Posts made by Amazoniac

Photodegradation of cobalamins in aqueous solutions and in human blood

"Human plasma contains a variety of cobalamins (Fig. 1) including methylcobalamin (MeCbl, 64%), adenosylcobalamin (AdCbl, 15%), hydroxocobalamin (OHCbl, 12%) and cyanocobalamin (CNCbl (sometimes called vitamin B12), 9%) [3]."

"It is known that intracellular cobalamins react rapidly with nitric oxide and superoxide [21,30-32], which can be generated in skin or blood during exposure to UVA [33,34]. Additionally, skin and blood contain many endogenous photosensitizers (porphyrins, flavins) absorbing in the UVA region, and exposure to UVA leads to the generation of reactive oxygen species [35,36]. Singlet oxygen, superoxide anions, hydrogen peroxide and triplet-state riboflavin radicals are generated under exposure of riboflavin (RF) to UVA [37]. Reactive oxygen species are quenched by antioxidants in human skin which may, due to this, indirectly be degraded. Cobalamins may also quench singlet oxygen and hydrogen peroxide, and it may photodegrade indirectly. However, the indirect photodegradation of cobalamins due to their antioxidant properties have not been studied."

"In the present study we have investigated the photodegradation of four major forms of vitamin B12 (MeCbl, AdCbl, OHCbl and CNCbl) under UVA exposure in aqueous solutions at physiological pH by absorption spectroscopy. The degradation of OHCbl exposed to UVA in the absence and presence of the endogenous photosensitizer RF was investigated. Serum vitamin B12 concentrations before and after summer were measured in four patients with psoriasis."

"All studied cobalamins degrade under UVA exposure in aqueous solutions at physiological pH (Fig. 4-5). OHCbl was found to be the most stable cobalamin under our experimental conditions (Fig. 4A and 5A)."

"However, OHCbl is an antioxidant, and may degrade indirectly in the presence of reactive oxygen and nitrogen species generated under UVA exposure. The presence of endogenous photosensitizer RF during UVA exposure increased the degradation of OHCbl (Fig. 7, 8A). RF and nicotinamide enhance the degradation of CNCbl in aqueous solution [24]. CNCbl is phototransformed to OHCbl [20,23]. It is possible that after entering a cell, OHCbl is transformed back to AdCbl and MeCbl, and thus may retain the biological activity of the vitamin, even in the case that the active forms will first be degraded in vivo. Nevertheless, high doses of solar radiation (or artificial UV radiation, e.g. sunbeds) may, at least theoretically, diminish the effectiveness of vitamin B12 and impair its organic functions. However, it is not simple to measure the changes of MeCbl, AdCbl or OHCbl concentrations in blood."

"AdCbl and MeCbl were extremely unstable and photodegrade in seconds (Fig. 4C-D and 5C-D). They were photoconverted to OHCbl (Fig. 6), which is in agreement with the earlier observations by others [18,21]. MeCbl was around 3-fold more sensitive to UVA radiation than AdCbl (Fig. 5CD)."

"The degradation rate of OHCbl in the presence of RF was around 3 times faster than alone (Fig. 8A), while the degradation rate of RF was not influenced by the presence of OHCbl (Fig. 8B)."

"The vitamin B12 status is most often assessed by measuring serum or plasma total cobalamins. Due to the fact that OHCbl is quite photostable, it is not surprising that seasonal variations of serum vitamin B12 were not observed in healthy people [47,48]. Our preliminary results on the influence of solar radiation on vitamin B12 levels in psoriasis patients demonstrate that sun exposure during a summer in Norway was not able to destroy the vitamin, while the same exposures increased the levels of 25-hydroxyvitamin D in serum by 66% (Table 1). This means that significant doses of UV radiation reached tissues below the stratum corneum. We also found that serum homocysteine levels were not significantly increased (indirect measurement of vitamin B12 and folate changes). However, longer exposure times in sunlight at lower latitudes or in sunbeds (which have several times higher UVA fluence rates than found in solar radiation [49,50]) may lead to increased plasma homocysteine concentrations due to the photodegradation of vitamin B12 but not to any photodegradation of folate, as was observed in patients with psoriasis by Osmancevic et al. [16]."

