Jenny – Page 17 – Effective Self Care info

December 30, 2020

Kale and carrots – super good right? maybe not for everyone.

The take home point about retinoid toxicity that is mind blowing to this dietitian (last post, & second half of this post) is that kale and carrots and other super nutritious beta-carotene rich foods might be part of the health problem for some people. If retinoid toxicity is occurring due to an enzyme change in the liver then the long held belief that we can’t really overdose on the carrot type of vitamin A may be wrong. Carnivore diet followers though, don’t rejoice too quickly, the animal product foods are sources of the active form of vitamin A and would definitely be part of the problem if excessive retinal was being activated to retinoic acid.

Thanks to everyone who responded to my survey on retinoid toxicity (last post/document). The summary points are that dry skin, seasonal allergies, and fibromyalgia type fatigue are fairly common symptoms and 100% of respondents (including me) were unfamiliar with all of the symptoms. Rewriting the survey and getting approval for research is needed. The initial effort did show that the topic is an unfamiliar one.

Change in the gene expression of enzymes involved in retinal/retinoic acid metabolism has been seen with infection with the Epstein Barr virus. (11) Chronic symptoms for years after an Epstein Barr infection have been known. The range of symptoms that can be due to retinoid toxicity could confuse the diagnosis process – see a dermatologist for the skin, an autoimmune/allergy specialist and a general practitioner might also be involved – would any one of them ask about all the possible retinoid toxicity symptoms? or suggest cutting back on food and supplement sources of vitamin A/beta carotene in order to just test the theory and see if any symptoms improve?

Retinoid toxicity may also help explain why smoking tobacco seems to have a somewhat protective effect against peripheral neuropathy while also being a risk – NAD+ deficiency could mean nicotine is helping provide a source of niacin – so the take home point there would be take niacin to help prevent nerve damage and fatigue (1, 2, 3) without providing smoke toxins that also worsen health risks. (post: Neuropathy can be a cause of extreme tiredness)

Nicotinamide adenine dinucleotide (NAD+) is an essential pyridine nucleotide involved in energy production within the mitochondria of cells and is protective against harmful effects of oxidative stress ( 2) – the chemical effects of physical or emotional stressors on the body. NAD+ is used in one enzyme involved in vitamin A metabolism. (9)

The following video connects Mast Cell over activity with niacin deficiency. Retinoic acid would add to mast cell activity as it is an activator of mast cells too. Mast cells can release histamine & then there can also be more supplied from foods, or produced in response to foods in mast cells in the intestinal lining. If the Epstein Barr virus causes retinoic acid metabolism gene changes maybe other infections can too. See: First Effective Treatment for Long Covid | Stunning Data from Huge New Study Dec 22, 2020 youtube.com, https://youtu.be/9-3V3h0ncIA

Low histamine/MCAS protocol
Niacin, zinc, selenium, vitamin C, D, quercetin, magnesium. – Dr. Ade Wentzel
Anti-histamine medications, over-the-counter generally
Prescription medications. Possibly ACE1 and ACE2 blockers, or Mast cell stabilizers or inhibitors.

The chemistry is complex, I am still learning, in the meantime though, cutting back on my daily intake of carrots, kale and then the addition of a lot of mango for a while – DID HELP – when did I ever think that I might be eating too much kale? or mango or my favorite anti-cancer vegetable – the carrot? answer – never. Learning about retinoid toxicity has been unexpected but helpful. Again carnivore diet fans – earlier in my symptom flare up history I found I had to cut out all animal products from my diet in order to get the new skin problem to resolve. Retinoid toxicity may have been a factor that I reduced without realizing why it helped but it worked so I stuck with it.

From a differential diagnosis perspective the range of symptoms that can be a result of retinoid toxicity would likely not be connected to each other. The patient might be seeing an allergy and autoimmune specialist, a psychiatric medical professional and talk therapist, and a general practitioner and as problems worsened a liver specialist, kidney specialist, and a neurologist might be added to the medical team – would they all talk to each other about the amount of carrots and liver in the patient’s average daily diet?

