects of COVID-19 on dyslipidemia incidence in a real-world population (228,266 individuals) residing in Naples in southern Italy. The pre–COVID-19 and COVID-19 groups were balanced for demographic and clinical factors using propensity score matching.

"RESULTS. Our analysis spans a period of 3 years during the COVID-19 pandemic (2020–2022), comparing dyslipidemia incidence with pre-pandemic data (2017–2019), with a follow-up of at least 1,095 days corresponding to 21,349,215 person-years. During the COVID-19 period, we detected an increased risk of developing any dyslipidemia when compared with the pre–COVID-19 triennium (OR = 1.29; 95% CI, 1.19–1.39). Importantly, these estimates were adjusted for comorbidities by a multivariate analysis."

[covid sequelae 3646]

Diabetes risk was more than doubled - all odds ratios refer to the entire population, infected or not. (2.4 million COVID-19 cases were reported in Campania during the 3 years of the pandemic among a total population of 5.5–6 million).

"Specifically, the increased risk of an incident composite dyslipidemia outcome was evident in subgroups based on age class (OR = 1.54, 95% CI 1.40–1.70), obesity (OR = 1.22, 95% CI 1.09–1.36), cardiovascular disease (CVD) (OR = 1.29, 95% CI 1.18–1.40), chronic kidney disease (CKD) (OR = 1.41, 95% CI 1.25–1.59), COPD (OR = 1.20, 95% CI 1.07–1.36), diabetes (OR = 2.07, 95% CI 1.90–2.25), and hypertension (OR = 1.30, 95% CI 1.18–1.43)."
https://www.jci.org/articles/view/183777 [3646]

Simon et al at Ruhr-University Bochum looked at anandamide and asthma.

"High concentrations of endocannabinoids have been detected in the lung. In this organ endocannabinoids also display functional effects on vessels as anandamide (AEA) and 2-arachidonlyglycerol (2-AG) were demonstrated to control pulmonary arterial tone. In isolated pulmonary arteries (PAs) of different species endocannabinoids were reported to induce vasorelaxation. Interestingly, in murine and rabbit whole lung preparations ex vivo as well as in mouse in vivo, we and others found a strong pulmonary vasoconstriction by AEA mediated by fatty acid amide hydrolase (FAAH). Our experiments revealed that this effect was specific for AEA and not found for 2-AG. In addition, we could show that this response is of physiological relevance as FAAH-dependent AEA degradation proved to be a central mechanism of hypoxia-dependent vasoconstriction. Because of its important physiological function in pulmonary vessels we then wondered if AEA can also affect airways and if this is of pathophysiological relevance."

Spoiler alert: it can and it is:

FAAH degrades anandamide, producing arachidonic acid, which in turn is converted to prostaglandin E2, which can dilate the bronchial tubes, she explains. Prostaglandin E2 acts via certain receptors and leads to an increase in the messenger substance cAMP (cyclic adenosine monophosphate).

It is precisely this, the increase in cAMP, that is targeted by well-established inhalation medications against asthma.

"Anandamide [AEA] induces airway relaxation"
"AEA-induced airway relaxation is mediated via FAAH-dependent metabolites"
"AEA induces airway tone decrease by activation of EP2 and EP4 receptors"*
"AEA enhances PGE2 and cAMP production in airways"
"AEA induces airway relaxation in precision-cut lung slices and reduces airway resistance in vivo"
"AEA levels and synthesis enzymes are reduced in the [ovalbumin] OVA-induced asthma model"
"AEA induces airway relaxation and limits airway hyperresponsiveness in the OVA-induced asthma model"
" The lack of these compounds and/or their metabolites could contribute to airway hyperreactivity in this disease."

*The EP(2) and EP(4) prostanoid receptors are two of the four subtypes of receptors for prostaglandin E(2) (PGE(2)) [aka dinoprostone]. They are in the family of G-protein coupled receptors and both receptors were initially characterized as coupling to Gs and increasing intracellular cAMP formation.

"Traditional Asian and African medicine applied cannabis in neurological disorders, infections and also lung disease such as bronchitis and asthma. Also more recent reports suggest a potential beneficial effect of plant-derived THC in human asthmatics."

and

"While FAAH was previously only considered as an enzyme that inactivates AEA, there is now accumulating evidence by us and others that also FAAH-dependent AEA metabolites initiate important signaling pathways."

and

"As a potential reason for the long-term reduction of AEA levels in OVA-sensitized mice in our experiments we identified reduced expression of enzymes responsible for AEA production such as NAPE-PLD [N-acetylphosphatidylethanolamine-hydrolysing phospholipase D], ABDH4 [alpha/beta-hydrolase 4], and GDE1 [glycerophosphodiesterase 1]. This is in accordance with the reported diminished transcription of NAPE-PLD in response to inflammatory stimuli in macrophages. While also other endocannabinoids may affect airway tone, the exogenous application of AEA or its FAAH-dependent metabolites can be an option to restore diminished AEA levels or metabolites to acutely counteract airway constriction. As a potential side effect, we have excluded pulmonary vasoconstriction of AEA inhalation in the lung at the concentration required for airway relaxation."
https://www.nature.com/articles/s41467-022-34327-0 [1749]

OVA - ovalbumin - is a chicken protein allergen mainly found in egg white. It is commonly used to sensitize immune reactions.

