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The relationship between nicotine and vitamin A
Click to access bmjcred00596-0030.pdf
Non-smoking: a feature of ulcerative colitis
The prevalence of cigarette smoking in the United Kingdom has decreased in the past 30 years,1 but the general household survey of 1980 showed that 42%' of adult males and 37% of adult females still smoked.2 Patients with Crohn's disease do not differ appreciably from the normal population in smoking habits,3 but we noticed that patients with ulcerative colitis tended to be non-smokers and therefore designed a questionnaire to assess this impression in more detail.
I can't recall off the top of my head how nicotine influences vitamin A metabolism but caffeine reduces symptoms of Hypervitaminosis A because it slows down vitamin A metabolism resulting in less production of retinoic acid. This means that caffeine users are likely more susceptible to bioaccumulation of vitamin A.
It's not the nicotine that dramatically depletes vitamin A, it's components within smoke. You could breath in wood smoke and it'll reduce vitamin A a lot as well. This is the first time since fire was discovered that humans are not exposed to smoke.
This is the video I did on smoking and vitamin A:
More discussion about smoke and vitamin A:
https://ggenereux.blog/discussion/topic/smoking-and-accutane/
Alcohol and Tobacco Smoke in Retinoid Metabolism and Signaling: Implications for Carcinogenesis
Abstract
Considerable evidence demonstrates that retinoids (retinol, retinoic acid, and retinyl ester, which are also the important metabolites from provitamin A carotenoids), may be effective in the prevention and treatment of a variety of human chronic diseases, including cancer. Substantial work has been done investigating the mechanisms by which tobacco smoke and excessive alcohol intake interfere with retinoid metabolism and signaling. Exposure to cigarette smoke subjects tissues to increased reactive oxygen species, which can induce cytochrome P450 enzymes and result in the degradation of retinoic acid, the bioactive form of vitamin A. Further, oxidative stress can result in cleavage of Β-carotene at positions other than the central double bond, decreasing the production of retinoic acid from this vitamin A precursor. This leads to aberrant retinoid signaling through nuclear retinoid receptors, while at the same time cigarette smoke also causes dysregulated signaling through the mitogen-activated protein kinase signaling pathways. Alcohol acts as a competitive inhibitor of vitamin A oxidation to retinoic acid involving alcohol dehydrogenases and acetaldehyde dehydrogenases, induces cytochrome P450 enzymes (particularly CYP2E1) that degrade retinol and retinoic acid, and alters retinoid homeostasis by increasing vitamin A mobilization from liver to extrahepatic tissues. Moreover, this alcohol-impaired retinoid homeostasis interferes with retinoic acid signaling by decreasing target gene expression and interfering with retinoic acid cross-talk with the mitogen-activated protein kinase pathways. The overall effect of both cigarette smoke and chronic, excessive alcohol intake is dysregulated apoptosis and uncontrolled cellular proliferation, which can act to promote the process of carcinogenesis. Nutritional interventions that serve to restore normal retinoid signaling and functioning may offer protection at the cellular level and represent a means to modify cancer risk in high-risk human populations.
Quote from tim on November 21, 2021, 8:21 amAlcohol and Tobacco Smoke in Retinoid Metabolism and Signaling: Implications for Carcinogenesis
Abstract
Considerable evidence demonstrates that retinoids (retinol, retinoic acid, and retinyl ester, which are also the important metabolites from provitamin A carotenoids), may be effective in the prevention and treatment of a variety of human chronic diseases, including cancer. Substantial work has been done investigating the mechanisms by which tobacco smoke and excessive alcohol intake interfere with retinoid metabolism and signaling. Exposure to cigarette smoke subjects tissues to increased reactive oxygen species, which can induce cytochrome P450 enzymes and result in the degradation of retinoic acid, the bioactive form of vitamin A. Further, oxidative stress can result in cleavage of Β-carotene at positions other than the central double bond, decreasing the production of retinoic acid from this vitamin A precursor. This leads to aberrant retinoid signaling through nuclear retinoid receptors, while at the same time cigarette smoke also causes dysregulated signaling through the mitogen-activated protein kinase signaling pathways. Alcohol acts as a competitive inhibitor of vitamin A oxidation to retinoic acid involving alcohol dehydrogenases and acetaldehyde dehydrogenases, induces cytochrome P450 enzymes (particularly CYP2E1) that degrade retinol and retinoic acid, and alters retinoid homeostasis by increasing vitamin A mobilization from liver to extrahepatic tissues. Moreover, this alcohol-impaired retinoid homeostasis interferes with retinoic acid signaling by decreasing target gene expression and interfering with retinoic acid cross-talk with the mitogen-activated protein kinase pathways. The overall effect of both cigarette smoke and chronic, excessive alcohol intake is dysregulated apoptosis and uncontrolled cellular proliferation, which can act to promote the process of carcinogenesis. Nutritional interventions that serve to restore normal retinoid signaling and functioning may offer protection at the cellular level and represent a means to modify cancer risk in high-risk human populations.