Probably not.

Updates are likely. Document with previous work on MCAS & a copy the survey.

Happy New Year’s Eve Eve!

Celebrating a new year and new health discoveries! (image: fireworks)

Excerpt from previous post – sources/types of vitamin A & retinoic acid

Might an excess or retinoic acid be overstimulating activity in the brain and causing hyperexcitability? (1, 2) Excess retinoic acid can have negative effects in the brain, particularly the hippocampus, (6), the area damaged initially in Alzheimer’s dementia, and may cause cell death. (7)

“The three active forms of vitamin A in the body are retinol, retinal, and retinoic acid.” … “Retinol and retinyl esters are often referred to as preformed vitamin A. Retinol can be converted by the body to retinal, which can be in turn be oxidized to retinoic acid, the form of vitamin A known to regulate gene transcription. Retinol, retinal, retinoic acid, and related compounds are known as retinoids. β-Carotene and other food carotenoids that can be converted by the body into retinol are referred to as provitamin A carotenoids (see the article on Carotenoids). ” (11)

Malfunction of CYP enzymes could increase the risk of excess retinoic acid as they are required to break down the active forms of vitamin A. (12)

Beta-carotene food sources

Beta-carotene, is an inactive form of vitamin A that is generally considered non-toxic, it provides the orange color of carrots, and since it is a fat soluble nutrient it can collect within our skin if eaten in excess and cause an orange color to the skin. (8, 13) It is unlikely to eat enough of the nutrient to cause the skin color change unless regularly drinking juice made with carrots, or kale or other fruits and vegetables that are very rich in beta- carotene. It is unlikely to cause any health problems other than to appear orange for a while (stop drinking so much carrot juice to make it fade). Infants and toddlers who are fed limited numbers of foods but daily may also develop the problem if carrots and sweet potatoes are given consistently instead of including more variety.

Beta-carotene may be broken down to the active retinal form in the intestinal lining or in the liver. (13)

Sources of Pre-formed vitamin A and Provitamin A – beta-carotene and other carotenoids.

“…vitamin A toxicity can occur from either topical or oral use. Oral vitamin A delivery comes in two forms: provitamin A (a prodrug that is metabolized to vitamin A) and preformed vitamin A. Pre-formed vitamin A is obtained from animal food sources, including dairy products and liver, and in most supplements. A list of other foods containing Vitamin A includes milk, cheese, margarine, butter, eggs, chicken, chicken liver, beef, beef liver, processed meats, pizza, fish, and cold breakfast cereals[1]. Provitamin A (beta-carotene and other carotenoids), found in plants such as green leafy vegetables, sweet potatoes, and carrots, must be metabolized to vitamin A. As a result, it is less likely to cause toxicity.” (9) [See Reference list from previous post/document)

From the survey:

Meals and snacks include meats, poultry, fish, milk and other dairy products. [and Vitamin A & D fortified milk equivalent drinks]
1. Several servings per day typically
2. At least one serving per day
3. At least one serving per week
4. One serving per month or less
5. No servings of animal products typically
6. Unknown
Meals and snacks include carrots, tomato products (fresh, or tomato sauce, ketchup, or salsa), sweet potatoes, winter squash or pumpkin, dark green leafy vegetables, cantaloupe, apricots, mango, papaya, peaches, nectarines.
1. Several servings per day typically.
2. At least one serving every other day
3. At least one serving per week
4. One serving or less per month
5. No servings of carotenoid rich plant foods typically

*2. Answer 2 is the amount menu planners have as a minimum goal – 1 beta carotene rich produce serving at least every other day.

My own symptoms & diet: I was having several servings of beta carotene rich foods daily and often several times a day, when I had a skin symptom flare up, reducing to the less frequent use helped the skin problem, cheilitis, finally get better. Cheilitis is nonhealing cracks/fissures at the corners of the lips and my problem didn’t get better with more vitamin Bs or iron which deficiencies of can also be a cause., but then got better within a few days of stopping the daily carrot, kale and mango intake. I have one serving occasionally now instead of several daily.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.