The penH equation is described here:
https://www.biopac.com/application/pulmonary-function/advanced-feature/full-body-plethysmograph-penh/ [1565]

More about penH at
https://pubmed.ncbi.nlm.nih.gov/16638630/ [1564]

Meanwhile on the psychedelics front, Flanagan et al (2020)

"...examined the ability of several agonists of differing chemical structures to prevent airways hyperresponsiveness (AHR) in a rodent model of allergic asthma, rather than a cell-based system. First, testing in an in vivo model of asthma provides greater translational relevance to results. Second, airway response in rodent models of asthma takes into account not only pulmonary inflammation but also other aspects of disease processes involving immune cell function. Demonstrating suppression of AHR in a rodent model of asthma indicates pleiotropic therapeutic effects are occurring that together prevent inflammation in the lung and enhance our ability to detect anti-inflammatory effects regardless of its nature or source."

[psychedelics rat ahr 1563]

As you can see from their Figure 1, psilocin - the active metabolite of psilocybin - is fully effective against AHR, whereas N,N-DMT is not effective at all. LSD is partially effective.

"Psilocin, which has significantly weaker affinity for the 5-HT2A receptor and less potency than [the 5-HT2 receptor selective agonist (R)-2,5-dimethoxy-4-iodoamphetamine] (R)-DOI at activating canonical signaling pathways, is potent at normalizing PenH (Figure7R), and a low sub-behavioral dose of 0.01 mg/kg (Figure​7S) inhaled is sufficient to completely prevent OVA-induced AHR to methacholine."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8033619/ [1563]

Meanwhile "Hypotheses on Mechanisms Linking Cardiovascular and Neurological/Psychiatric Disorders" (2009) observes that:

"Our data indicate that potential anti-inflammatory effects of agonists like (R)-DOI would be evident at doses far below that necessary to elicit behaviour effects like hallucinations."
https://downloads.hindawi.com/journals/specialissues/326342.pdf [1567]

In January 2022 Khan et al, explaining that...

"Mprotease is accountable for the cleavage of polyprotein downstream of non-structural protein 4 to form distinctive non-structural proteins that show important roles in the life cycle of the virus."

...show mechanisms by which...

"...psychedelic compounds such as psilacetin, psilocin, and psilocybine were screened and found to be inhibitors of SARS-CoV-2 Mprotease. It has been found that psilacetin, psilocin, and psilocybine bind to Mprotease with −6.0, −5.4, and −5.8 kcal/mol, respectively. Additionally, the psilacetin was found to inhibit human interleukin-6 receptors to reduce cytokine storm. The binding of psilacetin to Mprotease of SARS-CoV-2 and human interleukin-6 receptors changes the structural dynamics and Gibbs free energy patterns of proteins."

More about the

"Gibbs Free Energy Landscape
GFE landscape can suggest structural and conformational changes in Mprotease, Mprotease-psilacetin, HIK6, and HIK6-psilacetin molecules. For 2D and 3D conformational depiction, the GFE landscape was projected on PC1 and PC2 for Mprotease, Mprotease-psilacetin, HIK6, and HIK6-psilacetin, respectively.

"G(PC1, PC2)=−kBT1nP(PC1, PC2)

"The kB, T and P(PC1, PC2) denote Boltzmann constant, temperature, and normalized joint probability distribution for Mprotease, Mprotease-psilacetin, HIK6, and HIK6-psilacetin respectively."
https://www.frontiersin.org/articles/10.3389/fimmu.2021.794780/full [2471]

Sobańska et al (2026) recite some of the scarier aspects of psychedelics including the dreaded "thought disorders...mood changes...sexual excitement", but then...

"At the same time, some positive, long-term effects of low doses of LSD were reported, such as the following: symptoms in patients with schizophrenia or depression improved for periods of up to a few weeks even after a single LSD administration; potential applications of LSD also include the treatment of alcoholism and tobacco addiction. Similarly, other classic psychedelic drugs like psylocibin appear to improve emotional empathy and specific memory types such as semantic associations and associative learning. Psylocibin and its analogues seem to be useful in treatments of eating disorders, chronic pain, depression, fear and PTSD, and an interest in 'rediscovered' and 'repurposed' psychedelic drugs continues to surge. Unfortunately, despite the results suggesting that psychedelic drugs may have a positive influence on some psychiatric patients, natural and synthetic compounds associated with psychedelic experience are illegal in many countries."

It is not explained how ergolines, tryptamines and phenylethylamines pass from "medically useful" to "no medical uses" simply by crossing a national border. However they

"...were investigated in the context of their ability to cross the human placenta. Using a novel multivariate model involving compounds’ drug-likeness (according to Lipinski’s Ro5), caco-2 membrane permeability, fraction unbound to plasma proteins, steady-state volume of distribution and the total count of heteroatoms (non-carbon atoms with hydrogens included), it was established that the majority of studied compounds are likely to cross the placenta easily, most probably by the passive diffusion mechanism."
https://www.mdpi.com/1420-3049/31/2/212 [5951]

Despite feeling better already having been declared dangerous and illegal, and despite more research being necessary, a case study of a woman with long Covid suggests that its curative properties are unaffected by illegality:

"The patient reported a slower build-up without shivering and reported feeling very detached from LongCOVID symptoms. The patient's experience while under the influence of MDMA and psilocybin was reported as feelings of being in a childlike state, having an intense connection to nature, and of being in an alternate reality. Though the patient experienced transient nausea and emesis 40 min after ingestion of psychedelics, she endorsed 0/10 pain within 1 h of ingestion irrespective of the nausea. After this second dosing session, the patient subjectively reported significant improvement in her post-COVID symptoms including fatigue, depression, anxiety, joint pain, and headaches. The patient was able to return to work and her cognitive function improved, allowing her to resume her PhD studies. The patient's insomnia also improved, and she was able to stop taking antihistamines. The patient's unique headache, which was different from her migraines, decreased in severity and frequency. Headache frequency reduced to approximately once per week compared with a May 2022 baseline of 5 per week. Headache duration also decreased to less than 2–4 h per attack—an improvement from the typical 8–12 h duration in May 2022. After the July dosing session, her headaches intensity remained at 30% of their former peak intensity. Overall, the patient indicated her symptom improvement was approximately 80% when asked to self-report on a scale of 0%–100%.

