@Mr-X It took about three drops in an hour or more.

@DavidPS while he didn’t mention lactoferrin in the interview, I remember hearing Peat once say that an all milk diet would be sustainable for about a month before causing iron deficiency. Just another thing to think about in the role milk and its components seem to have on iron. I’ve had pretty rough teeth my whole life despite following dentists recommendations as a child/teen. I have found a ton of relief in lactoferrin, (helps with tooth sensitivity, color, (from yellow to white) and translucence). The color of my teeth reminds me of rust, (which when diluted is more of a yellow-orange than red). Another modality that has improved my teeth has been the work of Dr Manhart over at the Calcium Therapy Institute. His products combine calcium with zinc… And here we are again, zinc, iron. I wonder, if bones are holding iron instead of zinc what their appearance might be? Maybe yellowing from oxidized iron? How is the Calcium Therapy Institute able to recalcify teeth that have almost completely disintegrated, (they primarily focus on bacterial infections causing the decay-though this brings us back to iron potentially)? Another thing I think about regularly is copper plumbing. All the water that touches our body lives/travels in copper. I don’t know one way or that other if this matters, but it’s just another drop in the bucket of “what the heck is going on with iron, zinc, and copper?” Is it possible we’d be better off with pex tubing? I recall another interview with Peat where he mentioned that the plastics used for pex were actually some of the safest. I have become fully convinced that environmental factors are possibly the most important to our health, but maybe they aren’t the ones commonly considered. People seem very worried about pollution, and sprawl, and things of this ilk, (which obviously have their own issues) but no one really talks about copper plumbing as potentially problematic. I have no evidence it is to be clear, it’s just something that pops in my head from time to time. One final thing I consider is the number of times I heard Peat say that typically chelation is more deleterious than simply leaving it alone. This stops me from jumping on the HG7 bandwagon despite being interested. I sometimes wish Dr Peat was still with us, as l’d love to have his option on some of the newer modalities that pop up now and then. I also think that Peat tended to focus on simplicity over utility because of his understanding of the nature of those who are ill. It’s possible that a complex system like say HG7 could be beneficial, however Peat may have discounted it for its potential to harm, and the difficulty of adhering to it. This doesn’t mean however that something so complex is inherently non-beneficial.

