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Mineral Oil
Just sharing this old paper on mineral oil absorbing vA from the diet.
590 FREDERICK STEIGMANN ET AL Vol. 20, No.4
Influence of the intake of mineral oil upon the plasma vitamin A level If a standard diet with a vitamin A potency of 2500 loU. was given, the administration of 30 cc. of mineral oil mixed into the food during the noon meal (corresponding to 6.8% of the food on weight basis for the respective meal), was associated with a slight but steady drop of the average of the plasma vitamin A level during 4 weeks of administration (Table I). At the end of this period, the average plasma vitamin A level was 10 micrograms below the previous period.
It would make sense that mineral oil could also be used to prevent some of the re absorption of vA from bile in the intestinal tract.
Thoughts?
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Two things pop in my head:
- Of course, the authors render it a problem that mineral oil would hinder the absorbtion of vA and carotene. They view both of them as essential vitamins, not as toxins.
- Figure two shows how plasma concentration falls on a diet with 1.500 IU of vA. It raises on double the amount. So probably the cut-off point is somewhere in the middle, around 2.250 IU vA. Anything below would lead to depletion. Anyone being concerned, as I was, about eating eggs – you won't make yourself vA toxic because the four eggs are far below this cut-off point. In addition, as Andrew has pointed out many times, there are many beneficial nutrients in eggs, which actually improve the detox process. Among them, choline and the other one which is difficult to spell. Spyo ...?
- I've always thought that mineral oils should be ingested away from food, exactly for the purpose of better absorbtion, otherwise it would compete with food stuff. Turns out, mineral oil with food might not be such a bad idea, it will depress vA levels over some period of time. It might still be true that minerals won't get absorbed as well, but at least they hinder vAs absorbtion. And in a vA toxic Weltanschauung this is good news.
I'm not sure about the practical implications of the study. Maybe it's a good idea to down some mineral oil when one eats food with vA, as protective measure so to speak? Maybe eat your eggs with mineral oil. Sounds like the ultimate egg hack. Hahaha.
What exactly is mineral oil, and what is the purpose of ingesting it? That paper doesn't provide the composition or origin of the mineral oil used.
From a very brief search, it looks like the main application in humans is as a laxative and lubricant. It is not absorbable. And it is most often a byproduct of crude oil refinement.
Based on that, I would avoid ingesting it unless it was an emergency (e.g. you took too much retinol supplement by accident), similar to charcoal.
I haven't read the mineral oil paper more than your quote from it, but I have some thoughts on it since it reminds me of the non-absorbable synthetic fat Olestra.
Long-term use of Olestra seems to cause dysbiosis causing increased weight gain in mice after they previously had a diet that included Olestra, as per wikipedia:
"Consumption of olestra may encourage rats to eat too much of foods containing regular fats, due to the learning of an incorrect association between fat intake and calories. Rats that were fed regular potato chips as well as chips cooked with olestra gained more weight when subsequently eating a high-fat diet than rats that received just regular chips.[15]"
https://en.m.wikipedia.org/wiki/Olestra
Long-term use of Olestra, mineral oil or another possible laxative might permenatly harm beneficial bacteria in the colon. I read someone else propose that the reason we absorb vitamin A and other toxic substances is since the microbiota living further down are sensitive to toxicity. Too much toxins in the colon at one single point might seriously damage our microbiota, especially in the colon, after enterohepatic circulation.
I think using mineral oil or something similar to try and increase vitamin A excretion is not without risk but it might be possible to manage that risk.
Hi @david,
Yeah, I can see that mixing Olestra in with food could lead to long term issues, and weight gain, even though it was marketed as a diet supplement to reduce weight.
But, I was thinking more that food grade mineral oil could be used apart from meals, such as before bedtime. For the same purpose that some people are using activated charcoal in trying to capture some of the intestinal retinoids that get released with bile, and therefore before it gets reabsorbed. But, unlike activated charcoal inducing constipation, mineral oil would be a laxative too. Of course, used too much, or used too often, will cause side effects.
I’ve heard it claimed that the problem with going full carnivore (all muscle meats) is that it would not provide enough fiber to capture vA from bile in the intestinal tract. I don’t really buy into that argument because I think the extra fat in the carnivore diet would also capture some of the retinoids? Quite a few people have reported bad results with beans, and some other sources of plant fiber.