"Six weeks later (on July 16th), her head pressure returned at approximately 30% of its previous severity. After another 2 g dose of psilocybin cubensis mushrooms, her symptoms abated to 90% relief of symptoms. She was able to work part-time thereafter and return full-time in September.

"After several months of improvement, the patient reported experiencing an early November relapse of her post-COVID-19 symptoms in the setting of a nonCOVID-19 flu-like illness. Her headache returned, although it was less severe and not as frequent as before. The patient decided to try another dosing session with psychedelics on November 24th. This time, 2g of dried golden teacher psilocybin cubensis mushrooms led to a remission of her symptoms. The patient subjectively reported complete resolution of her symptoms. The patient was again able to return to work 3 days later and continue with her PhD studies."
https://onlinelibrary.wiley.com/doi/pdf/10.1002/ccr3.8791 [3105]

If you have a strong stomach, muscimol, found in Amanita muscaria, can fix your long Covid and Alzheimer’s too. According to the account of Winkelman et al (2023):

"In vivo rodent studies of AD treatment with muscimol showed potent enhancing effects on memory and learning (Pilipenko et al., 2015), even at very low doses (Pilipenko et al., 2018). This effect involves muscimol-mediated significant downregulation of hippocampal and cortical proteins involved in neuroinflammation and astrocyte reactive gliosis, such as GFAP, as well as modulated enzymes critical for GABA synthesis (Pilipenko et al., 2018). These results are very important, since large-scale neural network activity is abnormally increased in the brain of patients with AD, and animal models show decreased GABAergic inhibitory neuron activity may contribute to the observed Aβ-induced cognitive deficits (Xu et al., 2020). Chronic modulation of GABAAR with muscimol greatly reduces Aβ-induced neurotoxicity in cultured rat cortical neurons, an effect entirely inhibited/prevented by bicuculine, a specific GABAAR antagonist (Lee et al., 2005). Low-dose muscimol adiminstered directly into subthalamic nuclei also reversed Parkinsonism in a small human study (Levy et al., 2001), and ameliorated cognitive deficits and improved spatial memory in an APP/PS1 mouse model of AD (Fu et al., 2019), suggesting the therapeutic potential of muscimol in both Aβ and tau neuropathologies and homeostasis."

Their Figure 1 explains the different pathways of different psychedelics:

[psychedelics pathways 3722]

"Interaction of receptors and pathways involved in the therapeutic action of classic and non-classic psychedelic substances. Fig. 1 represents interacting pathways and typical receptors for psychedelics discussed in this paper. The center of the figure represents a neural or glial cell expressing these receptors. One pathway (upper left) involves glutamatergic presynaptic neurons that express 5-HT2A receptors that modulate glutamate release, leading to the ligation and activation of AMPA, NMDA, and metabotropic glutamate receptors (mGluR). Another pathway (upper right) involves presynaptic cholinergic neurons that release acetylcholine (ACh) activating muscarinic (M1-M5 type) and nicotinic cholinergic receptors (nAChR). Classic serotonergic pathways (LSD, DMT, psilocybin; upper center) mainly activate 5-HT2A receptors, which are 7-transmembrane G-protein-coupled receptors (GPCRs). Atypical psychedelics activate either other types of GPCRs (e.g., ibogaine modulates the kappa-opioid receptor – KOR), GABAA (muscimol), or muscarinic receptors (muscarine). DMT and 5-MeO-DMT-modulated pathways (middle left) exhibit affinity at sigma-1 receptor (Sig-1R) sites at the mitochondria-associated endoplasmic reticulum membranes. Upon activation by their specific ligands, these receptors converge into three major pathways: 1) Phospholipase C (PLC) - Protein kinase C (PKC) effector pathway that regulates intracellular Ca2+ levels and control transcription factors modulating cellular survival/death, neuroprotection and metabolic fine-tuning (in the center; involving diacylglycerol – DAG); 2) Catalyze the formation of cyclic AMP (cAMP) from ATP (Adenosine triphosphate) by AC (Adenylate cyclase), and thereby activating Protein kinase A that controls several survival- and neuroplasticity-related genes (lower left); 3) Phosphoinositide 3-kinase (PI3K) – AKT – mammalian target of rapamycin (mTOR) effector axis that regulates protein synthesis, stress-adaptation, neurorestorative and neuroplasticity-related genes and mechanisms. This effector pathway also likely involves genes controlled by the nuclear factor CREB (cAMP response element-binding protein; lower right). Both classic and non-classic psychedelics can modulate inflammation control via the modulation of the transcription factor Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and its target genes via unknown mechanisms. In immunocompetent glial cells, such as microglia and astrocytes, this mechanism involves pattern recognition receptors (PRRs) and inflammasomes that are expressed either on the cell surface or localized on intracellular membranes or in the cytoplasm. PRRs recognize various sets of pathogenic or self-derived structures (pathogen-associated molecular patterns – PAMPS, or endogenous damage-associated molecular patterns – DAMPs), and transduce signals through the NF-κB pathways. The interaction of a specific PAMP/DAMP with PRRs results in downstream signaling through various adaptor proteins. This receptor-adaptor interaction leads to the activation of specific kinases, and leads to the subsequent phosphorylation of NF-κB. This transcription factor then translocates into the nucleus regulating the transcription of inflammatory cytokine and chemokine genes, such as IL-1β, IL-6, IL-8, IL-18, and TNFα. Classic psychedelics, typically via 5-HT2A and/or Sig-1R signaling, can modulate intracellular Ca2+ levels through inositol trisphosphate (IP3). 5-HT2A and Sig-1R can also interfere with both PKC and PRR-mediated NF-κB signaling. Thus, the NF-κB and PKC downstream pathways may have a cardinal role in both the collaboration and essential signaling processes of PRRs, 5-HT2A, and Sig-1R in modulating inflammation-control in general, and local neuroinflammation in the brain. Arrows represent activation, red T-arrows represent inhibition/inhibitory effect."
https://www.sciencedirect.com/science/article/pii/S0924977X23001347 [3722]

