Posts made by Amazoniac

It directs to..

a) Professor Smith:

"If a person takes in more toxic "vit" A than they excrete on a regular basis, then they are ACCUMULATING it in their liver and bodyfat

If 306 mcg beta-carotene (that's 1020 IU, one carrot has 6000 IU!) took 58 DAYS to turn over...do you realize just how fast you are filling up with this toxin?

1 beta-carotene eventually has to split into 2 retinaldehydes"

b) Disciple:

"Wow.

And this is also a great study for showing how much beta-carotene is actually converted to retinol. They write a minimum of 62% is turned into retinol. So a lot will eventually go the retinol route.

"What is clear is that, by our estimates, a minimum of 62% of the absorbed β-carotene was cleaved to vitamin A and by this reasoning the vitamin A value of β-carotene dose was 0.53. [The calculation is as follows: Assuming central cleavage, 1 mol of β-carotene yields 2 mol of vitamin A. If 62% of the absorbed β-carotene were cleaved to vitamin A, 1 mol of β-carotene would yield 1.24 mol of vitamin A. Thus, the vitamin A value of the absorbed dose is 1.24. Yet, the dose was 42.6% absorbed. So, the actual vitamin A value is (1.24) (0.426) or 0.53.]"

1 molecule of beta-carotene turns into 2 molecules of "active vitamin A".

The 0.53 value means that 1mg of ingested beta-carotene will turn into 0.5mg retinol. In other words, one medium carrot (eaten with lots of fat) can be equivalent to 27g beef liver.

Due to the time-delayed conversion, an acute poisoning is not possible, but a chronic poisoning is."

Their claims:

• a) "[..]one carrot has 6000 IU!" (1,800 mcg)
• b) "[..]one medium carrot (eaten with lots of fat) can be equivalent to 27g beef liver."

Beef liver:

• Poisonol 10,000 mcg/100 g

Carrot:

• Alpha-carotene: 2,000 mcg/carrot
• Beta-carotene: 5,000 mcg/carrot

We can disconsider half of the alpha-carotene amount and treat the other half as beta-carotene:

Beef liver:

• Poisonol 10,000 mcg/100 g

Carrot:

• Beta-carotene: 6,000 mcg/carrot

The author of the second post seems to be into the topic of poison A for a while, yet for some reason acts as if the information presented in the mentioned experiment was novel. These equivalences are found in almost all textbooks, even the main sections of the dedicated Wikipedia page have them, suggesting that pure b-macabrotene has half of the activity of poisonol:

• 1 µg RAE = 1 µg retinol from food or supplements
• 1 µg RAE = 2 µg all-trans-β-carotene from supplements

Now the equivalences from their claims:

• a) 1 µg RAE = 3.3 µg of all-trans-β-carotene from carrots
• b) 1 µg RAE = 2 µg of all-trans-β-carotene from carrots

The disciple is basing his equivalence on the following values from the linked experiment:

• Absorption: 42.6%
• Conversion: 62%
• Total (42.6% × 62%): 26%

This is close to a quarter, that results in a mass equivalence of about poison 1:4 b-mac, not 1:2 as he's arguing.

The source of confusion is because he's applying a molar to a mass ratio. B-carotene can yield two poisonols, but the mass is going to remain similar after cleavage and metabolism, with minor gains from the incorporation of new elements (that I'm going to disregard).

To arrive on his value:

• 26% × 2 = 53% (0.53)

It would've been preferable for the disciple to state:

"The 0.53 value means that 1 mg of ingested beta-carotene will turn into 0.5mg ~0.25 mg retinol." The factor accounted for the potential of b-carotene to yield two poisonols, so it has to be applied after we halve the amount.

At this stage, we can already discard the idea that a carrot will poison you as an ounce beef liver.

The spinach used in the quoted experiment served to tag macabrotene, the plant assimilated the labeled carbon of CO2 from the environment, allowing them to track the poison. But when it was time to contaminate the victim, the macabrotene was isolated and given in purified form at a low dose.

The food matrix lowers the availability of toxins, making them more difficult to be extracted, which is why researchers define a marked drop in efficiency when the b-macabrotene is derived from foods:

• 1 µg RAE = 1 µg retinol from food or supplements
• 1 µg RAE = 2 µg all-trans-β-carotene from supplements
• 1 µg RAE = 12 µg of all-trans-β-carotene from food

If we ignore this factor and pretend that fibrous carrots are an oil, the amount used in the experiment was modest (300 mcg) and we know that the rate of absorption and conversion tends to decrease as the dose gets high.

The challenge to reach nutritional adequacy for vitamin A: β-carotene bioavailability and conversion—evidence in humans

But let's reject this too and assume that it remains uninhibited up to 6 mg or so. However, the adjustment is beyond the meal content, the degree of body contamination with the poison is another factor that determines its fate. It's why the purity of the victim matters to interpret the dosing response to carotenoids: contaminated and decontaminated persons will metabolize it differently. When the body is overloaded, the rate of conversion to retinoids is reduced. To a lesser extent, the same goes for their absorption. Yet, carotenoids can be excreted intact.