Reference List – includes excerpts & references not mentioned in the text.

Steve Hill, Niacin Increases NAD+ Significantly in Human Trial. June 8, 2020, lifespan.io, https://www.lifespan.io/news/niacin-increases-nad-significantly-in-human-trial/
Braidy N, Villalva MD, van Eeden S. Sobriety and Satiety: Is NAD+ the Answer?. Antioxidants (Basel). 2020;9(5):425. Published 2020 May 14. doi:10.3390/antiox9050425 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7278809/
Griffith GD, Griffith T, Byerrum RU, Nicotinic Acid as a Metabolite of Nicotine in Nkotiana rustica.* J of Biological Chemistry, Vol. 226, No. 12, December 1960 https://www.jbc.org/content/235/12/3536.full.pdf “It appears that the nicotinic acid derived from nicotine enters the metabolic pool and presumably is converted to bound forms such as the pyridine nucleotides, since the dilution of isotope increases somewhat with time.“
Nicotinic acid – an overview. sciencedirect.com https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/nicotinic-acid Niacin, V.K. Lule, … C.D. Khedkar, in Encyclopedia of Food and Health, 2016, https://www.sciencedirect.com/science/article/pii/B9780123849472004839 Interactions of Niacin with Drugs: “Taking nicotinic acid and/or nicotinamide and using a nicotine patch can increase the possibility of becoming flushed and dizzy.” – may increase the risk of the niacin flush reaction, also a side effect risk of the nicotine patch:
Niacin and Niacinamide (Vitamin B3) , webMD.com, https://www.webmd.com/vitamins/ai/ingredientmono-924/niacin-and-niacinamide-vitamin-b3
Pirinen E, Auranen M, Khan NA, Brilhante V, Urho N, Pessia A, Hakkarainen A, Kuula J, Heinonen U, Schmidt MS, Haimilahti K, Piirilä P, Lundbom N, Taskinen MR, Brenner C, Velagapudi V, Pietiläinen KH, Suomalainen A. Niacin Cures Systemic NAD+ Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy. Cell Metab. 2020 Jun 2;31(6):1078-1090.e5. doi: 10.1016/j.cmet.2020.04.008. Epub 2020 May 7. Erratum in: Cell Metab. 2020 Jul 7;32(1):144. PMID: 32386566. https://pubmed.ncbi.nlm.nih.gov/32386566/
Luis Rajman, Karolina Chwalek, and David A. Sinclair https://www.cell.com/cell-metabolism/pdf/S1550-4131(18)30122-0.pdf “NMNATs are also attractive targets for raising NAD+ in cells because they have dual substrate specificity for NMN and nicotinic acid mononucleotide (NaMN), and they contribute to both de novo and salvage pathways (Zhou et al., 2002). The green tea compound epigallocatechin gallate has been reported to activate NMNAT2 by more than 100% and NMNAT3 by 42% at 50 mM, although this needs to be confirmed, as no data were presented in the paper (Berger et al., 2005). … An alternative approach to raising NAD+ is to inhibit its degradation either by inhibiting PARPs or NADases, also known as glycohydrolases. The major NADase in mammals, CD38, is inhibited in vitro at low micromolar concentrations by flavonoids including luteolinidin, kuromanin, luteolin, quercetin, and apigenin (IC50 < 10 mM) .” …niacin/niacinamide supp may help reduce risk of kidney injury which involves low NAD+ … bloodflow and muscle and nerve function also may be improved by adequate niacin