So, if someone is having constipation trouble with a lower fat carnivore type diet then the addition of mineral oil might be a good option.
@ggenereux2014
I think the assumption and working principle when using any mineral oil, as a laxative, is that it is not well-absorbed. Though liver samlpes from rat studies and human biopsies tells us mineral oils can accumulate over time. The absorbtion might just be a slow passive diffusion with almost non-existent acute toxicity, but with enough constant accumulation mineral oils might cause lipogranulomas in the lymphatic system, the liver and the spleen. [From the safety review paper below: "Lipogranuloma is a nodule of lipoid material associated with granulomatous inflammation; Granuloma is a localised collection of chronic inflammatory cells with epithelioid cells and giant multinucleated cells."].
Using a specific mineral oil which have minimal accumulation might be useful in the short-term for those that have problems with constipation.
Here is a 64 page safety review (2019) on mineral oils called:
"Evaluating the risk to humans from mineral oils in foods: Current state of the evidence"
https://doi.org/10.1016/j.fct.2019.110966.
Here are a few quotes from the paper starting with the paper's abbrevations:
Mineral hydrocarbons (MHCs);
Mineral oil hydrocarbons (MOH);
Mineral oil saturated hydrocarbons (MOSH);
Mineral oil aromatic hydrocarbons (MOAH);
"2.2.1 Human data
Despite the wide use of MOH and, consequently, the high potential for human oral exposure, there is an absence of reports of human toxicity relating directly to MOSH consumption. However, clear evidence of absorption in the form of lipid lesions (lipogranulomas3) from human autopsy samples has been reported. Boitnott and Margolis (1970) found a correlation between the level of saturated hydrocarbons present in liver and the occurrence of histological lipid lesions; at levels < 0.2 mg/g tissue lesions were absent, minimal lesions were apparent at levels between 0.2 and 1.0 mg/g, and multiple foci (lipogranulomas) were evident at levels between 1.0 and 2.5 mg/g tissue. No epithelioid granulomas, of the type seen in F-344 rats, were reported in any of the cases evaluated by the authors. MOSH levels of 3.4 to 4.2 mg/g tissue were measured in spleen samples that demonstrated severe follicular lipidosis, compared to 0.3 mg/g in histologically negative spleens (Cruickshank and Thomas, 1984). Where present, human lesions have been reported as lipoid granulomas characterised by histiocytic clusters around oil drops, i.e. a non-immunological response, similar to that seen in Sprague-Dawley rats (Duboucher et al., 1988). These were significantly different to the epithelioid granulomas characterised by the presence of activated, cytokine-secreting giant cells seen in F-344 rats (Nochomovitz et al., 1975; Blewitt et al., 1977; Fleming et al., 1998; Carlton et al., 2001)."
"More recently, liver biopsy samples from patients with a number of types of chronic liver disease (including hepatitis C, fatty liver disease, autoimmune hepatitis, and primary biliary cirrhosis) were reviewed by Zhu et al. (2010). Findings suggested that most lipogranulomas identified in humans result from the presence of liver disorders/disease, although the authors suggest that MOH may play a role in the development of some. This was also noted by Lagana et al. (2010) who reported that approximately 4% of human liver biopsy samples contained granulomas and of these 90-95% had known causes, including systemic immunological disorders and infectious diseases; fewer than 5% were considered idiopathic, which it can reasonably be assumed includes those caused by exposure to MOH. In contrast, in a study of multiple tissue samples from 37 subjects, an average saturated hydrocarbon content of 0.131 mg/g, liver was reported, with very few granulomas observed (Barp et al., 2014)."
Continuation of my comment:
"2.2.2 Animal data
The toxicity of MOSH and MOAH has been extensively studied in animals and previously reviewed elsewhere (e.g. EFSA, 2012). In summary, MOSH and MOAH have low acute oral toxicity. Bioaccumulation is associated with the formation of microgranulomas in liver and mesenteric lymph nodes, and also increased organ weights, notably liver and spleen. MOH are mutagenic due to the presence of 3-7 ring MOAH (including alkylated and non-alkylated PAHs) that can be activated by P450 enzymes to form genotoxic carcinogens. Some MOAH (e.g. naphthalene) can also act as non-genotoxic carcinogens. MOSH are not carcinogenic, but in a two-stage mouse skin tumour model, at high concentrations C10 – C16 MOSH have been shown to act as tumour promotors, as do highly alkylated MOAH. MOSH is not considered to alter immune function following oral exposure.