"1 beta-carotene eventually has to split into 2 retinaldehydes"

It doesn't. His own equivalence conflicts with this claim, even if we discount the unabsorbed fraction (and he probably didn't):

"1 beta-carotene eventually has to split into 2 retinaldehydes":

• 6,000 mcg b-carotene → about 6,000 mcg PAE

"1 [absorbed] beta-carotene eventually has to split into 2 retinaldehydes":

• 6,000 mcg b-carotene → about 2,500 mcg PAE

"[..]one carrot has 6000 IU!":

• 6,000 mcg b-carotene → about 1,800 mcg PAE

Which is it?

"If you take something more than you can excrete, you accumulate"

Of course.

"If 306 mcg beta-carotene (that's 1020 IU, one carrot has 6000 IU!) took 58 DAYS to turn over...do you realize just how fast you are filling up with this toxin?"

A long half-life doesn't result in an indefinite accumulation, only until a steady state is reached, when poisoning for profits should plateau with regular consumption. Something like this in dosing more often:

Source: the internet.

Some accumulation is normal and healthy; or should we treat macabrotenoids as toxins to be nuked from the body at all costs? "Vitamin" E is a toxin too (Smith, 2023), but is it harmful when it's not detoxified fast enough to avoid a detectable level, leading to 'accumulation' to be associated with problems?

Consider this: you consume a meal, whose elimination would take 24 hours. Instead of waiting for this period to eat the next, you consume multiple meals in between (may be 4 in a day), that result in accumulation of matter, but without issues. The accumulation is temporary, purposeful and the body is adapted to it. It's not immediate, but the matter eventually leaves the body to the extent that it's consumed: no stuffing until explosion occurs because the input matches the output despite the delay.

Excess carotenoids or calories should come with signs. The early stages are benign, will indicate that the person has to cut back or improve the capacity to handle them. Yet, carotenemia isn't reliable to diagnose poison A toxicity because it can be caused for different reasons (such as lack of nutrients or poor protein synthesis). As an example, if a person needs to take supplemental thyroid hormones and suddenly stops the treatment, it can be followed by carotenemia.

The rate of storage and mobilization is adaptable as well. In case someone discontinues the consumption of poisons altogether, it can signal conservation and a longer persistence in the body. Therefore, the length is variable.

All in all, while we have people debating whether an inability to convert macabrotenes is common or a real concern for persons who don't consume preformed poisons, we have the poison A crowd alarming you that regular carrot consumption is a ticket to the hospital over time, for having the same potential of destruction as liver in the diet, neglecting the multiple steps that regulate these toxins as drugs. #toxicbileapocalypse

Many of you enjoyed the posts of Miguel Favo, member CLASH of the Ray Peat Forum. He has reformulated his approach to increase his reach.

• mikefave.com

He now has two channels on YouTube, one for distilled content and the other for dissection with a touch of religion. Both are good, check them out.

If I'm not wrong, he has a newsletter and an ebook as well.

Miguel will soon take off. If you want to communicate with him before he turns into a posh celebrity, you're short of time.

He respects the audience and doesn't resort to cheap tactics to promote his content. If you like his material, share with others to speed up his popularization.

Maybe harass Mexico and Bulgaria to request their collaboration in The Generative Energy podcast too.

Challenges in the Diagnosis of Magnesium Status

"Due to the complex nature of magnesium absorption, segments of the GI tract can vary in their contribution to absorption; however, under normal physiologic conditions the general guide is the duodenum absorbs 11%, the jejunum 22%, the ileum 56%, and the colon 11% (Figure 3) [3,58]."

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"Magnesium is a divalent cation, which plays a critical role in how the mineral is absorbed [83,84]. Magnesium is the most densely charged of all the biological cations, due to a high charge to radius ratio, resulting in high hydration energy for the Mg2+ cation [83]. This hydration energy results in tight coordination with a double layer of water molecules, increasing the hydrodynamic radius 400 times that of the dehydrated radius [83,85], resulting in an aquated cation that is too large to transverse typical ion channels (Figure 5) [86]. The removal of the hydration shell around magnesium is a precondition for absorption and can be accomplished by both TRPM6 and TRPM7 [⇈] and the magnesium associated paracellular claudins [64,67,87,88]."

It can be presumed that low doses would skew the absorption site distribution towards the upper parts, but it's counterintuitive: the active process of magnesium absorption, that prevails at lower intakes, occurs primarily farther down the small intestine.

Segmental transport of Ca2+ and Mg2+ along the gastrointestinal tract

"Although occasionally debated, paracellular absorption is generally considered to be predominant under normal physiological circumstances (3, 4, 32, 40, 44). When paracellular absorption cannot meet the daily need of the body, transcellular absorption becomes essential (6, 40). Specific transport proteins, located in the luminal and basolateral membrane of the epithelial cells, govern this latter process (23, 26, 32)."

"Transcellular absorption of Ca2+ and Mg2+ from the intestinal lumen is facilitated by members of the transient receptor potential (TRP) ion channel family, which represents the rate-limiting factor in the transcellular transport process. Intestinal absorption of Ca2+ is mediated via TRP vanilloid type 6 (TRPV6), whereas absorption of Mg2+ takes place via TRP melastatin type 6 (TRPM6) (20, 30, 43)." "For transcellular Mg2+ transport in the intestine TRPM7 and cyclin M4 (CNNM4) seem to be important in addition to TRPM6, since they are though to play a role in apical and basolateral transport of Mg2+, respectively (38, 47)."