treatment. … “Since then, numerous studies have reinforced the view that NAD+ levels are key to neuronal function and survival. This includes the dependence on NMNAT2 and its NAD synthesis activity for axonal survival (Yan et al., 2010). ” Supplementing may help protect against Parkinson’s Disease and Alzheimer’s dementia and other neurologic conditions. “NAD-boosting regimens prevent and in some cases can reverse neuronal degeneration associated with hearing loss, prion toxicity, retinal damage, traumatic brain injury (TBI), and peripheral neuropathy (Brown et al., 2014; Dutca et al., 2014; Hamity et al., 2017; Lin et al., 2016; Vaur et al., 2017; Yin et al., 2014; Zhou et al., 2015) ” https://www.cell.com/cell-metabolism/pdf/S1550-4131(18)30122-0.pdf
Fricker RA, Green EL, Jenkins SI, Griffin SM. The Influence of Nicotinamide on Health and Disease in the Central Nervous System. Int J Tryptophan Res. 2018;11:1178646918776658. Published 2018 May 21. doi:10.1177/1178646918776658 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5966847/
Seung-Hye Hong, Ho-Phuong-Thuy Ngo, Hyun-Koo Nam, Kyoung-Rok Kim, Lin-Woo Kang, Deok-Kun Oh. Alternative Biotransformation of Retinal to Retinoic Acid or Retinol by an Aldehyde Dehydrogenase from Bacillus cereus, Applied and Environmental Microbiology Jun 2016, 82 (13) 3940-3946; DOI: 10.1128/AEM.00848-16 https://aem.asm.org/content/82/13/3940 “This enzyme converted not only small aldehydes to carboxylic acids but also the large aldehyde all-trans-retinal to all-trans-retinoic acid with NAD(P)⁺.“
1.1.1.105: all-trans-retinol dehydrogenase (NAD+). https://www.brenda-enzymes.org/all_enzymes.php?ecno=1.1.1.105&table=Natural_Substrates_Products Epstein-Barr virus lytic infection induces retinoic acid-responsive genes through induction of a retinol-metabolizing enzyme, DHRS9.17244623 From table https://www.brenda-enzymes.org/enzyme.php?ecno=1.1.1.105&onlyTable=Disease
Jones RJ, Dickerson S, Bhende PM, Delecluse HJ, Kenney SC. Epstein-Barr virus lytic infection induces retinoic acid-responsive genes through induction of a retinol-metabolizing enzyme, DHRS9. J Biol Chem. 2007 Mar 16;282(11):8317-24. doi: 10.1074/jbc.M608667200. Epub 2007 Jan 22. PMID: 17244623. https://www.jbc.org/content/282/11/8317.long “Abstract: Lytic Epstein-Barr virus (EBV) replication occurs in differentiated, but not undifferentiated, epithelial cells. Retinoic acid (RA) induces epithelial cell differentiation. The conversion of retinol into its active form, retinoic acid, requires retinol dehydrogenase enzymes. Here we show that AGS gastric carcinoma cells containing the lytic form of EBV infection have enhanced expression of a gene (DHRS9) encoding an enzyme that mediates conversion of retinol into RA. DHRS9 expression is also increased following induction of lytic viral infection in EBV-positive Burkitt lymphoma cells. We demonstrate that the EBV immediate-early protein, BZLF1, activates the DHRS9 promoter through a direct DNA binding mechanism. Furthermore, BZLF1 expression in AGS cells is sufficient to activate DHRS9 gene expression and increases the ability of retinol to induce the RA-responsive gene, CYP26A1. “