Two Korean and one Latvian studies show that the health landscape has changed, increasing the utility of anti-inflammatory cannabis and psychedelics in the mRNA-vaccinated population:

In a South Korean study of 519,330 vaccinated and 38,687 unvaccinated.

mRNA Vaccinated at 3 months:
+140% higher Mild Cognitive Impairment (MCI)
+23% higher Alzheimer's Disease (AD)

"Findings showed an increased incidence of MCI and AD in vaccinated individuals, particularly those receiving mRNA vaccines, within three months post-vaccination. The mRNA vaccine group exhibited a significantly higher incidence of AD (Odds Ratio [OR]: 1.225; 95% Confidence Interval [CI]: 1.025-1.464; p = 0.026) and MCI (OR: 2.377; CI: 1.845-3.064; p < 0.001) compared to the unvaccinated group. No significant relationship was found with vascular dementia or Parkinson's disease."

and the conclusion:

"Evidence suggests a potential link between COVID-19 vaccination, particularly mRNA vaccines, and increased incidences of AD and MCI."
https://pubmed.ncbi.nlm.nih.gov/38806183/ [3183]

From Larsson et al (2023) of IFM-chemistry, Linköping University, Linköping Sweden, we learn that "SARS-CoV-2 Spike amyloid fibrils specifically and selectively accelerates amyloid fibril formation of human prion protein and the amyloid β peptide."
https://www.biorxiv.org/content/biorxiv/early/2023/09/01/2023.09.01.555834.full.pdf [5016]

Nyström and Hammarström (2022) are also interested in the "Amyloidogenesis of SARS-CoV-2 Spike Protein":

"SARS-CoV-2 infection is associated with a surprising number of morbidities. Uncanny similarities with amyloid disease associated blood coagulation and fibrinolytic disturbances together with neurologic and cardiac problems led us to investigate the amyloidogenicity of the SARS-CoV-2 spike protein (S-protein). Amyloid fibril assays of peptide library mixtures and theoretical predictions identified seven amyloidogenic sequences within the S-protein. All seven peptides in isolation formed aggregates during incubation at 37 °C. Three 20-amino acid long synthetic spike peptides (sequence 192−211, 601−620, 1166−1185) fulfilled three amyloid fibril criteria: nucleation dependent polymerization kinetics by ThT, Congo red positivity, and ultrastructural fibrillar morphology. Full-length folded S-protein did not form amyloid fibrils, but amyloid-like fibrils with evident branching were formed during 24 h of S-protein coincubation with the protease neutrophil elastase (NE) in vitro. NE efficiently cleaved S-protein, rendering exposure of amyloidogenic segments and accumulation of the amyloidogenic peptide 194−203, part of the most amyloidogenic synthetic spike peptide. NE is overexpressed at inflamed sites of viral infection. Our data propose a molecular mechanism for potential amyloidogenesis of SARS-CoV-2 S-protein in humans facilitated by endoproteolysis. The prospective of S-protein amyloidogenesis in COVID-19 disease associated pathogenesis can be important in understanding the disease and long COVID-19."
https://pubs.acs.org/doi/pdf/10.1021/jacs.2c03925 [5017]

Askenova et al (2022) think "The Increased Amyloidogenicity of Spike RBD and pH-Dependent Binding to ACE2 May Contribute to the Transmissibility and Pathogenic Properties of SARS-CoV-2 Omicron as Suggested by In Silico Study":

"Interaction with other proteins can be influenced by the Spike amyloidogenic tracts. It has been shown that Spike induces structural changes in β and γ fibrin(ogen), complement 3, and prothrombin, increasing their resistance to trypsinization, which, among other mechanisms, may contribute to hypercoagulation in patients with COVID-19. A recent preprint suggests that SARS-CoV-2 induces amyloid aggregation of several proteins involved in neurodegenerative diseases such as APLP1, ApoE, clusterin, α2-macroglobulin, PGK-1, ceruloplasmin, nucleolin, 14–3-3, transthyretin, and vitronectin."
https://www.mdpi.com/1422-0067/23/21/13502/pdf?version=1667552886 [5018]

After finding that fully vaccinated Alzheimer's patients were at greater risk of breakthrough infections with Covid...

