There are some problems here. The first is ideological: longitudinal studies of the incidence of HCC in medical marijuana/recreational marijuana (MM/RM) jurisdictions do not fit the prohibition narrative. "Drugs" are only supposed to do bad things.
You were supposed to believe "someone" had checked all this out and that this assumption justifies your belief and police powers. But you don't know who that "someone" is. Nor does anyone else. And this suits the very simpleminded sort of opinions required to motivate the kinds of Action Man activities confronting the illegal population.
Funding might be hard to obtain for research not adhering to the institutionalised cant of "drug abuse". "Cannabis use disorder" ICD codes would have to be used, which would make the codes themselves look ridiculous - as in the ElTelbany study [1735]. It would be hard to square these terminologies if the study produced the "wrong answer" for the drug warriors and other believers.
Another problem is the time lag. Cannabis's proposed mechanism against HCC operates primarily through CB2 receptor activation in hepatic stellate cells - reducing fibrosis progression - and through autophagy/apoptosis in dysplastic hepatocytes. Cirrhosis leading to HCC is a 15-30 year process, which fibrosis reversal or slowing could interrupt at any point. A reasonable lag between population-level cannabis exposure increasing and HCC incidence changing might be 15-25 years for the anti-fibrotic effect, possibly shorter for anti-proliferative effects.
The mainstream explanation for the US decline is direct-acting antivirals (DAAs) for hepatitis C: sofosbuvir (Sovaldi) approved December 2013, sofosbuvir/ledipasvir (Harvoni) October 2014. DAAs achieve >95% SVR (cure) for HCV, and HCV is the dominant HCC risk factor in the US. Medicaid access studies show that more liberal DAA access correlates with sharper HCC mortality declines. This is a powerful confounder. However: DAAs cure the viral infection but do not immediately eliminate HCC risk in already-cirrhotic livers. HCC risk declines only slowly after HCV cure - one study found annual HCC probability dropping from 0.81% at one year post-DAA to 0.10% at five to six years. A DAA rollout starting in 2014 would not produce measurable population-level HCC decline until roughly 2019-2020, not 2016. This tension in the mainstream account has not been satisfactorily resolved and creates space for additional contributing factors such as cannabis access.
A third problem is the divergent aetiology of HCC between the country where the DAA confounder argument has its empirical basis and the country under discussion. The US HCC burden is substantially HCV-driven. The Global BRIDGE study and subsequent analyses place HCV as the leading HCC risk factor in the United States, accounting historically for roughly 35% of cases. The Baecker et al. [6219] analysis of GLOBOCAN 2012 data put the US population-attributable fraction for HCV-related HCC at around 30-35%, with alcohol (ALD) accounting for a further 20-25% and NAFLD/NASH rising rapidly from below 10% toward 25-30% by 2015-2020. At the population level, HCV prevalence in the US is 1%-2.4% depending on study methodology and demographic, driven in large part by the opioid epidemic and associated injecting practices.
Slovenia is an entirely different population. HCV seroprevalence in the Slovenian general population is estimated at approximately 0.3%, and the infected pool is concentrated almost entirely among people who inject drugs (PWID), in whom seroprevalence is 23-27%. That cohort is small in absolute terms relative to the general population.
Slovenian clinical oncology has not published a dedicated HCC patient series documenting aetiology in a form comparable to the Slovak or German data above. This is not surprising in a country of two million with perhaps 100-200 new HCC diagnoses annually; patient numbers accumulate slowly. It may also reflect less neutral factors. Slovenia recorded the highest standardised death rate in the European Union for disorders related to alcohol use in 2020, at 17.3 deaths per 100,000 inhabitants according to Eurostat - nearly three times the EU average. A country where alcohol occupies this position in the mortality statistics, and where production, tourism, and cultural identity are tied to it, has limited institutional motivation to publish a prominent series confirming that alcohol is also its primary liver cancer pathway. The absence of Slovenian data is not a neutral gap; it is consistent with the institutional reluctance documented elsewhere in these proceedings.
The best available proxy for Slovenian HCC aetiology is the Slovak data (Stefanikova et al., Curr Oncol 2023 [6218], n=429 consecutive patients 2010-2016 from centres across Slovakia, a country with closely comparable alcohol culture, HCV prevalence and demographics). In Slovakia: ALD alone - 48.3% of HCC; chronic HCV - 14.9%; chronic HBV - 10%; NAFLD - 12.6%; ALD in combination with viral hepatitis - a further 2.1%; cryptogenic and other - 12%. The Global Burden of Disease Study [6220] put the ALD-attributable fraction of liver cancer deaths in Central Europe at 46%. Baecker et al. [6219] calculated the ALD population-attributable fraction for Central Europe at 36%, rising to 50-60% in Eastern Europe. The HCV fraction in the same Central European analyses is correspondingly small.