December 21, 2020

Retinoid Toxicity Symptom Questionnaire

Surveymonkey/Symptom Questionaire

The second half of this post goes into more detail about retinoid toxicity. Retinoid acid is an active form of vitamin A and it can activate mast cells of the immune system and is involved in many other functions of the body including skin health and calcium balance. The activation of mast cells can affect mood by increasing histamine release which affects brain excitability. Mast Cell Activity & Hyperexcitable Mood.

If the theory about retinoic acid is correct, then the liver is overactivating too much vitamin A and a solution for reducing symptoms might involve significantly reducing vitamin A sources in the diet. Adding liver healing nutrients and herbs might also be part of a solution aimed at restoring normal function and avoiding other mast cell activating foods or histamine releasing foods might also be part of a symptom resolution process.

This is complex physiology. Gathering more information from many people can help to show whether there is a pattern connecting excess vitamin A/retinoic acid and vaccine or medication injury.

Thanks in advance for completing the survey.

November 25, 2020

‘Allergic’ to flickering lights?

Flickering lights, whether shadows of trees on the road on a bright sunny day, or fast action movies, or actual strobe lights, have all been problems for me in the past. Migraine headaches after a light show at a music concert became expected. I stopped going to them or action movies – or once or twice went but wore sunglasses the whole time.

Epilepsy? Strobe lights of a certain timing can trigger epileptic seizures but I haven’t had seizures of any typical sort. I recently consulted a neurologist who ordered an EEG – which I wasn’t informed included intense strobe lights, for many minutes. I didn’t have a seizure during the EEG but I did have a bad mood meltdown/reaction almost immediately after leaving the office and it lasted for an hour or two instead of a few minutes to a half hour which has been more typical of my odd behavior symptoms.

I had been fairly stable ever since finding out more about Mast Cell Activation Syndrome, and avoiding most of the ‘avoid list’ foods. So search engine – yes, theoretically, someone else also wondered about why people with overactive mast cell problems are also sensitive to flickering lights – may be suggesting to the brain nystagmus of the eyes: (How Flickering Light can Cause an Allergic (MCAS) Response), – or it really could be the EMF of electronic screens too – but that wouldn’t explain why I was triggered by strobe lights used for an EEG screening, or the lights of an action movie. Just a busy black and white pattern can give me a slight headache feeling.

Not a definitive answer, however there often aren’t definitive answers with unusual health symptoms. Getting the problem under control is the goal, applying labels is more about society or insurance claims.

So – if you see me in sunglasses – it may be because I’m ‘allergic’ to the flickering of lights.

Fluorescent lighting causes flickering. In animal-based research it was found to affect inflammation and immune responses. Cellular perception of oxidative stress may lead to an increase in IL1-beta and TNF. Seeing flickering lights may suggest to innate genetic pathways that we may need to make an additional immune effort – and does.

“In all three organisms, Fluorescent light (FL) induced transcriptional changes of the acute phase response signaling pathway and modulated inflammation and innate immune responses. Our pathway and gene clustering analyses suggest cellular perception of oxidative stress is promoting induction of primary up-stream regulators IL1B and TNF. … Overall, the conserved nature of the genetic responses observed after FL exposure, among fishes and a mammal, suggest the presence of light responsive genetic circuitry deeply embedded in the vertebrate genome.” (2)

“Art is not what you see, but what you make others see.” – Edgar Degas

Confirmation or congeniality bias – we tend to believe information that supports our current belief far more readily than information that contradicts it. We may be twice as likely to find and believe information that is in agreement with our belief than to give credence to information that contradicts it. (Hart et al, 2009, 3) (Decision making ebook/WiseInsights)

To see a new idea or solution we may first have to take off our blinders that keep us focused on an old idea or more limited scope of what might be possible answers. Flickering lights give me a headache and can affect my mood when more intense or for more extended length of time – am I just imagining it? or it did happen? many times – yes, and wearing dark sunglasses is protective for me, whether watching an action movie, rock concert, walking around a grocery store lit by fluorescent lights, or driving at night in urban areas with a lot of highway lights and headlights from oncoming traffic.

The mechanism of action of flickering lights triggering an immune reaction may involve a health status pathway of normal immune function that may include detecting nystagmus like light patterns as theorized regarding MCAS, (1, 5), and/or it may involve intense blue light over activating light sensing TRP channels until depolarization doesn’t occur as rapidly as in normal vision. (6) Whatever the mechanism – flickering lights inducing illness may have been weaponized. (4)

Sunglasses – check.