"Cobalamins circulate in blood bound to two transport proteins, haptocorrin and transcobalamin [51-53]. The major part of cobalamins are bound to haptocorrin (80-96%) [53], which has an unknown function, but it has been proposed that haptocorrin serves to protect cobalamins [22,51]. It was demonstrated that haptocorrin protects MeCbl from 442 nm photodegradation [22]. Calculations show that this mechanism may be of significance at light doses penetrating the skin, and act to protect cobalamins [22,51]."

"It is interesting to note that vitamin B12 deficiency may cause cutaneous hyperpigmentation [56-61]. The dominant mechanism of hyperpigmentation is an increase in melanin synthesis [62]. This clearly demonstrates that vitamin B12 is involved in melanin synthesis, and that vitamin B12 might have had a more important evolutionary role than folate (which absorbs only in the UVB region) in the development of different skin colours. American and British black-skinned persons have significantly higher serum vitamin B12 concentrations than white persons have [63-66]. The ethnic differences in vitamin B12 levels probably arise from combinations of hereditary and acquired properties unrelated to cobalamin intake, storage, or deficiency [67]."

@ilovethesea said in New "Mission" of RPF:

@Amazoniac He’s taken the entire site off the wayback machine. Stolen all our content, banned us from accessing it, and now we can’t even look up prior versions. Unbelievable!

Did you, BioEclectic and other members have the chance to open the initial version of the forum, at the time when Ray agreed with its creation? The appearance was almost a variation of his website, with a picture of him and some of his favorite foods.

It's thanks to the limited access that I had to resort to the Internet Archive and could compare the initial to a recent version of the front page, which was a wall of warnings, pushy subscriptions, misinformation campaigns, and senseless slandering.

"CO2 , The Gas of Life" | William Happer

"If I see a madman driving a car into a group of innocent bystanders, then I can’t simply wait for the catastrophe and then comfort the wounded and bury the dead. I must try to wrestle the steering wheel out of the hands of the driver."

Contrary to Ray, the lion isn't a 'killer', but the apathy of some participants in being spectators of power abuses by him is perplexing.

The forum has become the antithesis of the person that it represents.

I wonder what are the thresholds for protesting for those who remain indifferent. They need a footage of the lion incinerating members with ethanol retinol to act?

At this stage, I'm more wary of people who haven't positioned than those who are enraged.

As for the few supportive militants, they're intriguing. They identify themselves as the open-minded camp while watching unfazed the tyranny in front of them. If these people were liberals as claimed, they would repudiate the administration and wouldn't be willing to be part of it.

The recent access restrictions were based on the forum being under attack, but what about everything that was already archived? These were a threat to defend against too?

Even CloudFlare takes a more balanced approach than radical blocking:

• The Trouble with Tor | CloudFlare

"We didn’t want to make blocklisting easier because, again, we believe there’s value in the anonymous web surfing that Tor offers."

• The Trouble with CloudFlare | The Tor Project

@T-3

Another topic that appeared in conversations with my pastors is how work that starts to get complex can bring hesitation in modifying it in further, for fear of losing parts by accident or messing up. Despite being possible to undo changes or resort to file history offered by some programs, it's more guaranteed to advance the work through duplicate files, relying on a copy of the latest version.

• If the modification goes well, the duplicate file is adopted and the original is kept as record.
• If the modification goes bad, the experimental copy is abandoned and you're left at where you were, with an intact material.