@DavidPS DavidPS said Lithium has been known to benefit the brain. Small amount of lithium found in the water table had great benefit. Excerpts from the study (main points): Here we show that endogenous lithium (Li) is dynamically regulated in the brain and contributes to cognitive preservation during ageing. Of the metals we analysed, Li was the only one that was significantly reduced in the brain in individuals with mild cognitive impairment (MCI), a precursor to AD. Li bioavailability was further reduced in AD by amyloid sequestration. Replacement therapy with lithium orotate, which is a Li salt with reduced amyloid binding, prevents pathological changes and memory loss in AD mouse models and ageing wild-type mice. These findings reveal physiological effects of endogenous Li in the brain and indicate that disruption of Li homeostasis may be an early event in the pathogenesis of AD. Li replacement with amyloid-evading salts is a potential approach to the prevention and treatment of AD. Analyze Yes, but … The amount is so light that it’s hard to measure without an appropriate tool. I’ve decided to make a search with LucH’s pendulum (1) when I saw last month an article in a medical review. We have to make a distinction between a pathology (AD) and cognitive preservation by anticipation. First, note that the improvement has been obtained on mice. Not only, but well in the referenced study. The improvement observed in the axons is fine / real but there is no feedback on the long term. A mouse doesn’t talk and doesn’t feel good but shows an ability to target sth (behavior to recognize, to memorize a way to get a sweat). The mouse acts in order to obtain a reward in the form of food or a punishment when it makes a mistake. I explain the restriction: Synaptic reuptake is a key process for regulating neurotransmitter concentration in the synapse. Lithium acts on this process to modulate neuronal activity. How much lithium is found in brain axons and how much is sequestered by cortical amyloid plaques has been studied. It has been done with human beings. See further details on the link beneath. For the other readers: Overall, lithium readjusts the balances between excitatory and inhibitory neurotransmission, as well as between catecholamines and acetylcholine. It is the adjustment of these balances, rather than the isolated effect on a single neurotransmitter, that partly allows for the improvement and stabilization of mood. End of the parenthesis. Dose range The effective dose range for lithium is relatively narrow, and exceeding it can lead to adverse effects. The specific mechanisms by which lithium exerts its effects on the brain are still under investigation (…). In case of supplementation, toxic effects are to be expected, such as concentration problems, but not only that. Plasma concentration is reached within 2 to 4 hours after oral administration of a supplement. (1) The plasma half-life is approximately 24 hours. Equilibrium is reached between the 5th and 8th day. More quickly if the kidneys' elimination capacity is reduced. Be careful, apprentice chemists, especially in the case of insufficient sodium intake. Final thought: Yes, Li is a cofactor in the absorption of certain vitamins, helps the body produce serotonin, supports the transmission of neural messages and much more. But I’d rather try to get my Li through food, provided you don’t suffer from intolerance, as there is a lot of Li in milk, cheese, eggs and sea food or liver (chicken or beef). Not yet official, but lithium is gradually being considered an essential trace element, with a recommended daily intake of 1 mg for a 70 kg adult. (2) Studies also suggest that lithium's effectiveness depends on the availability of other minerals and works synergistically with them to maximize its effectiveness on mood, longevity, and cognitive support. (3) In another human study, a daily microdose of just 300 mcg of lithium was found to significantly reduce age-related cognitive decline just three months after starting a lithium supplement. (4) NB1: Alzheimer is a complex pathology. We need to act in many directions. In short: exercise (mental and physical), K2 MK4, tocos, iodine and other well-known ones. For another article. NB2: I won’t trust a labo when they say lithium orotate could do the job. (5) Low supplementation (e.g., 5 to 20 mg/day of lithium orotate) may produce transient or subtle effects, but does not guarantee stable maintenance of brain levels. Sources & references My article on lithium https://mirzoune-ciboulette.forumactif.org/t2124-le-lithium-ameliore-l-humeur-optimise-les-cellules-souches-la-longevite-et-plus-encore#30285 Lithium: occurrence, dietary intakes, nutritional essentiality. J Am Coll Nutr, 2002) DOI: 10.1080/07315724.2002.10719188 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443601/ https://pubmed.ncbi.nlm.nih.gov/22746245/ Une supplémentation faible (ex : 5 à 20 mg/jour de lithium orotate) peut produire des effets transitoires ou subtils, mais ne garantit pas un maintien stable des niveaux dans le cerveau (cf. étude Human brain 7Li-MRI: 10 à 60 µM, stable après 2-4 semaines). Human brain 7Li-MRI following low-dose lithium dietary supplementation in healthy participants - ScienceDirect 2024

@LucH - thanks for your analysis. I tend to underthink some of these studies and often I do not make connections to other studies. I stopped eating grapefruit moths ago but I had not given a second thought to eating mandarin oranges. I am goig to rethink my dietary sources of Vitami C.

@pittybitty said in The artificial/accelerated aging effects of ultra-filtered sunlight: Full spectrum light bulbs (aka grow lights) are quite easy to get I find it easier to get sunlight than grow bulbs. Sunlight is much more intense than the light emanating from the bulbs. Grow lights are typically positioned very close the plants to get the best results. The image in Fgure 4(d) posted above shows how rapidly the incandescent light fades from it source. I would expect the same from grow lights. https://en.wikipedia.org/wiki/Radiant_intensity Winndow pane glass filters the portion of sunlight that the body uses to make vitamin D. If you go outside for 10-20 minuts during the day you can make enough vitamin D. The manufacturers of e-glass are charging a hefty premium for this specialty glass. I would expect that home buliders would not want to build using this glass.

@Mauritio said in Sirtuins, Klotho and Ray Peat: Im courios what you guys think of that ? @DavidPS I've seen you post about sirtuins from time to time. I try not to overthink the effects of sirtuins. My posts about sirtuins have mostly been to support the effects of healthy foods. Here are my posts from the RPF. https://lowtoxinforum.com/search/2681847/?q=sirtuins&c[users]=David+PS&o=relevance Dr. Peat's quote about sirtuins needs to read in context. It may have been written many years ago. In addition, it does not distinguish which of the numbered sirtuins applies. If Peat says sirtuins are bad because they block p53, the context matters here aw well. Peatbot: P53 is a well-known tumor suppressor protein that plays a critical role in regulating the cell cycle and preventing cancer. It is often referred to as the "guardian of the genome" because of its role in maintaining genomic stability by preventing mutations. When p53 is functioning properly, it can help protect against cancer by repairing DNA or initiating apoptosis (programmed cell death) if the DNA damage is irreparable. However, mutations in the p53 gene can lead to a loss of its tumor-suppressing functions, which can contribute to the development of cancer.