Reference List

Russell Irvin Johnston, @russjj, How Flickering Lights can Cause an Allergic (MCAS) Response. March 9, 2019, medium.com, https://medium.com/@russjj/how-lights-flickering-can-cause-an-allergic-mcas-response-c0e250ef37f9
Boswell M, Lu Y, Boswell W, et al., Fluorescent Light Incites a Conserved Immune and Inflammatory Genetic Response within Vertebrate Organs (Danio Rerio, Oryzias Latipes and Mus Musculus). April 2019, Genes 10(4):271, DOI: 10.3390/genes10040271 https://www.researchgate.net/publication/332195692_Fluorescent_Light_Incites_a_Conserved_Immune_and_Inflammatory_Genetic_Response_within_Vertebrate_Organs_Danio_Rerio_Oryzias_Latipes_and_Mus_Musculus
Hart W, Albarracín D, Eagly AH, Brechan I, Lindberg MJ, Merrill L. Feeling validated versus being correct: a meta-analysis of selective exposure to information. Psychol Bull. 2009;135(4):555-588. doi:10.1037/a0015701 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4797953/
Yasemin Saplakoglu, Russia Claims Strobe-Light Weapon Causes Nausea & Hallucinations. Is That Even Possible?, February 15, 2019, livescience.com, https://www.livescience.com/64774-russia-navy-weapon-hallucinate.html
Naren Srinivasan, Oliver Gordon, Susan Ahrens, et al., Actin is an evolutionarily-conserved damage-associated molecular pattern that signals tissue injury in Drosophila melanogaster. eLife 2016;5:e19662 DOI: 10.7554/eLife.19662 https://elifesciences.org/articles/19662 “Thus, extracellular actin detection via a Src-family kinase-dependent cascade is an ancient means of detecting cell injury that precedes the evolution of adaptive immunity.“
Katz B, Payne R, Minke B. TRP Channels in Vision. In: Emir TLR, editor. Neurobiology of TRP Channels. Boca Raton (FL): CRC Press/Taylor & Francis; 2017. Chapter 3. Available from: https://www.ncbi.nlm.nih.gov/books/NBK476112/ doi: 10.4324/9781315152837-3 https://www.ncbi.nlm.nih.gov/books/NBK476112/ “These studies have led to the identification and characterization of TRP as a light-sensitive and Ca²⁺-permeable channel (Minke, 2010; Montell, 2011; Hardie, 2011). Illumination of fly photoreceptors induces a cascade of enzymatic reactions, which result in activation of the light-sensitive TRP channels (Minke, 2010; Devary et al., 1987). To function as a reliable light monitor, each stage of the phototransduction cascade needs an efficient mechanism of activation as well as an equally efficient mechanism of termination, ensuring that, at the cessation of the light stimulus, the photoreceptor potential will rapidly reach dark baseline. … Failure of response termination at the stage of R activation was designated the prolonged depolarizing after (PDA) potential by Hillman, Hochstein, and Minke (Hillman et al., 1983; Minke, 2012). The PDA, like the light coincident receptor potential, arises from light-induced opening of the TRP channels in the plasma membrane. However, in contrast to the light coincident receptor potential, which quickly declines to baseline after the cessation of the light stimulus, the PDA is a depolarization that continues long after light offset (Figure 3.4) (see Hillman et al., 1983; Minke, 2012 for reviews). … Thus, massive R to M photoconversion by intense blue light induces a PDA, while M to R photoconversion by intense orange light suppresses the PDA. … In summary, the PDA is observed only when a considerable amount of photopigment (>20%) is converted from R to M. The larger the net amount of R to M conversion, the longer the PDA. ”

November 21, 2020

Note about notes, an open notebook.

I write about many topics because I am interested in many topics. Health itself is a vast topic – interconnected though. Research silos with specialists focusing on the minutia of one area of study creates disconnect that may prevent seeing the greater whole needed for health.

I like health and haven’t had it consistently since early childhood. Many genetic differences in metabolism is part of my problem I’ve learned which makes it easy for me in some ways to see how important a body function may be in every day life – because I don’t have it. This also means solutions that work for me may not work the same for people with typical genetic metabolism. It may help some people though. Metabolic problems can occur due to illness, older age, or malnutrition.