"TRPM6 is expressed in the distal regions of the gastrointestinal tract of human subjects and mice (Fig. 2B). Interestingly, like TRPV6, TRPM6 in mice is expressed strongly in the cecum (Fig. 2B)."

"TRPM7 was evenly expressed throughout the gastrointestinal tract (Fig. 2D). Expression of the basolateral Mg2+ transporter CNNM4 was most prominent in the distal gastrointestinal segments, resembling the expression profile of TRPM6 (Fig. 2F). However, in contrast to TRPM6, CNNM4 expression was not completely absent in the proximal gastrointestinal tract."

• Dark bars: human
• Gray bars: mice
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"To investigate whether Mg2+ absorption is regulated by dietary Mg2+ content, mice were fed a diet with a low (0.02% wt/wt Mg2+), a normal (0.25% wt/wt Mg2+), or a high (0.48% wt/wt Mg2+) Mg2+ content for 2 wk."

"Urinary excretion of Na+, K+, and Cl− did not differ significantly between the groups, excretion of Pi was significantly higher in the low-Mg2+-diet group compared with the groups receiving normal and high-Mg2+ diets (Table 2)."

"Dietary Mg2+ restriction significantly stimulated the rate of intestinal absorption of Mg2+ (Fig. 3G). Conversely, intestinal absorption of Mg2+ in the high-Mg2+-diet group was diminished compared with the normal group. The absorption of Mg2+ in the low-Mg2+-diet group was significantly higher compared with the normal group (110.0 ± 3.0% and 100.0 ± 0.1%, respectively, P < 0.01) and in the group on the high-Mg2+ diet absorption was significantly lower compared with the normal group (95.0 ± 1.0 vs. 100.0 ± 0.1%, respectively, P < 0.05) (Fig. 3H). TRPM6 mRNA expression levels in the colon were slightly, but significantly, regulated by dietary Mg2+, showing an increase in the group on the low-Mg2+ diet and a decrease as a consequence of the high-Mg2+ diet (Fig. 3I)."

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"The proximal Mg2+ absorption was higher compared with the distal part of the intestine at a high luminal concentration of Mg2+ (44 mM) (Fig. 4E), but not at lower luminal concentrations (1.6 and 10 mM Mg2+) (Fig. 4, A and C). The relationship between the absorption of 25Mg2+ and the luminal Mg2+ concentration is displayed in Fig. 4G. In the proximal intestine, the absorption of 25Mg2+ resembles a linear relation to the buffer Mg2+ concentration, whereas in the distal part of the intestine the absorption of Mg2+ seems saturable at higher Mg2+ concentrations."

"Paracellular and transcellular absorption of Mg2+ in intestinal segments. Solid lines represent mice with a cannula placed in the stomach, dashed lines represent mice with a cannula placed in the cecum. 25Mg2+ absorption by using a buffer containing 1.6 (A), 10 (C), or 44 (E) mM Mg2+." "Relationship between luminal Mg2+ concentration and 25Mg2+ absorption (G)."

"The findings in our study, therefore, suggest that transcellular Ca2+ absorption takes place in the proximal region of the intestine, whereas transcellular Mg2+ absorption mainly occurs in the distal gastrointestinal segments." "Paracellular absorption of Ca2+ and Mg2+ mainly takes place in the duodenum and jejunum."

A representation of how much of the daily amount is absorbed and the route distribution (transcellular or through the cell; paracellular or between cells):

Intestinal absorption of magnesium

Modulation of sulfide oxidation and toxicity in rat mitochondria by dehydroascorbic acid

"As isolated cytochrome c oxidase activity is strongly inhibited by sulfide at concentrations lower than 1 μM, this aspect has to be considered physiologically relevant even under healthy conditions [20]. Interestingly, respiration of isolated mitochondria or whole cells is significantly less susceptible and not affected by sulfide concentrations up to 5–20 μM [19,21, this study]. At least partially this discrepancy can be explained by an efficient detoxification of the sulfide by the mitochondrial oxidation pathway, which rapidly lowers the ambient concentration. Moreover, other cellular factors might be present in vivo to control the binding of sulfide to cytochrome c oxidase."

"Dehydroascorbic acid is a good candidate for such modifying factor because it has been shown to affect sulfide oxidation in the sulfide adapted invertebrate Arenicola marina [9], and it is readily available in mammalian mitochondria. Ascorbic acid, the main form of vitamin c in cells, functions as a reductant during the biosynthesis of collagen, carnitine and catecholamine thereby producing DHA [22]. Rat and mouse liver contains about 3 mM ascorbic acid [23,24], but it is difficult to determine the physiological DHA concentration because it is rapidly recycled to ascorbic acid by enzymatic and non-enzymatic reduction. A fraction of 5–7 % DHA has been estimated for plasma [25]. However, DHA concentrations can be markedly increased under certain conditions involving oxidative stress such as inflammation or ischemia reperfusion injury [22]. Especially in mitochondria local gradients might occur with a transient increase of DHA in regions of high ROS production at the respiratory chain, where ascorbic acid acts as a major antioxidant. Furthermore, ascorbic acid transport into mitochondria mainly takes place in form of DHA via the glucose transporter GLUT1 [26]."