Interesting info.
I see that these studies seem to commonly conclude that supplementation could help undue these "negative" effects. But there have been studies done with supplements to test this idea and they turn out poorly. A study involving supplementing smokers with Vitamin A comes to mind. Do they offer any ideas of why supplementation led to worse outcomes?
New study.
Wood smoke particle exposure in mice reduces the severity of influenza infection
Abstract
Elevated ambient temperatures and extreme weather events have increased the incidence of wildfires world-wide resulting in increased wood smoke particle (WSP). Epidemiologic data suggests that WSP exposure associates with exacerbations of respiratory diseases, and with increased respiratory viral infections. To assess the impact of WSP exposure on host response to viral pneumonia, we performed WSP exposures in rodents followed by infection with mouse adapted influenza (HINI-PR8). C57BL/6 male mice aged 6-8 weeks were challenged with WSP or PBS by oropharyngeal aspiration in acute (single dose) or sub-acute exposures (day 1, 3, 5, 7 and 10). Additional groups underwent sub-acute exposure followed by infection by influenza or heat-inactivated (HI) virus. Following exposures/infection, bronchoalveolar lavage (BAL) was performed to assess for total cell counts/differentials, total protein, protein carbonyls and hyaluronan. Lung tissue was assessed for viral counts by real time PCR. When compared to PBS, acute WSP exposure associated with an increase in airspace macrophages. Alternatively, sub-acute exposure resulted in a dose dependent increase in airspace neutrophils. Sub-acute WSP exposure followed by influenza infection was associated with improved respiratory viral outcomes including reduced weight loss and increased blood oxygen saturation, and decreased protein carbonyls and viral titers. Flow cytometry demonstrated dynamic changes in pulmonary macrophage and T cell subsets based on challenge with WSP and influenza. This data suggests that sub-acute WSP exposure can improve host response to acute influenza infection.
Given many of the different anecdotal and evidence surrounding nicotine consumption and Vitamin A depletion throughout this and other threads, I thought this topic deserved a closer look and more analysis.
Anecdotally, I have been Vitamin A free (as well as other known inflammatory proteins like Gluten, Casian, and those found in Egg Yolk) for only about two months. Over the years, I have enjoyed smoking a pipe about once a week. However, since being VA free, I have noted an increase in desire to smoke my pipe more often. Granted, the addictive effects of nicotine could be playing a significant role, but I do wonder if there is some other mechanism at play, here. Over the past two months, I have also been able to eliminate a long standing (and fairly large) dosage of Allegra antihistamine I was using to control eczema, and that could be playing into this as well in terms of my body seeking a way to "deal" with the effects of body wide VA.
I do wonder, though, what is one to do with research that apparently shows a relationship between cigarette smoke, reduction of Vitamin A, and an INCREASE risk of lung cancer in rats?
Here's a study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4605095/
Findings from this study suggest that cigarette smoke-induced lung retinoic acid depletion may involve two independent pathways, RARα- and RARβ-mediated, responsible for the increased cancer risk associated with cigarette smoke-induced vitamin A deficiency.
How could this be explained? Could it, once again, be the diet the rats are being fed (as we read in "Poisoning for Profits). Given the nature of what Grant has uncovered, in research like this, up can be down, left can be right. What would the potential mechanisms of action here?
Because smoke contains many carcinogenic compounds. It also creates carcinogenic compounds indirectly. For example it creates retinoid and carotenoid breakdown products which are carcinogenic. Sunlight is also carcinogenic and creates carcinogenic retinoid breakdown products. We don't need to strictly avoid smoke or sunlight exposure but we should avoid excess smoke and sunlight exposure. I think it's probably true that people that consume a lot of retinol and carotenoids are more likely to get cancer from smoke and sunlight exposure.
Smoking is a shortcut to reducing liver retinol stores but of course it does have downsides. I smoke organic tobacco very conservatively. If smoking it is important to consume high vitamin C fruit daily.