Learning is teamwork. I study what others have written and make notes so I may more easily find the information that I read again. The internet is a big place, full of wonderful information – finding it again is not always easy. My blogs are my notebook – open access in the hope that it may help lead others to finding useful information for their own purposes.

I like health and current medical system does not focus on prevention or early treatment guidance. You have to be quite sick to prove a need for a diagnosis or treatment and the treatment may just be a medication that makes overall health worse rather than being guidance to correct underlying differences and improve natural function. My approach is the early identification of problems and how to restore natural function. Genetic differences and nutritional needs are my main focus and area of more experience. I am learning, there is a lot to learn.

Based on what I have learned about my body’s differences and chronic issues, paralysis, Alzheimer’s dementia, liver and kidney injury may be in my future – I would rather not have to experience any of those – which means I have to figure out what I may need to do to prevent them – because the focus of western medicine is on treating problems after they are fairly severe and show up on a lab test.

If my notes can help other people or researchers too, on their own path towards learning, bonus.

*mentioned to my sister this morning – I would need a graduate degree (or several) to understand all of this stuff – and then it would still be hard. This is very advanced information – I am not an expert – point is – no one is. Prevention of organ damage in sepsis is not happening across the US with the Covid epidemic – prevention requires early treatment before too much damage and irreversible scar tissue is formed.

” The main mechanisms involved in the pathogenic cascade and in the evolution of sepsis are represented by the inflammatory response, immune response, and redox activity, followed by the involvement of cellular defects, which all lead to severe organ dysfunction. Adding to this phenomenon are severe respiratory infections; tissue hypoxia; acute kidney injury (AKI); metabolic imbalances; and, last but not least, derangements of the biological system as a whole. Through the augmentation of the inflammatory status and through the concomitant derangement of several organ functions, a high percentage of critical patients with sepsis develop multiple organ dysfunction syndrome (MODS), and finally death [8,10–12]. ” (1)

“However, recent results have proven that cannabinoids are responsible for a decrease in the expression of certain pro-inflammatory cytokines such as IL-6, IL-12, IL-1, IL-2, and TNF-α.” (1)

Reference List (my notes for further study re last post)

Anca Raluca Dinu, Alexandru Florin Rogobete, Tiberiu Bratu, et al., Cannabis Sativa Revisited—Crosstalk between microRNA Expression, Inflammation, Oxidative Stress, and Endocannabinoid Response System in Critically Ill Patients with Sepsis. Cells 2020, 9, 307; doi:10.3390/cells9020307, 28 January 2020 https://www.dropbox.com/sh/ux0r70xaszbnlj8/AAB4k6QoFRRM-XyKzacCs4-Pa?dl=0 “Furthermore, a series of important implications on inflammation and the immune system that are induced by the activity of cannabinoid receptors stimulated by the delta-9-tetrahydrocannabinol (∆9-THC) and cannabidiol (CBD) have been noticed. One of the most important is their ability to reduce the biosynthesis of pro-inflammatory mediators and the modulation of immune mechanisms. Different studies have reported that cannabinoids can reduce oxidative stress at mitochondrial and cellular levels. … we wish to present the possible implications of cannabinoids in the most important biological pathways involved in sepsis, such as inflammation, redox activity, immune system, and epigenetic expression.”
Tafti M, Ghyselinck NB. Functional Implication of the Vitamin A Signaling Pathway in the Brain. Arch Neurol. 2007;64(12):1706–1711. doi:10.1001/archneur.64.12.1706 https://jamanetwork.com/journals/jamaneurology/fullarticle/794818
Kathleen L. McCoy, “Interaction between Cannabinoid System and Toll-Like Receptors Controls Inflammation”, Mediators of Inflammation, vol. 2016, Article ID 5831315, 18 pages, 2016. https://doi.org/10.1155/2016/5831315 https://www.hindawi.com/journals/mi/2016/5831315/