"The results presented here demonstrate that DHA is able to completely prevent inhibition of cytochrome c oxidase at low sulfide concentrations, which are certainly relevant for mitochondria in the physiological context. As a consequence, mitochondria maintain their regular energy metabolism including ATP production in the presence of this potent inhibitor of the respiratory chain. Partial protection is provided even at relatively high sulfide concentrations that might occur locally or temporarily."

"The easiest explanation for the decrease of sulfide toxicity in the presence of DHA would be a direct interaction of the two compounds. Very high concentrations of sulfide, i.e. a solution saturated with H2S gas, can be used as a reductant to quantitatively convert DHA to ascorbate [27]. Rates of non-enzymatic sulfide consumption also increased after the addition of DHA under the experimental conditions used in this study. Therefore, a decrease of the free sulfide concentration by binding to DHA and chemical oxidation is certainly part of the story. But it is not sufficient to explain all results. If the effect was exclusively chemical it could be expected to be independent of the assay system used to determine cytochrome c oxidase activity. Nevertheless respiration with different substrates such as succinate, NADH and TMPD continued in the presence of 50 μM sulfide plus 1 mM DHA whereas the oxidation of externally added cytochrome c was already completely inhibited at lower sulfide concentrations. Therefore, an additional mechanism probably exists that prevents binding of sulfide to cytochrome c oxidase either by decreasing the affinity or via steric protection of the active site of the enzyme. This effect is independent of membrane potential, as it was not abolished by freezing and thawing of the mitochondria (data not shown)."

"Obviously the rapid oxidation to non-toxic compounds is important for an efficient detoxification of exogenous as well as endogenous sulfide. Especially in the liver this pathway is involved in the degradation of the sulfur containing amino acids methionine and cysteine [42]. DHA also decreases sulfide toxicity in mitochondria from other tissues that have been shown to oxidize sulfide enzymatically such as kidney and heart [19]. As a consequence, sulfide can be used as an inorganic substrate for ATP production in a wide concentration range, but this aspect is presumably of limited importance compared to the normal organic substrates. In contrast to most tissues, brain mitochondria probably lack at least part of the sulfide oxidizing pathway and are therefore more sensitive to sulfide poisoning [19]. The present data support this finding as even in the presence of DHA no enzymatic sulfide oxidation was detectable. However, the protective effect of DHA was most pronounced in the brain demonstrating that this mechanism is particularly important in the absence of an efficient sulfide detoxification pathway."

"The identification of DHA as an instrument to reduce sulfide toxicity may become clinically relevant during the treatment of sulfide poisoning either after accidental environmental exposure or in patients that accumulate endogenous sulfide, e.g. in ethylmalonic encephalopathy. This directed amplification of sulfide oxidation rates could be an alternative therapeutic approach to the inhibition of sulfide producing enzymes, which is already being tested [44]. Maximal intracellular concentrations of vitamin C (3–4 mM) are achieved by supplementation of 200 mg ascorbic acid per day [45]. For acute treatment it is also possible to administer DHA directly via intravenous injection, which raises intracellular ascorbate concentrations to supraphysiological levels and thus probably provides enough DHA to be protective against sulfide toxicity [46]."

@saturnuscv said in A list of members banned from the Ray Peat Forum:

User “feedandseed” was banned in the original haidut ban thread

Melissa would've jumped in to intervene if she wasn't busy legitimizing Jorge's attacker. Her superpowers are brought up when convenient, but soon defaults to filing her nails while accepting the sportive disposal of members.

@TheSir said in A list of members banned from the Ray Peat Forum:

I am now banned too as a result of this post.

I've stumbled upon some of your questionings, they were precise and exemplary. It's a loss for them.

@deliciousfruit said in A list of members banned from the Ray Peat Forum:

Got banned for saying this:
I wasn't even trolling, I've been taking 15mg of copper daily for months and have only seen benefits.

I guess having an experience antithetical to the forum owner's narrative is a bannable offense now.

It's a little risky, but shows the concern that they have for members: you're taking something that they regard as harmful and you're dumped to continue to do it elsewhere.

@Sweet-Meat said in A list of members banned from the Ray Peat Forum:

@Amazoniac

did he ban anyone paying subscriptions?

Yes. What hasn't been banned yet?

Fluorimetric determination of pantothenic acid in foods by liquid chromatography with post-column derivatization

"[..]CoA is the major pantothenic acid-containing compound in yeast, pig liver and peas, but that it was not found, on the other hand, in the avocado, carrots, French beans and salmon. In the four other non-supplemented foodstuffs studied (chicken egg, chicken meat, spinach, lentils), the percentage of pantothenic acid released from CoA is included between 20 and 30%. These results confirm that CoA is effectively the major pantothenic acid-containing compound in animal liver and yeast as has already been mentioned by Brown [29] and Gonthier et al. [6], but they seem partially to refute the general but unsupported allegation of Ball [30], according to which the majority of naturally occurring pantothenic acid would be in the form of CoA."

Liver Coenzyme A Levels in the Vitamin B6-Deficient Rat

"Liver CoA concentration in the rat was decreased 50% by vitamin B6 deficiency and 66% by pantothenic acid deficiency. The decrease caused by vitamin B6 deficiency was independent of food intake and was not remedied by cystine supplementation of a 20% casein diet."