The key adverse effect following oral exposure to MOHs has been identified in F-344 rats as the formation of microgranulomas, and this is discussed in more detail in the following section. A specific consideration is the applicability of this finding to other rat strains and, in particular, to humans."
"Granuloma formation in the liver has been used as the pivotal toxicological end point in previous risk assessments of mineral oil consumption. However, the suitability of the F344 rat model for human risk assessment has been repeatedly questioned, stemming from a lack of granuloma formation in the livers of Sprague Dawley rats and other strains given identical diets. Grob (2018) has proposed that changes in the weight of the mesenteric lymph nodes, spleen and liver (due to MOSH accumulation) represent a toxicological effect that is consistent between rat species. There is agreement that accumulation is a critical element of MOH toxicity and in humans MOSH (C20 – C40) are strongly accumulated and can reach concentrations in excess of 1000 mg/kg tissue. However, further studies are needed to confirm the utility of this toxicological endpoint and whether or not it represents an adverse effect."
"Exposure of F-344 rats to the broad range of MOSH was associated with a non-linear accumulation of MOSHs with respect to dose, primarily in liver and, to a lesser extent, in spleen and adipose tissue. Steady state was not reached at the highest dose at 120 days and body burden was decreased (by 40%) during the recovery period [30 days recovery after 90 days of exposure]. Accumulation in liver was associated with a statistically significant increase in absolute and relative liver weights, with maximum retention occurring in liver for C29 and in adipose tissue for n-C15/16. MOSHs in liver and spleen were identified as highly branched and cyclic hydrocarbons, and those in adipose tissue as n-alkanes and compounds with n-alkyl moieties. Granuloma formation was apparent in liver tissue of the highest dose group following >90 days of exposure and were not reversible during the recovery period.
For the defined MOSH mixtures, accumulation was also predominately seen in hepatic tissues, with statistically significant increases in absolute and relative liver weights for the L-C25 and L-C25W groups. In addition, absolute and relative spleen weights were statistically significantly increased in these two groups; no increases were apparent in liver or spleen weights for the S-C25 groups. The highest observed accumulation in liver and spleen tissue was for MOSH with carbon chain lengths between C26 and C30, with wax constituents (n-alkanes, n-alkyl monocyclic naphthenes) being more highly retained in adipose tissue. Hepatic granuloma formation was significantly higher than in controls for the highest dose of S-C25 and for all doses of L-C25W; no liver granuloma formation was apparent following exposure to L-C25 at any dose tested. Where hepatic granulomas were present, animals additionally showed the presence of lymphoid cell clusters in liver parenchyma and the portal tract, reaching significance at the highest doses of S-C25 and for the portal tract only at the highest dose of L-C25W. The authors suggest that n-alkanes may play a significant role in hepatic granuloma formation."
"Barp et al. (2017) compared the findings from the Cravedi et. al (2017) study with those from human studies (Barp et al., 2014; Biedermann et al., 2015) to assess the potential translation of animal study data to human risk evaluation for MOSH. The authors concluded that the high concentrations of MOSH measured in human tissues shows that previous estimates derived through extrapolation from animal data are underestimates. However, there was good agreement between the classes of hydrocarbons showing maximum retention; n-C25 in animals and n-C25 to n-C29 in humans. MOSH accumulation is also dependent on composition in both animals and humans as this widely affects elimination rates, with strongly branched hydrocarbons being retained to the highest degree."
There also exists the weigth-loss supplement "alli" which is touted as reducing fat-absorbtion from the intestines, recommending one to take a multivitamin 2 hours after the meal in order to get one's fat soluble vitamins. I just heard it existed but I am sceptical at best of using un-natural things in the long-term. I have no idea if it helps people with constipation.
https://www.myalli.com/
So is vaseline not a good thing to use on chapped lips and cracked fingers?
I kind of thought it would be veg-toxin free and it works good.