"Among the fully vaccinated patients with dementia, the overall risk of COVID-19 breakthrough infections ranged from 8.6% to 12.4%. Patients with dementia were at increased risk for breakthrough infections compared with patients without dementia, with the highest odds for patients with Lewy body dementia (LBD) (adjusted odds ratio or AOR: 3.06, 95% confidence interval or CI [1.45 to 6.66]), followed by vascular dementia (VD) (AOR: 1.99, 95% CI [1.42 to 2.80]), Alzheimer's disease (AD) (1.53, 95% CI [1.22 to 1.92]), and mild cognitive impairment (MCI) (AOR: 1.78, 95% CI [1.51 to 2.11]). The incidence rate of breakthrough infections among fully vaccinated patients with dementia increased since December 2020 and accelerated after May 2021. The overall risk for hospitalization after breakthrough infections in patients with dementia was 39.5% for AD, 46.2% for VD, and 30.4% for MCI."
https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12669 [3518]

...Wang et al (2022) found a higher Alzheimer's risk among over-85s in the 360 days following Covid infection:

"An infectious etiology of Alzheimer’s disease has been postulated for decades. It remains unknown whether SARSCoV-2 viral infection is associated with increased risk for Alzheimer’s disease. In this retrospective cohort study of 6,245,282 older adults (age ≥65 years) who had medical encounters between 2/2020–5/2021, we show that people with COVID-19 were at significantly increased risk for new diagnosis of Alzheimer’s disease within 360 days after the initial COVID-19 diagnosis (hazard ratio or HR:1.69, 95% CI: 1.53–1.72), especially in people age ≥85 years and in women. Our findings call for research to understand the underlying mechanisms and for continuous surveillance of long-term impacts of COVID-19 on Alzheimer’s disease."

In fact the 95% CI hazard ratios show a similar association in all 65 and over groups, from 1.59 for the 65-74 group, 1.69 for the 75-84 group, and 1.89 for the 85-and-over group.

[covid 360 day alzheimers 3517]

The Defendant thinks the 180 day limit mentioned in the caption of Figure 1 is a misprint as no such period is mentioned elsewhere.
https://content.iospress.com/download/journal-of-alzheimers-disease/jad220717?id=journal-of-alzheimers-disease%2Fjad220717 [3517]

Another 2024 paper by Hong Jin Kim et al is "Psychiatric adverse events following COVID-19 vaccination: a population-based cohort study in Seoul, South Korea" study of 4,348,412 individuals living in Seoul, South Korea:

"Cumulative incidence of depression, anxiety, dissociative, stress-related, and somatoform disorders, sleep disorders, and sexual disorders at three months following COVID-19 vaccination were higher in the vaccination group".

Depression +68%
Anxiety, dissociative, stress, somatoform +44%
Sleep disorders +93%
Sexual disorders +++
https://www.nature.com/articles/s41380-024-02627-0 [3184]

And Lazareva et al published "New-onset psychosis following COVID-19 vaccination: a systematic review" (2024)

"Our systematic review aimed to examine cases of new-onset psychosis following COVID-19 vaccination."

A total of 21 articles described 24 cases of new-onset psychotic symptoms following COVID-19 vaccination

54% were female, mean age 34 years, mean onset time was 6 days.

Duration of psychotic symptoms ranged between 1 and 2 months with a mean of 52 days.

Overall, 50% of patients achieved full recovery. (50% didn’t)

CONCLUSION: “Data suggest a potential link between young age, mRNA, and viral vector vaccines with new-onset psychosis within 7 days post-vaccination.”
https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2024.1360338/pdf [3185]

So when you get your COVID-19 Vaccine, after 3 months you get these bonuses:

+140% Mild Cognitive Impairment
+23% Alzheimer's Dementia
+68% Depression
+44% Anxiety, dissociative, stress, somatoform
+93% sleep disorders
++ sexual disorders
increased risk of psychosis within 7 days, especially if you're in your 30s, with only 50% chance of recovery

Nevertheless, Scott et al (2024) insist that:

"Vaccinations remain one of the most effective preventative methods against severe COVID-19 outcomes and the development of long-term COVID-19."

But...

"However, individuals with underlying health conditions may not mount an adequate protective response to COVID-19 vaccines, increasing the likelihood of severe symptoms, hospitalization, and the development of long-term COVID-19 in high-risk populations. This review explores the potential therapeutic role of cannabinoids in limiting the susceptibility and severity of infection, both pre- and post-SARS-CoV-19 infection. Early in the SARS-CoV-19 infection, cannabinoids have been shown to prevent viral entry, mitigate oxidative stress, and alleviate the associated cytokine storm. Post-SARS-CoV-2 infection, cannabinoids have shown promise in treating symptoms associated with post-acute long COVID-19, including depression, anxiety, post-traumatic stress injury, insomnia, pain, and decreased appetite."

Explaining that, like the Ugandan chimpanzees [3154, 3155] the marijuana users seemed to know something the regular doctors could not contemplate...

"With the legalization of cannabis being relatively new in many countries at the onset of the pandemic, several studies have been conducted to investigate changes in cannabis usage during the pandemic compared to the pre-pandemic period. A study by Statistics Canada found a 7% increase in cannabis use among the overall population, with 34% of previous cannabis consumers reporting an increase in their usage compared to the pre-pandemic period. Similar trends were observed in European countries such as France, Italy, and the Netherlands."