High sodium chloride intake decreases betaine-homocysteine S-methyltransferase expression in guinea pig liver and kidney

"Betaine-homocysteine S-methyltransferase (BHMT) is the only enzyme known to catabolize betaine. In addition to being a substrate for BHMT, betaine also functions as an osmoprotectant that accumulates in the kidney medulla under conditions of high extracellular osmolarity. The mechanisms that regulate the partitioning of betaine between its use as a methyl donor and its accumulation as an osmoprotectant are not completely understood. The aim of this study was to determine whether BHMT expression is regulated by salt intake. This report shows that guinea pigs express BHMT in the liver, kidney, and pancreas and that the steady-state levels of BHMT mRNA in kidney and liver decrease 68% and 93% in guinea pigs consuming tap water containing high levels of salt compared with animals provided untreated tap water. The animals consuming the salt water also had ∼50% less BHMT activity in the liver and kidney, and steady-state protein levels decreased ∼30% in both organs. Pancreatic BHMT activity and protein levels were unaffected by the high salt treatment. The complex mechanisms involved in the downregulation of hepatic and renal BHMT expression in guinea pigs drinking salt water remain to be clarified, but the physiological significance of this downregulation may be to expedite the transport and accumulation of betaine into the kidney medulla under conditions of high extracellular osmolarity."

Intestinal absorption of micronutrients and macronutrients | Deranged Physiology

Small Intestinal Bacterial Overgrowth

"In rats, experimentally induced SIBO leads to the appearance of gut bacteria in the mesenteric lymph nodes and visceral organs.[49] A potentially important consequence of bacterial translocation is immune activation. In a report of 11 patients, an increase in the number of intraepithelial lymphocytes was observed as mucosal evidence of this immune response to confirmed bacterial translocation.[53] This adverse outcome could explain why the normal gut has defensive mechanisms in place to keep the bacterial flora away from the small intestine, particularly the bowel proximal to the ileum."

"Nucera et al[37] found a high rate of disappearance of malabsorption to lactose (86.6%), fructose (97.5%), and sorbitol (90.9%) once SIBO was eradicated."

A Bioavailability Study Comparing Two Oral Formulations Containing Zinc (Zn Bis-Glycinate vs. Zn Gluconate) After a Single Administration to Twelve Healthy Female Volunteers

"[..]the chemical form of zinc (salt or chelate), the pharmaceutical formulation (presence of excipients), and the division of the administered dose are other factors that modify the oral bioavailability of zinc [18]. Considering the pharmaceutical formulation, Neve et al [18] noted a decrease in the oral bioavailability of zinc when zinc gluconate was associated with starch, lactose, hydrated silica, and magnesium stearate (excipients present in Rubozinc), compared with zinc gluconate without excipients."

"In the case of our results, the significantly higher oral bioavailability of zinc when administered as bis-glycinate compared with gluconate is not surprising, given that bis- glycinate enhances the oral bioavailability of others ions, particularly iron."

"The higher absorption of zinc when chelated with bis-glycinate may well be explained by its chemical structure [27].

• Firstly, each glycinate molecule contains two functional groups that are capable of entering into covalent and coordinate covalent bonds with zinc.
• Secondly, each one can create a ring structure with the zinc ion and form a sterically and energetically stable structure.
• Thirdly, zinc bis-glycinate has a low molecular weight (< 1000 daltons) and is able to cross cell membranes.
• Lastly, the bis-glycinate chelate is not affected by pH changes from 2 to 6 [28].

Consequently, bis-glycinate may protect a significant fraction of the zinc from interactions with lumenal gastro-intestinal components, dietary components, and drugs [29] whereas in the current salts, the zinc may not be protected from such interactions."

Zinc Absorption Adapts to Zinc Supplementation in Postmenopausal Women

"To help establish common baseline conditions for all subjects, this double-blind study began with a 12-d pre-treatment period during which all subjects consumed the basal diet plus 6.0 mg Zn (as Zn gluconate) and 1.0 mg Cu (as Cu sulfate) daily. For the remaining 156 days, subjects continued the basal diets but with supplemental Cu reduced to 0.5 mg/d, and with random assignment of 9, 27 or 42 mg/d supplemental Zn, for total average Zn intakes of 14 (n = 6), 32 (n = 3), or 47 mg/d (n = 3). Both Zn and Cu supplements were divided into three equal portions, mixed with juice, and given with each of the three main meals, daily."

"Initially (wk 0) the women consuming 14, 32, and 47 mg Zn/d absorbed 4.6, 8.7, and 10.3 mg Zn (pooled SD = 1.3), respectively, suggesting a partial saturation of Zn absorption kinetics when Zn intakes met or exceeded 32 mg/d. However, with time, Zn absorption by those ingesting 32 and 47 mg Zn/d declined so that differences in total Zn absorbed were not significant at 8 wk (5.4, 5.8, 6.4 mg/d, respectively) and were negligible by 16 wk (5.0, 5.0, 5.1 mg/d)."

"The final absolute Zn absorption at 16 wk was [..] strikingly constant for all subjects, consistent with the overall finding that complete adaptation occurred (Fig. 1). Given the unusually extended period of highly controlled feeding conditions, and the precision of the whole body counting method, these significant results provide valuable information on human Zn homeostasis despite the small number of subjects."