C16.:0 Palmitic acid C18:0 Stearic acid C12:0 lauric acid or C4:0 butyric acid or C6:0 Caproic acid Note: Some people could have allergy problem with stearic acid when suffering from leaky gut or border bross inflamed (stomach). When consumed on a regular base, from supplements, e.g. It depends on the amount and the frequency. As a whole food or re-combined as a soluble vehicle when adding e.g. essential oils. When you take it with food and not directly injected in the blood (fatty muscle leg or arm), is quite different. I haven't the answer. Edit: If you meant "does the mixture change the assimilation" when fluid, no. Up to 10 carbons, direct assimilation from the liver to the muscles (or in the Krebs cycle) (portal vein). Between 12-14, +/ half and half (half with VLDL and LDL vehicle). Higher carbon chains with these two last conveyors. From ChatGPT (confirmation asked): MCT oil is indeed utilized by muscles for energy, not just for the Krebs cycle in the liver. While MCTs are readily metabolized in the liver and can be converted into ketone bodies, they are also transported to other tissues, including muscles, where they can be directly used as fuel. This direct utilization contributes to muscle energy production and can potentially enhance muscle function and growth.

@LucH @wrl thanks for the interestng links.

Prebiotics Improve Blood Pressure Control by Modulating Gut Microbiome Composition and Function: A Systematic Review and Meta-Analysis (2025) Results: Of the 3010 records screened, nineteen studies met the inclusion criteria (seven human, twelve animal). A random-effects meta-analysis was conducted on six human trials reporting post-intervention BP values. Prebiotics were the primary intervention. In hypertensive cohorts, prebiotics significantly reduced SBP (−8.5 mmHg; 95% CI: −13.9, −3.1) and DBP (−5.2 mmHg; 95% CI: −8.5, −2.0). A pooled analysis of hypertensive and non-hypertensive patients showed non-significant reductions in SBP (−4.5 mmHg; 95% CI: −9.3, 0.3) and DBP (−2.5 mmHg; 95% CI: −5.4, 0.4). Animal studies consistently showed BP-lowering effects across diverse etiologies. Prebiotic interventions restored bacterial genera known to metabolize DFs to SCFAs (e.g., Bifidobacteria, Akkermansia, and Coprococcus) and increased SCFA levels. Mechanistically, SCFAs act along gut–organ axes to modulate immune, vascular, and neurohormonal pathways involved in BP regulation. [image: 1755345967207-110ba5d4-966b-4f7d-a2cb-6f51cf377aa4-image.png]

Hi, In my research on the effects of phytotherapy against inflammation in order to relieve pain, I found this. Boswellic acid from boswellia serrata is effective against these “agents”: Board: [image: 1755328102838-tableau-docx-partiel.jpg] So effective against these agents. Abréviations: RA = Rhumatisme arthritique / Rheumatoid Polyarthritis (often calle « PR », in French) PGE = Prostaglandines. IL-1B = cytokine, mediator involved in particular in RA (destruction of cartilage/synovium). TNF-a = facteur de nécrose tumorale alpha (cytokine, messenger involved in the inflammatory process). MMP = matrice métalloprotéinase (MMP stands for enzymes that selectively hydrolyze peptide bonds and degrade structural proteins; they play a crucial role in the breakdown of joint tissues). NF-kB = facteur nucléaire-kappa B (controls many genes involved in inflammation). PLA2 = Phospholipase A2. NO = monoxyde d’azote synthase (=>inhibited nitric oxide production). LPS = Lipo-polysaccharides (immune reaction induced by an excess of bacterial residues destroyed by macrophages). AO = anti-oxydant. (x) => (moderate effectiveness) (if into brackets) X? => A single source found. NB: Unchecked boxes only indicate that I have not found any "reliable studies" mentioning this action. We will complete this later, if possible... See this post, on my forum, for analyze and comments: Understanding the inflammatory response (AA cascade). Substances naturelles anti-douleur. Tableau https://mirzoune-ciboulette.forumactif.org/t266-substances-naturelles-anti-douleur-tableau#15733 (update 04/2020) : Comment: I’d combine Boswellia with Celadrin to target as much possible the other factors. These molecules only acts on inflammation, not on the pain. Celadrin is a brand name and is made of “unsaponifiables”, often coming from of avocado and soy. Lubricates joints. 350 mg 3X/jr. Comment: Don’t forget these molecules have to be taken in staples, with recovery periods, not to weaken the detox pathway Cyp450 (accumulation of toxins could happen, otherwise). So pause every 6 weeks, according to your feelings, as well. Some substances have an impact on platelet aggregation, as well. E.g. curcumin and aspirin (white willow bark). Not Celadrin. The body is able to manage and fight against pain, if not overburden. Need to be covered against oxidation, to preserve homeostasis (interaction). B6 PLP could be useful too but mind the side effects when overload. I associate 100 mg of each B1, B2, B3 niacinamide, B6 PLP + 500 mg TMG, but only 5 days a week, for 3 weeks. Then 2 weeks stop (to avoid problem with GABA when excess B6).