Fears that happiness (aka elevated hedonic tone) might get in the way of antidepressant sales were expressed as follows:

"Although it remains unknown whether depressive symptoms associated with post-COVID-19 syndrome are a consequence of the viral infection itself or related to the socio-economic outcomes of the pandemic, this increase in prevalence calls for novel approaches for the treatment of depression."
https://pmc.ncbi.nlm.nih.gov/articles/PMC10779964/ [3778]

As for cannabis use in Canada pre- and post-legalization, a rare longitudinal study from McDonald et al (2025) found that use increased slightly after legalization, but "misuse" as defined by the "Cannabis Use Disorder Identification Test - Revised" (CUDIT-R) declined.

[use canada pre and post legal 4951]

The Defence says this method of classifying misuse based on frequency of use is non-empirical and arbitrary. It proceeds from unargued assumptions, which may be summarised as "cannabis is bad so the people who use the most must be the worst", and "cannabis must be bad for you because it's illegal".

But the Defence says this is a false lemma. The Defence says that cannabis is a net benefit to the population in health terms. At the very least no fair empirical test has been conducted to test the hypothesis that this is not true.

The Defence says the practitioners of prohibition did not know what they did not know, and the Defence says they still don't. And very probably don't want to know. The Defence draws the Court's attention to the Eichmann Defence.

To prop up the false lemma, numerous reasons other than belonging in a "disorder" category, explanatory of why frequencies of use might vary, including product variety and quality, quantity of pain, the presence of PTSD or other conditions, life schedules, and supply conditions are not considered by this dogmatic metric.

During the pandemic, cannabis use became less "problematic" - but this is not, according to the false lemma, because of people using it to avoid dying or long-term symptoms.

[misuse canada pre and post legal 4951]

"CUDIT-R scores (on scale of 0 to 32) decreased significantly overall (β = −0.08 [95% CI, −0.10 to −0.06] per year; −0.4 over 5 years; P < .001), most notably with the onset of the COVID-19 pandemic."

Elsewhere:

"Interestingly, a notable decrease was observed in cannabis misuse that occurred during the early phase of the COVID-19 pandemic (April to October 2020)."

And:

"The COVID-19 pandemic was not a significant moderator for changes in cannabis use frequency but was for cannabis misuse."

And with the Ugandan chimps in the back of our minds we eventually hear that:

"Another longitudinal study similarly found that among pre–COVID-19 frequent cannabis users cannabis use frequency increased early in the pandemic while cannabis use disorder symptom severity decreased slightly."

The Defence responds that extension of the self-aggrandising "CUD" into an important-sounding measurement fit for JAMA makes for an oversimplistic overview.

However, the prohibitionists have been hoisted by their own petard:

"As shown in Table 2, a significant interaction between time and prelegalization cannabis use frequency was found (omnibus test for time × prelegalization cannabis use frequency: P < .001). eFigure 2 in Supplement 1 shows an interaction plot estimated from the LMM to facilitate interpretation. Figure 1B shows longitudinal changes in cannabis use frequency since legalization, stratified by prelegalization cannabis use frequency. We observed a significant decrease among individuals using daily at baseline, little change for those using weekly at baseline, and slight increases among those using monthly or less at baseline. To qualitatively characterize the patterns of change, eFigure 3 in Supplement 1 provides a person-centered alluvial plot showing transitions between cannabis use frequency groups from the first wave (before legalization in September 2018) to the last wave (5 years after legalization in October 2023). Wave-by-wave transitions are also shown in eFigure 3 in Supplement 1."

Finally:

"To our knowledge, this study uses the longest follow-up of any within-individual longitudinal study evaluating recreational cannabis legalization, providing a more nuanced understanding of cannabis behavior changes following legalization. The cohort had a high retention rate, with a mean of 90% retention across all follow-up waves, with 87% remaining at the 5-year mark."
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2833180 [4951]

Once again science struggled to find the cure that everyone knows about:

"Mangoo et al. (2022) examined the efficacy of 129 patients treated with cannabis-based medicinal products (CBMPs) for depression. Their results found that CBMP treatment was associated with a reduction in depression severity and an increase in health-related quality of life after 1, 3, and 6 months of treatment."

Instead Scott et al set about trying to show that people smoke cannabis so they can get depressed, for reasons they do not elucidate:

"Epidemiological studies have shown that non-medicinal or recreational use of cannabis, which is typically high in ∆9-THC, may be associated with an increased risk of developing depressive symptoms. Studies on cannabis abuse as a risk factor for depression found that in participants with no baseline depressive symptoms, those with a diagnosis of cannabis abuse were four times more likely to develop depressive symptoms than those without a diagnosis of cannabis abuse. Similar results were seen in studies by Lee et al. (2008), which found that heavy cannabis users, defined as those who smoke six or more cones of cannabis daily, were four times more likely to report moderate to severe depressive symptoms across three Aboriginal communities."

But a quick delve into these references show one, their 52, is actually "a summary of cannabinoid effects in support of possible therapeutic applications for major depression, bipolar disorder, anxiety, posttraumatic stress disorder, and schizophrenia. Considering this evidence, highlighted benefits and risks of cannabinoid use in the management of these illnesses..."
https://www.mdpi.com/2077-0383/13/1/227 [3364]

Their 53 - the "four times more likely" were from Baltimore, famous for its gun violence and the first major city to be fluoridated, in 1952.

"Baltimore tied for top five in violent crime rate (140th), while ranking 105 in overall safety."

And

"146 out of 148 in high school graduation rate."

And as a further lesson in skepticism:

"Despite this study's findings, another recently named Baltimore one of the happiest cities in the world."
https://www.wmar2news.com/local/study-ranks-baltimore-leadership-among-least-effective-in-nation [3365]

Aborigines - the subject of Bovasso's third supporting reference that cannabis makes you depressed - have no other reasons to be depressed, apparently.