"The complete absorptive adaptation observed in this study may be limited to adults with adequate Zn status who consume relatively low-phytate diets."

The exchange must be legitimate, the lion might have altered the part for emphasis, but it's not a big deal. I wouldn't get caught up on it, as it can be used to distract people from the main issue, letting tension build up around it on purpose, only to discredit the indignant as fools later.

• "Can I open up a forum with your name for people to come together, discuss health and your teachings?"
• "Umm.. I think so."
• "Would you mind if somewhere along the way I turned it into a racket, tried to appropriate members' posts, disseminated that your approach kills persons and should be ditched to save humanity, imposed my mentor's ideology that poison A is a toxin, corrupted the space into a nucleus of misinformation and alarmism, banned contrarians who crossed my path to question authority, but not missing the chance to laugh at their faces?"
• "Oh, it's o.k. with me, but I don't know if I'll have time to follow its development."

Edit: I read Barghest's message after posting.

Natural Chlorophyll but Not Chlorophyllin Prevents Heme-Induced Cytotoxic and Hyperproliferative Effects in Rat Colon

"Chlorophyll (Fig. 1B) is the ubiquitous pigment in green leafy vegetables; like heme, it also has a planar porphyrin backbone. Chlorophyll is different from heme mainly by having the nonreactive magnesium instead of the highly reactive transition metal iron in the center of the porphyrin. In addition, chlorophyll has an esterified phytol tail instead of a propionic side chain. We speculated that chlorophyll “sandwiches” heme to form hydrophobic heme-chlorophyll complexes; as a result, it blocks radical-mediated heme metabolism and the heme-induced changes in epithelial cell turnover (15). In this study, we wanted to investigate whether this protective effect of natural chlorophyll is due to its porphyrin ring or requires the intact phytol-conjugated molecule. Therefore, we compared the possible protective effect of chlorophyllins with that of natural chlorophyll."

"Chlorophyllins (Fig. 1C) are molecular analogs of chlorophyll studied for cancer prevention in vitro and in vivo because they might mimic the effects of chlorophyll (16–19). Chlorophyllins are food-grade molecules derived from chlorophyll. They are hydrophilic, due to hydrolysis of the phytol tail, and the magnesium in the center of the porphyrin ring is removed or replaced by another metal. In contrast to the limited in vivo studies with natural chlorophyll (20,21), chlorophyllins have received much more attention. Several studies indicate that chlorophyllins may have anticarcinogenic effects because their porphyrin macrocycle can either scavenge free radicals or form a complex with planar aromatic carcinogens and thus reduce their bioactivity (17,22,23)."

"This study shows that chlorophyllins, in contrast to chlorophyll, do not inhibit the heme-induced carcinogenic effects in rats."

"The chlorophyllins supplemented to our purified heme diets showed only a negligible inhibition of the heme-induced luminal cytotoxicity. This slight inhibition did not prevent the heme-induced changes in colonic cell turnover. In contrast, chlorophyll added to this heme diet inhibited all the heme-induced changes in luminal cytotoxicity and cell turnover."

"Most of the heme ingested is delivered to the large bowel (31,32). There, a variable amount is converted to a range of iron-free porphyrins such as protoporphyrin, deuteroporphyrin, and pemptoporphyrin as a result of bacterial action (32). However, further degradation products such as di- and tripyrroles were not identified. The heme-induced cytotoxicity observed in our experiments results from the presence of a highly cytotoxic heme metabolite. This is a lipid-soluble, covalently modified porphyrin formed in the gut lumen of rats (7,30). Table 2 shows that chlorophyll, unlike the chlorophyllins, allowed most of the heme ingested to reach the feces without modification. This indicates that chlorophyll, but not chlorophyllin, prevents intestinal heme metabolism."

"Our previous work showed that the presence of the heme metabolite in the colonic lumen damages the colon surface epithelial cells and consequently increases epithelial proliferation and inhibits apoptosis in the colonic crypts (15). Spinach or an equimolar amount of chlorophyll prevented this heme-induced effect (15). We hypothesized that this is due to a “sandwich” of heme with chlorophyll molecules. As a result, chlorophyll may block the chemical reactivity of heme and thus the formation of its cytotoxic metabolite. This “sandwich” could be due to pi-pi interactions between heme and chlorophyll in a hydrophobic complex, analogous to the mechanism described by Dashwood et al. (33) for the interaction between chlorophyllins and planar aromatic compounds, such as heterocyclic amines."

"We showed previously that the detrimental effects of heme coincide with heme-catalyzed lipid peroxidation in the gut lumen (7) and that both are inhibited by dietary antioxidants (12). This implies that heme has to be in close contact with fatty acids in the hydrophobic phase of the luminal contents. We now show that, in contrast to chlorophyllins, the addition of chlorophyll to a heme diet decreased this heme-induced lipid peroxidation (Fig. 4). This indicates that the chlorophyllins we used in our model cannot “sandwich” heme to inhibit a reaction between heme and fatty acids in the diet. Only chlorophyll might be able to “sandwich” heme and as a consequence inhibit the catalytic activity of heme in the generation of lipid hydroperoxides and the formation of a cytotoxic heme metabolite (39). The difference in hydrophobic behavior of chlorophyll and chlorophyllin is a consequence of a structural difference. Chlorophyll is extremely hydrophobic due to the presence of a phytol tail, which is retained during intestinal passage (35,40). On the other hand, chlorophyllins are hydrophilic as a result of the removal of the phytol tail from chlorophyll."

