I looked a little into the literature on how much alcohol consumption actually affects rates of oral cancers in populations with ALDH polymorphism, and this particular study seems to be helpful in modelling how the likelihood of oral cancer increases with alcohol consumption for this group of people (found in this meta-analysis).
The specific categories of drinking frequency don’t seem to be too nice here, given that it was split between drinking <=4 days a week, drinking >=5 days a week and having less than 46g of ethanol per week, and drinking >=5 days a week and having more than 46g of ethanol per week. Only in the latter category was there an actual significant increase in oral cancer rates (4.4x), although there is some non-significant evidence for about a 1.5x increase in the high-moderate group and the moderate group. Comparing the ~77 mg/week ingestion rate from the document to the 10-40g range I would estimate the high-moderate group to have, I would imagine that there is probably a much more minor effect for Lumina (if I had to estimate, maybe like a 1.1x risk, which might be offset by the benefits of lower levels of lactic acid at that level).
One other argument against this (which I would put a lower epistemic status on given my basic intuition of enzyme kinetics) would be that since people probably tend to have more than 10 milligrams of alcohol every time they have a gulp of an alcoholic beverage, ALDH2 deficiency would be much more of a bottleneck as acetaldehyde levels rise rapidly after consuming alcohol compared to the rather low background generation of acetaldehyde we might see for Lumina users.
As I am being slightly a “man of one study” here, I’d be interested to see if you’ve found any studies of your own that demonstrate more of an effect of alcohol consumption on oral cancer for ALDH2 deficiency than I’ve been listing here.
There are a lot of studies to regarding the assocation between ALDH2 deficiency and oral cancer risk. I think part of the issue is that
AFR people are less likely to become alcoholics, or to drink alcohol at all.
Japanese in particular have a high proportion of ALDH2 polymorphism, leading to subclinical but still biologically significant levels of acetaldehyde increase after drinking among the non-AFR group.
Drinking even small amounts of alcohol when you have AFR is really really bad for cancer risk.
Note that ALDH2 deficiency homozygotes would have the highest levels of post-drinking acetaldehyde but have the lowest levels of oral cancer because almost none of them drink. As in, out of ~100 homozygotes, only 2 were recorded as light drinkers, and none as heavy drinkers. This may be survival bias as the definition of heavy drinking may literally kill them.
The source for #4 looks like a pretty good meta-study, but some of the tables are off by one for some reason. Might just be on my end.
ADH polymorphism is also pretty common in Asian populations, generally in the direction of increased activity. This results in faster conversion of ethanol to acetaldehyde, but often isn’t included in these studies. This isn’t really relevant for this discussion though.
As always, biostatistics is hard! If X causes less drinking, drinking contributes to cancer, and X increases drinking’s effects on cancer, X may have positive, neutral, or negative overall correlation with cancer. Most studies I’ve looked at had a pretty string correlation between ALDH2 deficiency and cancer though, especially after you control for alcohol consumption.
It also looks like most researchers in the field think the relationship is causal, with plausible mechanisms.
I looked a little into the literature on how much alcohol consumption actually affects rates of oral cancers in populations with ALDH polymorphism, and this particular study seems to be helpful in modelling how the likelihood of oral cancer increases with alcohol consumption for this group of people (found in this meta-analysis).
The specific categories of drinking frequency don’t seem to be too nice here, given that it was split between drinking <=4 days a week, drinking >=5 days a week and having less than 46g of ethanol per week, and drinking >=5 days a week and having more than 46g of ethanol per week. Only in the latter category was there an actual significant increase in oral cancer rates (4.4x), although there is some non-significant evidence for about a 1.5x increase in the high-moderate group and the moderate group. Comparing the ~77 mg/week ingestion rate from the document to the 10-40g range I would estimate the high-moderate group to have, I would imagine that there is probably a much more minor effect for Lumina (if I had to estimate, maybe like a 1.1x risk, which might be offset by the benefits of lower levels of lactic acid at that level).
One other argument against this (which I would put a lower epistemic status on given my basic intuition of enzyme kinetics) would be that since people probably tend to have more than 10 milligrams of alcohol every time they have a gulp of an alcoholic beverage, ALDH2 deficiency would be much more of a bottleneck as acetaldehyde levels rise rapidly after consuming alcohol compared to the rather low background generation of acetaldehyde we might see for Lumina users.
As I am being slightly a “man of one study” here, I’d be interested to see if you’ve found any studies of your own that demonstrate more of an effect of alcohol consumption on oral cancer for ALDH2 deficiency than I’ve been listing here.
The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption—PMC (nih.gov)
There are a lot of studies to regarding the assocation between ALDH2 deficiency and oral cancer risk. I think part of the issue is that
AFR people are less likely to become alcoholics, or to drink alcohol at all.
Japanese in particular have a high proportion of ALDH2 polymorphism, leading to subclinical but still biologically significant levels of acetaldehyde increase after drinking among the non-AFR group.
Drinking even small amounts of alcohol when you have AFR is really really bad for cancer risk.
Note that ALDH2 deficiency homozygotes would have the highest levels of post-drinking acetaldehyde but have the lowest levels of oral cancer because almost none of them drink. As in, out of ~100 homozygotes, only 2 were recorded as light drinkers, and none as heavy drinkers. This may be survival bias as the definition of heavy drinking may literally kill them.
The source for #4 looks like a pretty good meta-study, but some of the tables are off by one for some reason. Might just be on my end.
ADH polymorphism is also pretty common in Asian populations, generally in the direction of increased activity. This results in faster conversion of ethanol to acetaldehyde, but often isn’t included in these studies. This isn’t really relevant for this discussion though.
As always, biostatistics is hard! If X causes less drinking, drinking contributes to cancer, and X increases drinking’s effects on cancer, X may have positive, neutral, or negative overall correlation with cancer. Most studies I’ve looked at had a pretty string correlation between ALDH2 deficiency and cancer though, especially after you control for alcohol consumption.
It also looks like most researchers in the field think the relationship is causal, with plausible mechanisms.