The solitary author of the "four times more depressed" study, Bovasso, considers users to be "abusers". The concept of "abuse" is repeated no less than 85 times.

Bovasso is obviously biased. His claims are self-contradictory, e.g.:

"The results underscore the importance of cannabis abuse prevention rather than treatment because they address the incidence (i.e., new cases) of depressive symptoms rather than the prevalence of depressive disorder. This finding extends those of the national ECA study, which found that alcohol abuse and cocaine, but not cannabis or other drugs, were risk factors for suicide over the initial 1–2-year period of the study (1980–1981)."
https://psychiatryonline.org/doi/10.1176/appi.ajp.158.12.2033 [3367]

Maybe, these "abusers" simply became more aware of their surroundings, more politically engaged with reality, and dissatisfied. After all, we do not cheer when we are surrounded by fear: we ought to be depressed when things are bad. Maybe the "non-abusers" of Baltimore, like their Slovenian counterparts, simply concentrate their efforts on drinking and making things worse.

Bovasso denies this, but his students' reviews were mixed, with a general theme of rote learning, do not question, and "My way or the highway". He seems extremely unpopular with a large minority, placing his knowledge of psychology in some doubt. Psyc167 says:

"I'm just here to forewarn students NOT to take this man's classes. For the sake of your sanity, don't do it..."

"Gregory Bovasso clearly doesn't enjoy his job. His sole purpose is to humiliate and put students down for any feeble attempted [sic] at pleasing him. In my honest opinion, this man should retire."

Psyc211 says:

"Don't ever take a class with this teacher."

And Psyc101 simply says:

"Stay far away from this man."
https://www.ratemyprofessors.com/professor/661422 [3366]

Bovasso did not like cannabis and it shows. Bovasso, like many teachers, may have become convinced of his infallibility and the eternal worth of the opinions he picked up in his early career. Bovasso misleads his readers. His 2001 paper and only contribution to Psychiatry Online received the following reply, useful in the wider context of "Problems With Odds Ratios":

"The 4.49 figure and the 4.00 figure are odds ratios, which have a well-known propensity to exaggerate relative risk. In this case, the odds ratios are at least a twofold exaggeration of the relative risk, which I calculate to be 2.16—(10/15)/(257/834).

"Odds ratios may be useful in retrospective case-control studies (in which the incident rate of meeting the criteria is unknown); however, this study had a longitudinal cohort design. Odds ratios are also useful in logistic regression, but when estimates from a logistic regression are reported, they should be clearly identified as odds ratios. In this article, the abstract stated only that depressive symptoms were 'four times more likely' (p. 2033); there was no mention of odds ratios or logistic regression. Even when logistic regression is used, there is a method for converting the odds-ratio estimates to relative risks. For this study, the method yielded a covariate-adjusted relative risk of 2.08, with a 95% confidence interval of 1.15–2.77.

"None of this will be apparent to readers who see only the abstract. Additionally, since the abstract mentioned Ns of 1,920 (the entire group), 849 (the subjects with no depressive symptoms at baseline), and 1,837 (the subjects with no cannabis abuse at baseline), readers who see only the abstract will be unaware that the N for the group of interest—the group for which the article was named—is 15. The work described in the article is interesting, and the findings may be important. However, they merit more careful reporting."
https://psychiatryonline.org/doi/10.1176/appi.ajp.160.1.190-a?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed [3368]

Bovasso and his 15-strong cohort of cannabis "abusers" (but not the above response) is still quoted. Good weed was evidently wasted on these 15, but nowhere is it explained why they repeatedly spent money to become depressed.

Nor, if they did, why this attempt to reify an opinion about a subjective psychiatric diagnosis (no scales e.g. the Hamilton Depression Rating Scale (1960, 1967) or Beck's Depression Inventory (1961, 1978, 1996) are mentioned) doesn't apply to an actual depressant. This was 2001 of course.

Refusing to accept that "medical users" are indivisible from "recreational users" in the factual sense, O'Dell et al (2025) nevertheless insisted on this pointless and artificial legalistic comparison in "Chronic Disease Symptoms Self-Managed by Cannabis During the COVID-19 Pandemic: Results from the COVID-19 Cannabis Health Study":

"The COVID-19 Cannabis Health Study is an ongoing study among adults ≥18 who self-report cannabis use. Analyses included 1,466 responses received between March 21, 2020, and March 23, 2022, from participants who self-reported cannabis use and a chronic health condition. We examined comorbidities, symptoms managed with cannabis during the COVID-19 pandemic, and fear regarding COVID-19 diagnosis and transmission using the COVID-19 Cannabis Health Questionnaire. Descriptive statistics, Chi-squared, and T-tests were conducted. Results were stratified by those who reported using cannabis to manage a chronic health condition (medicinal cannabis user, n = 1,333) and those who did not use cannabis to manage chronic health condition (non-medicinal cannabis user, n = 133).