@Milk-Destroyer - Evidently, the study has its limitations.

Oxygenated, You're making one categorical affirmation after another with a conviction that contrasts with the attitude of authors in this field, who are conservative for being aware of the volume of unreliable or contradictory information on the topic. Already in the title, you declared that fat oxidation is the main source of cellular ROS, but how did you conclude this? [image: 1754347668994-029bee82-cd38-4ff1-aeb7-28846684e250-image.png] ⠀(10.1242/jeb.221606) In pink are the major sources: [image: 1754347697643-dac6e475-a2b8-42a9-babc-92ed6b2fc234-image.png] ⠀(10.1038/s41580-020-0230-3) [image: 1754347722481-da7b76ab-128b-4dfb-8524-02fee5516ac3-image.png] ⠀(10.1038/s41580-020-0230-3) It would be worth clarifying how each of these H₂O₂ is generated, as we could have yet another statement put to question: that ROS formation involves unpaired electrons. Example: "[..]complex I could mediate one- or two-electron reduction of oxygen[..]" (10.1016/j.bbabio.2013.01.002) [image: 1754347771554-786c9b7d-f263-4d02-ad31-1196acfc643a-image.png] ⠀(10.1146/annurev.arplant.55.031903.141701) We know that oxidases generate H₂O₂, which already challenges the exclusive association of ROS with one-electron reactions. Nevertheless, even if we relax the criteria to include other ROS sources related to fatty acids (peroxidation and eicosanoid metabolism as examples), we would still be left with comparable alternatives to consider, such as NADPH oxidases (NOX). [image: 1754347859260-7c318a3d-f274-44da-9199-9fa83e96b037-image.png] ⠀(10.1016/j.redox.2020.101722) [image: 1754347869418-2f9790b8-96fe-438d-81f6-21dbb7593dd7-image.png] ⠀(10.1242/jeb.221606) You can tell that a fraction is attributed to mitochondria. Then, only part of this mitochondrial (and peroxisomal) ROS will come from fatty acid oxidation in normal conditions. Cellular ROS > Mitochondrial ROS > Fatty acid oxidation ROS With conclusive information about the contribution of each compartment, we would have to discount all ROS sources unrelated to the oxidation of fatty acids, our latest carcinogens on the block. Funnily, with glucose oxidation, every opportunity to maximize ROS production is taken as a room for cancer therapy. With fatty acids, when the opportunity appears, the picture is carcinogenic and let's leave the interpretation at that, without conceiving exploiting this "massive" burst of ROS to potentiate eradication therapies. Different from many doctors, most researchers in the field are well-aware of the association of stimulated oxidative phosphorylation with lower ROS production, an observation that has been circulating since early publications: "Addition of succinate speeds up H₂O₂ production by a factor of six and, after that, the addition of ADP (state 4 → state 3 transition) (Chance & Williams, 1956) decreases it to a value similar to that in the absence of substrate. When all the added ADP is phosphorylated, there is an acceleration paralleling the changes in the mitochondrial metabolic state. A further addition of ADP produces the transition to the active state, with the corresponding slow rate of H₂O₂ production." (10.1042/bj1280617) But a higher metabolic rate doesn't inherently lower ROS production. It's a matter of electron availability around susceptible sites. Oxygen consumption is usually tied to ATP production, and increasing the need for ATP tends to increase the rate of respiration. Then, with a higher metabolic rate, the demand for electrons tends to decrease their availability, clearing the way for an orderly electron movement while reducing the chances of leakage. Likewise, a low metabolic rate with accompanying low rate of substrates oxidation must be able to get respiratory ROS production under control. ⠀ "Not only does reverse flow result in a dramatic shift of