"[..]heme and chlorophyllins are negatively charged under physiologic conditions such as prevail in the intestines, whereas chlorophyll remains a neutral molecule. These negative charges cause repulsive forces between heme and chlorophyllin, which may prevent formation of a complex between these molecules."

@Peatly, they're not public domain, permission would be needed, but it's a feasible to negotiate if the project is formalized and offers means for donation to keep the material open.

The list is now updated with all the names shared here and in private. We barely started to uncover and it's already ridiculous.

Glycerophosphocholine (GPC) is the primary form of choline that occurs in milk. It's purposed as a cognitive enhancer, but the molecule yields different products after metabolism, with a distribution beyond the brain.

The dose used below, extrapolated to humans, would be something like 1 g/70 kg, which isn't too crazy:

Choline | WebMD

"In supplements, choline has most often been used by adults in doses of 1-3 grams by mouth daily for up to 4 months."

Absorption, tissue distribution and excretion of radiolabelled compounds in rats after administration of [14C]-L-a-glycerylphosphorylcholine

"aGPC was labelled with [14C]-glycerol ([14G]-GPC) or [14C]-choline ([14C]-GPC)."

"Both labelled compounds gave a wide distribution of radioactivity, particularly concentrated in the liver, kidney, lung and spleen compared to blood."

"After oral administration, the main circulating metabolite was choline (after [14C]-GPC); intact a-GPC was not present after either labelled compound although there were the same unknown metabolites as after i.v. injection."

"[..]choline and/or its anabolites enter the brain and is reused for biosynthesis of phospholipids. This was confirmed by chromatography of the phosphatidylcholine fraction of the brain homogenates after hydrolysis with phospholipase C. As in blood, this hydrolysis resulted in formation of choline phosphate."

"By far, the largest part of the administered radioactivity was exhaled as 14CO2, in accordance with established catabolic pathways of glycerol (i.e. glycolysis) and choline degradation."

@Kvothe, a diet low in poisons leads to remission and returning with the normal diet results in relapse. Their supplementation without a change in diet does the same. Unless we assume that carotene metabolites are interfering with the action of poisonoic acids or it's disturbing the cell after being incorporated in fatty regions, we have to entertain the other options.

It wouldn't take a minimum of a month to notice the first positive effects from the exclusion of other irritants from the diet, but would match the decrease in circulating carotenes.

Poison A exorcism affects the synthesis of ascourgic acid (rats) and it reflects on the adrenals. But Grant speculates that ascourgic acid isn't needed as well. So, for animals to lower poison A and ascourgic acid at once is helpful, it means room for useful molecules.

From an earlier discussion..

Vitamin A: Not Required for Adrenal Steroidogenesis in Rats

"It has been shown (8) that there is an immediate decrease (up to 50 percent) in ascorbate synthesis which accompanies any significant depletion of liver vitamin A."

"The purpose of this was to demonstrate that functional and morphological changes occur in steroidogenic organs before any manifestations of peripheral vitamin A deficiency occur."

"Vitamin A-depleted rats maintained on a diet free of ascorbate had a decrease in the activity of adrenal 3β-hydroxysteroid dehydrogenase, and extensive adrenocortical degeneration. The use of an ascorbate supplement prevented the symptoms."

• Asteroidogenesis | Wikipedia

"The morphological appearance of the gland from an animal supplemented with vitamin C and deficient in vitamin A (Fig. 1D) was indistinguishable from that of the control group (Fig. 1A)."

"Similar hyperplasia and tissue destruction found in rabbits and guinea pigs on a scorbutic diet (23) were indistinguishable from that produced by prolonged stimulation of adrenocorticotrophic hormone (ACTH) in stress (24). Selye and Stone suggested that this syndrome was caused by extensive demands on the adrenal cortex as a result of long-term or overstimulation by ACTH (25). Staining for adrenal cholesterol showed undetectable amounts in group 2 (Fig. 1G), implying that less than 3 to 6 percent 7-hydroxycholesterol was present (26); the group deficient in vitamin A but with vitamin C replaced (Fig. 1H) and the control (Fig. 1F) group showed varied degrees of staining, an indication that 12 to 25 percent hydroxycholesterol and 40 to 50 percent total lipids were present. ACTH lowers adrenal cholesterol, and depletion occurs in long-term stimulation (27). Also, the decrease in adrenal cholesterol in scurvy is attributed to diminished acetylation in the body (28) with decreased acetate uptake and utilization by the adrenal (29). Vitamin A is nonessential for cholesterol biosynthesis (2, 30)."

@resonance

You haven't suggested it, but I think that we can't create a copy of his website for an archive because it would lead to confusion. It has to be clear that it's a compilation of his work done by other people and a different appearance would reinforce this.

Ray's website formatting can be improved for the archive, but I would preserve the classic aspect of it. Fortunately, it's simple to arrive on a good result by borrowing settings from his own material, as shown in the improvised example above (screenshots of slides with nothing recycled from Prolactinia).