"Results: Most (90.9%, n = 1,333) of the total sample (mean age: 47.1 years [standard deviations {SD} = 15.0]) reported using cannabis to manage a chronic health condition, of which 46.1% (n = 615) reported having a medical card/recommendation, and 4.6% received recommendations to use cannabis to manage COVID-19 from health professionals. There were significant differences in age, gender, race/ethnicity, and education by medicinal cannabis use status. Comorbidities prevalent among medicinal cannabis consumers were mental health-related (66.1%), pain (58.5%), cardiometabolic-related (30.5%), immune-related (21.9%), and respiratory-related (20.8%). The most reported symptoms self-managed with cannabis during the pandemic were sleep (69.2%), chronic noncancer pain (49.7%), acute pain (46.5%), headaches/migraines (39.0%), muscle spasms (33.6%), nausea/vomiting (30.6%), and appetite stimulant (29.9%). There were no statistical differences in COVID-19 testing, fear of diagnosis, fear of transmission, or isolation due to COVID-19 between medicinal and nonmedicinal cannabis consumers in this sample."
https://www.liebertpub.com/doi/abs/10.1089/can.2023.0234 [4787]

In a study of seven experimental and three placebo Covid patients by Kuntzman et al (2025):

"Clinical outcomes were better in the patient group that received sublingual CBD vs. patients receiving placebo treatment. Serum cytokine mean concentration levels showed differences between the two groups but of mixed trends.
https://ima-files.s3.amazonaws.com/679579_041db2de-131d-4688-a98c-0012d699a78c.pdf [5185]

Back et al (2024) examined whether psychedelics protected Covid medical staff from burnout:

"This randomized clinical trial found that psilocybin therapy resulted in a significant, sustained reduction in symptoms of depression experienced by clinicians after frontline work during the COVID-19 pandemic. The findings establish psilocybin therapy as a new paradigm of treatment for this postpandemic condition."
https://jamanetwork.com/journals/jamanetworkopen/articlepdf/2827553/back_2024_oi_241372_1732641695.29897.pdf [3803]

This was followed in 2025 by "Psilocybin-Assisted Group Psychotherapy + Mindfulness Based Stress Reduction (MBSR) for Frontline Healthcare Provider COVID-19 Related Depression and Burnout: A Randomized Clinical Trial" from Lewis et al:

"25 participants were enrolled and randomized. There were 12 study-related AEs recorded that were Grade 1-2 and no serious AEs. There was larger decrease in QIDS score for the MBSR+PAP arm compared to MBSR-only from baseline to 2-weeks post-intervention and significant between-group differences favoring MBSR+PAP on subscales of the MBI-HSS-MP as well as the DS-II and WCS.

"Conclusions Group psilocybin-assisted therapy plus MBSR was associated with clinically significant improvement in depressive symptoms without serious adverse events and with greater reduction in symptoms than MBSR alone. Study findings suggest that integrating psilocybin with mindfulness training may represent a promising treatment for depression and burnout among physicians and nurses."
https://www.medrxiv.org/content/10.1101/2024.12.31.24319806v1.full.pdf [5444]

Amid mixed results and difficulties designing experimental approaches to naturalistic use - particularly in hostile prohibition conditions - Bălăeţ et al (2025) were able to discern that "Naturalistic use of psychedelics is associated with longitudinal improvements in anxiety and depression during global crisis times".

So obviously it would be unpopular with governments who want you to be anxious and depressed about global crises all the time:

"Of the few studies that specifically examined the relationship of substance use with mental health during the pandemic, most have focused on alcohol, tobacco or cannabis, often grouping other psychoactive substances and overlooking their unique effects (Zolopa et al., 2022). However, recent efforts have targeted the psychedelics and entactogens associations with mental health outcomes such as mood and resilience, distinct from other drugs (Kopra et al., 2023). This is timely given the increased interest in the potential use of psychedelics for therapeutic purposes (Carhart-Harris et al., 2021) and their use among the general population to try and self-manage well-being, including those without severe mental health issues (Keyes and Patrick, 2023; Livne et al., 2022). This interest is driven by the therapeutic potential of psychedelics like psilocybin for severe depression (Carhart-Harris et al., 2021), as well as research suggesting mood-enhancing effects in ‘naturalistic settings’, that is, as they are commonly used in the real world (Forstmann et al., 2020)."
https://journals.sagepub.com/doi/10.1177/02698811251346729 [5125]

Uncovering mechanisms of AD-like deposition of amyloid in Covid, Miller et al (2025) found that

"...pharmacological inhibition of neuropilin-1 resulted in reduced amyloid-β deposition in human retinal explants treated with SARS-CoV-2 Spike 1 protein. These results suggest that Spike 1 protein, during infection with SARS-CoV-2, can induce amyloid-β aggregation, which may be associated with the neurological symptoms experienced in COVID-19"
https://www.science.org/doi/10.1126/sciadv.ads5006 [5138]

Cannabinoids do indeed inhibit NLP-1. See for instance Cárdenas-Rodríguez et al (2024) [3136], Juknat et al (2013)
https://journals.plos.org/plosone/article/file?type=printable&id=10.1371/journal.pone.0061462 [5139]

and Sarkar et al (2021)

https://www.tandfonline.com/doi/full/10.1080/07391102.2021.1905556 [5140]

 

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The Englishman stands for the rights of everyone disadvantaged, discriminated against, persecuted, and prosecuted on the false or absent bases of prohibition, and also believes the victims of these officially-sanctioned prejudices have been appallingly treated and should be pardoned and compensated.

The Englishman requests the return of his CaPs and other rightful property, for whose distraint Slovenia has proffered no credible excuse or cause.

The Benedictions represent both empirical entities as well as beliefs. Beliefs which the Defence evidence shows may be reasonably and earnestly held about the positive benefits of CaPs at the population level, in which the good overwhelmingly outweighs the bad. Below, the latest version of this dynamic list.


THE BENEDICTIONS                            REFERENCES                        TIMELINE OF DRUG LAW v. SCIENCE