the redox status towards reduction, but the build-up of ROS leads to direct structural damage to various cell proteins, as well as any intracellular structure containing polyunsaturated lipids." More like the other way around: an abnormal change of the redox status in favor of reduction results in reverse electron flow. Electron accumulation precedes the redistribution. ⠀ "What has not been widely acknowledged is that in the absence of exogenous agents capable of blocking or more of the ETC complexes (e.g rotenone, metformin, etc), reverse electron flow happens quite easily and is in fact responsible for the majority of ROS production simply as a result of shifting the metabolic substrate from glucose to fat (Randle Cycle). Namely, if the Randle Cycle (RC) shifts sufficiently in favor of fat oxidation, that results in depletion of the FAD co-factor, and thus a block at ETC Complex II. In other words, all that is needed for massive generation of ROS is to switch from oxidizing primarily glucose to oxidizing primarily fat. That sounds shocking and counter-intuitive, considering the world (and medicine) has gone crazy over low-carb diets lately, but it is well-known and undisputed biochemical fact." Putting aside the authoritative "undisputed biochemical fact", you have constructed the argument concerned with ROS overproduction from acute substrate alternation ("to switch"), only to then abruptly invoke chronic fatty acid oxidation ("low-carb diets"). These are different scenarios that can't be lumped together. Why the need for alarmism? The term "massive" might be more suitable for describing Kvothe's reproductive organ (..I've heard) or the overwhelming ROS production that often occurs when blood flow is restored after a period of interruption, leading to severe tissue damage. However, reverse electron flow can also occur in a controlled, transient fashion, serving to induce beneficial adaptations. It's odd that you reduced the problem to SDH 'blockage' from FAD depletion. If this was the case, why would it trouble cells that are primed to metabolize fatty acids as an adaptation to frequent exposure? Once the body synthesizes enough flavins to meet predictable needs (including everyday perturbations), it's a matter of maintenance to replenish obligatory losses from flavoproteins, and these are modest in relation to their extensive recycling in reactions. Fatty acid metabolism has to remain dependable in stressful conditions, and these are associated with micronutrient shortage. Also, how do you explain the ability of mitochondria to oxidize copious amounts of plain succinate when incubated with it? Not only in isolation, but especially in the presence of other substrates that help to clear inhibitory oxaloacetate. If other substrates can enhance the oxidation capacity, it becomes questionable to argue in terms of flavins repurposing. For succinate to become a SDH inhibitor itself, levels have to get extremely high while possibly involving an inability to wash it out, as when local blood circulation stops. Nevertheless, FAD should remain intact in SDH, which is why succinate can be readily oxidized when oxygen levels are restored in the tissue. In some situations, the purported SDH blockage could actually be protective, such as when SDH is intentionally inhibited by malonate to prevent ROS overproduction in classical reverse electron flow. Complex I ← UQ ← SDH ← Succinate Complex I ← UQ ← SDH ↚ Succinate If you had in mind reverse electron flow in the broad sense, the immediate concern in the respiratory chain for upstream processes would be impaired Complex I activity due to competition for available ubiquinone. Complex I is responsible for reoxidizing NAD for matrix dehydrogenases dependent on it, that in turn are overlooked sources of ROS. Altogether, it's a peculiar approach. What to make of it?