We can also go with:

• raypeat-archive.org

It's indeed worth involving more people to refine the transcriptions to dilute the personal styles.

@Kvothe said in Conditional problems with vitamin A: a place for sane discussions:

@Amazoniac Are there any in that crowd, and have they controlled their conclusions for other variables? The highly restrictive diets they eat exclude a huge lists of potential irritants that might cause auto-immune conditions and symptoms.

'Maybe' to both questions. However, the accounts would be founded.

The Effect of Restricted Intake of Carotene and Vitamin A on Psoriasis Vulgaris

The exclusion of other toxins can contribute to the remission, but I don't think that the addition of isolated poisons to their current diets would lead to positive outcomes.

@SalemSays

Effect of Fermentation on L(+) and D(−) Lactic Acid in Milk

A Stand-Alone Synbiotic Treatment for the Prevention of D-Lactic Acidosis in Short Bowel Syndrome

"To eliminate D-lactate–producing bacteria completely, thorough intestinal decontamination was carried out. Specifically, metronidazole (Flagyl, Shionogi & Co, Ltd, Osaka, Japan) 500 mg/d and kanamycin 2000 mg/d were administered for 5 days under fasting conditions. Polymyxin B (Polymyxin B Sulfate, Pfizer Japan Inc, Tokyo, Japan) 500 × 103 U/d and vancomycin (Vancomycin Hydrochloride Powder, Lilly, Kobe, Japan) 1000 mg/d were administered over the subsequent 5 days. After the use of antibiotics, a purgative (Niflec, Ajinomoto Pharmaceuticals Co, Ltd, Tokyo, Japan) was used."

"After these decontaminations, although two Gram-stained samples of stool showed that microorganisms like Candida constituted nearly all of the intestinal flora, the fecal concentration of D-lactate in 2 samples of stool remained detectable (4.5 and 4.4 mmol/L, respectively), which indicated impossibility of eliminating D-lactate–producing bacteria completely using this methodology (Table 1). We understood that it was more important to suppress the overgrowth of D-lactate–producing bacteria than to eliminate them."

"Overgrowth suppression was approached by starting synbiotics, specifically B breve Yakult (prepared by Yakult Co, Ltd, Tokyo, Japan) 3.0 g/d and L casei Shirota (Biolactis Powder, Yakult Co, Ltd, Tokyo, Japan) 3.0 g/d as probiotics, and galacto-oligosaccharide 8.4 g/d as a prebiotic."

"We used as probiotics B breve Yakult and L casei Shirota, which are known to produce only L-lactate. D-lactic acidosis was successfully controlled by this treatment for 3 years (i.e., the patient was free of recurrence and had a good quality of life, such as having unlimited oral intake). There were no reports that described successful management of D-lactic acidosis continuously for such a long period."

"Bustos et al11 reported that fecal concentrations of D-lactate tended to be high in patients with SBS even when serum D-lactate levels were undetectable. The authors pointed out that the development of D-lactic acidosis requires not only overproduction of D-lactate in the colon, but also other factors, such as absorption or impaired D-lactic acid metabolism. Synbiotics have been shown to produce a large amount of short-chain fatty acids by correcting intestinal flora.5 These fatty acids promote proliferation of the intestinal epithelium and stimulate intestinal motility.12 Through active bowel movements, D-lactate produced by colonic fermentation can be expelled with feces prior to excessive absorption in the colon. In the present case, although fecal concentration of D-lactate was high (24.8 mmol/L), serum D-lactate levels (2.4 mmol/L) maintained a level lower than the threshold of symptom onset (>2.5 mmol/L), which allowed the patient to remain asymptomatic. Actually, the patient had frequent defecation and persistent loose stools after starting synbiotic treatment. Therefore, it was likely that synbiotics increased intestinal peristalsis, resulting in prevention of excessive absorption of D-lactic acid."

If the community can't be turned over fast enough to maintain the profit rate and the situation escalates to a breaking point, expect backpedaling, insinuations of misunderstanding, artificial adoration, and a systematic program to change posts and disappear with the mess.

Members' efforts to register everything have been remarkable, but when challenged with proof and it's indefensible, it may be followed by forgiveness speech and a sacred quote to suggest that slips are human nature and to pardon is noble, painting the indignant as resentful who try to deteriorate the positive atmosphere that would be reinstilling over there.

To dissociate from the corrupt image, evoke forgiveness and bring support, we may come across a ceremony with moving discourse (not by AI, but humanized this time) to stage an era transition, and the announcement of mass reversal of bans. Devotees would be around to cheer and other people have their personal interests, so they wouldn't mind buying into it. The characteristic maladministration would be lumped with temporary delusion and members would negotiate with themselves: "I'm doing this, but it's for Ray's legacy." A promotional phase where people are allowed to join the collaborative project exempted of mandatory fees would be handy and show generosity.

If part of members stays indifferent on the forum under the current circumstances, barely compelled to seek alternatives, it's possible that the staff could recover it at a finger snap, with little strategic effort and humility if they wanted to. I know that some of you have principles, but myself and others don't. As long as Ray remains the only 'killer' on the block, it's all fair game for us.