The statistical error implicit in transposing the DAA confounder from US data to Slovenia is therefore compound.
First, HCV accounts for roughly 15% of Slovenian HCC versus 35% in the US - less than half the attributable fraction.
Second, the absolute HCV-infected population in Slovenia is far smaller: with a general prevalence of 0.3% in a country of two million people versus 1.5% in a country of 330 million, the HCV pool is approximately 6,000 in Slovenia against roughly 4.5 million in the US.
Third, the Slovenian PWID cohort that carries most of the HCV burden would not typically access DAA treatment at the same rate as the general US Medicaid population used in the studies showing DAA-HCC correlations, further attenuating any plausible DAA effect on Slovenian HCC incidence.
The compound result is that DAAs, even granting full credit for the US HCC decline, would be expected to reduce Slovenian HCC incidence by perhaps one-fifth of the US magnitude - an effect too small to account for any detectable trend at the population level, and certainly too small to serve as a credible alternative explanation to alcohol-related mechanisms or to cannabis.
The dominant Slovenian HCC risk factor - alcohol - is not addressed by DAAs at all. This matters for the cannabis hypothesis because cannabis's proposed CB2-mediated anti-fibrotic and anti-proliferative effects are at least as plausibly applicable to alcohol-induced hepatic fibrosis as to HCV-induced fibrosis.
Hepatic stellate cell activation and the consequent fibrosis cascade is shared across ALD, HCV and NAFLD pathways. A population where alcoholics constitute roughly 50% of HCC cases, not 20%, is precisely the population in which a cannabis effect on fibrosis progression would be most relevant, most detectable in principle - and least likely to be confounded by antivirals.
See Figure 1 (below): HCC aetiology by cause, Central European countries vs USA.
Figure 1. HCC aetiology breakdown by underlying liver disease (% of HCC cases). Data sources and years: Slovakia/Slovenia proxy: Stefanikova Z et al., Curr Oncol 2023 [6218], n=429 consecutive HCC patients from Slovak centres, 2010-2016 - this is the primary clinical comparator for Slovenia given closely matched alcohol culture, HCV prevalence, and demographics. Czech Republic and Poland: regional population-attributable fraction estimates for Central Europe and Eastern Europe respectively, derived from GBD 2015 [6220] and Baecker et al. 2018 [6219], referring to approximately 2012 base year. Germany: Schütte et al., Digestion 2013;87:147-153 [6233], n=650 consecutive HCC patients, single centre (Magdeburg), approximately 2000-2012; ALD figure is "sole identified risk factor for cirrhosis" category. USA: composite from deLemos et al. 2020 [6221] (ALD-HCC US multi-centre), Baecker et al. 2018 [6219], and GBD 2015 [6220]; approximately 2010-2018. All figures are approximate. These are clinical/epidemiological patient-series and attributable-fraction estimates, not ICD-10 death-certificate counts (the Eurostat ICD-coded standardised death rate for alcohol use disorders, which uses F10 codes, gives a distinct and higher metric). "ALD+viral" = co-diagnosis of alcoholic liver disease and viral hepatitis. "Crypto/other" = cryptogenic cirrhosis and minor aetiologies. The four Central/Eastern European series cluster consistently: ALD 46-52%, HCV 10-15%. The USA is the outlier: ALD 20%, HCV 35%. Germany sits at the boundary (ALD 52%, HCV 14%): a high-alcohol Western European country still shows an Eastern-style ALD-dominant pattern. This structural divergence means the DAA confounder - which is powered by the US HCV fraction (~35%) - operates on less than one-third of that fraction in any Central European comparator, and in Slovenia specifically on roughly 15%.
Furthermore, HCV prevalence in Slovenia is estimated at approximately 0.3% in the general population - somewhat higher than earlier estimates but still far below the 1%-2.4% in the USA - and concentrated in the PWID population. In the US HCV is driven by the opioid epidemic and associated intravenous activities which are ameliorated by CaPs. These have nothing to do with cannabis or psychedelics - so Officer Galun's evidence that "all drugs are the same" is not useful here.
From what the Defendant has been able to establish the evidence certainly does not contradict a hypothesis of reduced HCC associated with cannabis. That the medical profession would prefer to associate this with wonder drugs should surprise nobody, and it is true that legalisation may not have instantly encouraged cannabis use.
The one study which claims that cannabis causes liver cancer is by a
religious nut.
http://www.12v.si/rc [6223]
Probably this is the one Slovenia's doctors will reach for. Indeed the Defendant's own experience, when he was finally admitted to the ZZZS system after 15 years of bureaucratic incompetence, began with a doctor who interrupted a conversation about Hb1c to ask if the Defendant goes to church. Apparently some kind of recruitment drive, or maybe obviously you are going to be ill if you don't.
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