Ai Key Strategies to Improve Your Microbiome 1. Increase Dietary Fiber Benefits: Fiber acts as a prebiotic, feeding beneficial gut bacteria. Sources: Aim for 21 to 38 grams of fiber daily from: Legumes (beans, lentils) Whole grains (oats, quinoa) Fruits (berries, apples) Vegetables (leafy greens, sweet potatoes) Nuts and seeds >2. Stay Hydrated Importance: Water supports digestion and nutrient absorption. Recommendation: Drink enough water to prevent dehydration and maintain gut health. >3. Incorporate Fermented Foods Examples: Yogurt, kefir, sauerkraut, kimchi, and kombucha. Benefits: These foods contain probiotics, which can enhance gut diversity. >4. Limit Processed Foods Impact: Ultra-processed foods can negatively affect gut health. Advice: Focus on whole, unprocessed foods to support a healthy microbiome. >5. Manage Stress Connection: Stress can disrupt gut health. Techniques: Practice relaxation methods like meditation, yoga, or deep breathing. >6. Regular Exercise Effect: Physical activity promotes a diverse microbiome. Goal: Aim for at least 150 minutes of moderate exercise weekly. >7. Get Enough Sleep Recommendation: Aim for 7 to 9 hours of quality sleep each night. Benefit: Good sleep supports overall health, including gut health. Conclusion Improving your microbiome involves a combination of dietary changes, hydration, stress management, exercise, and sleep. By adopting these practices, you can enhance your gut health and overall well-being.

Defining a vitamin A5/X specific deficiency – vitamin A5/X as a critical dietary factor for mental Health Abstract: A healthy and balanced diet is an important factor to assure a good functioning of the central and peripheral nervous system. Retinoid X receptor (RXR)-mediated signaling was identified as an important mechanism of transmitting major diet-dependent physiological and nutritional signaling such as the control of myelination and dopamine signaling. Recently, vitamin A5/X, mainly present in vegetables as provitamin A5/X, was identified as a new concept of a vitamin which functions as the nutritional precursor for enabling RXR-mediated signaling. The active form of vitamin A5/X, 9-cis-13,14-dehydroretinoic acid (9CDHRA), induces RXR-activation, thereby acting as the central switch for enabling various heterodimer-RXR-signaling cascades involving various partner heterodimers like the fatty acid and eicosanoid receptors/peroxisome proliferator–activated receptors (PPARs), the cholesterol receptors/liver X receptors (LXRs), the vitamin D receptor(VDR), and the vitamin A(1) receptors/retinoic acid receptors (RARs). Thus, nutritional supply of vitamin A5/X might be a general nutritional-dependent switch for enabling this large cascade of hormonal signaling pathways and thus appears important to guarantee an overall organism homeostasis. RXR-mediated signaling was shown to be dependent on vitamin A5/X with direct effects for beneficial physiological and neuro-protective functions mediated systemically or directly in the brain. In summary, through control of dopamine signaling, amyloid β-clearance, neuro-protection and neuro-inflammation, the vitamin A5/X – RXR – RAR – vitamin A(1)-signaling might be “one of” or even “the” critical factor(s) necessary for good mental health, healthy brain aging, as well as for preventing drug addiction and prevention of a large array of nervous system diseases. Likewise, vitamin A5/X – RXR – non-RAR-dependent signaling relevant for myelination/re-myelination and phagocytosis/brain cleanup will contribute to such regulations too. In this review we discuss the basic scientific background, logical connections and nutritional/pharmacological expert recommendations for the nervous system especially considering the ageing brain. [image: 1753642620660-195305d5-1b58-4f65-a688-e795b5b0457c-image.png] [image: 1753642742365-868bf21c-c9f8-4fdc-b2bb-754445da7072-image.png]

@LucH Thanks for the info! There are some animal studies on restricting only omega-6, and the effect is to increase the metabolism of omega-3 and decrease that of omega-6: Fifteen weeks of n-6 PUFA deprivation compared with adequate diet decreased the mean unesterified plasma concentration of n-6 PUFAs by 84% (Table 1). The change in the total unesterified n-3 PUFA concentration was statistically insignificant, although unesterified DHA and EPA concentrations were increased by 53% and 79% The total n-3 PUFA concentration in brain was increased by 15%, reflecting largely an 11% increased DHA concentration (Igarashi et al. 2009). Expression of enzymes of the 20:4n-6 cascade, cPLA2-IVA and COX-2, was downregulated, whereas expression of DHA-preferring calcium independent iPLA2-VIA (Garcia and Kim 1997; Strokin et al. 2004; Ramadan et al. 2010; Basselin et al. 2011) and of 15-lipoxygenase (LOX) was up-regulated (Kim et al. 2011). COX-2 mRNA was decreased significantly (−23%, p b0.05) (Fig. 3A) in the n-6 PUFA deprived rats compared with adequate rats, as was COX-2 protein (−32%, pb0.05) (Fig. 3B). The deficient diet did not change COX-1 or mRNA significantly