This makes experimentations riskless and must contribute to creativity.
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Learning in double time: The effect of lecture video speed on immediate and delayed comprehension

"We presented participants with lecture videos at different speeds and tested immediate and delayed (1 week) comprehension. Results revealed minimal costs incurred by increasing video speed from 1x to 1.5x, or 2x speed, but performance declined beyond 2x speed. We also compared learning outcomes after watching videos once at 1x or twice at 2x speed. There was not an advantage to watching twice at 2x speed but if participants watched the video again at 2x speed immediately before the test, compared with watching once at 1x a week before the test, comprehension improved. Thus, increasing the speed of videos (up to 2x) may be an efficient strategy, especially if students use the time saved for additional studying or rewatching the videos, but learners should do this additional studying shortly before an exam. However, these trends may differ for videos with different speech rates, complexity or difficulty, and audiovisual overlap."

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Examining Increasing Playback Speed in Recorded Lectures on Memory, Attention, and Experience

"Recorded lectures represent a popular means of delivering educational content. These lectures afford increasing the playback speed which could be used to reduce time demands and increase the likelihood that a lecture is consumed. In two experiments (N = 320), we examined the impact of increasing the playback speed of lectures across a range of speeds on memory for the lecture material, mind wandering, and the learner’s experience of the lecture. For speeds up until 2x, findings revealed no significant differences in memory for the material, mind wandering, and learner’s subjective experience of the lecture, with the exception that “enjoyment of speed” decreased as speed increased. Beyond a speed of 2x, however, significant impairments in memory for the lecture material and decreases in liking toward both the video lecture and the speed were observed. Moreover, the increase in mind wandering with time on task often observed in recorded lectures was not modulated by lecture playback speed. These results reinforce extant results in the literature on the effects of increasing playback speed on memory for lecture material and add new insights in terms of this strategy’s influence on mind wandering and learner’s subjective experience of the lecture."

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I'm not shure why lavalier microphones aren't favored over radio station ones. They work well, are cheap, give the person some mobility, don't clutter the view with an alien arm and nor make the video obsolete by the time that it's published.

Perhaps it helps to feel less vulnerable when there's an object between the speaker and the camera? If this is the case, increasing comfort may be a valid reason to keep it. Otherwise, the clean option seems better.

Member jwayne will help us in the comparison between lavalier and vintage mics:

I think that it's advantageous for the forum to keep material containing unproven miraculous cures and baseless rules in the Junkyard, so that visitors aren't caught off-guard. But it's my opinion, and it's simple to disconsider.

Tissue-specific effect of colitis on protein synthesis in mice: impact of the dietary protein content

"As previously reported, acute inflammation severely affects colon metabolism by stimulating protein anabolism [4, 9, 18]. Because colon protein content was not modified along the colitis course and resolution despite a higher protein synthesis rate, this increase in biosynthesis might reflect colon repair after epithelium erosion, with possibly a higher epithelial cell loss in the lumen. The locally induced inflammation is known to provoke an increased amino acid need for protein synthesis in the colon, not only when inflammation is maximal (day 7–10) [19], but also likely during the healing process. This increase, notably at a time when dietary daily intake was reduced, could have been compensated by amino acids supplied by other tissues, such as muscle. A reduced protein synthesis in muscle would also spare amino acids for increased protein synthesis in the colon, liver and spleen. Indeed, muscle is a major contributor to restore protein and energy losses in situations where protein catabolism is manifest such as starvation [20], acute injury [21] or chronic inflammation [9]."

"The present study shows that the protein metabolism modifications are modulated by the dietary protein content. The moderately high-protein diet (P30%), which has been recently shown to improve epithelial repair after an acute colitis episode [14], was associated with a lower protein synthesis rate, restoring initial level in colon compared to the two other diets [14% and 55% protein]. It is noteworthy that several colitis induced alterations were restored earlier with P30 diet consumption compared to the two other diets, such as body weight, caecal protein content, spleen and muscle protein synthesis rates. These changes coincided with the recovery of P30-fed mice that showed less inflammation and bacterial translocation (as evidenced by measuring the circulating LPS-BP concentration [14]) and faster colon repair in accordance with an earlier restoration of initial protein synthesis colon as shown in the present study."

"Our finding that the P30 diet restores rapidly and sustainably the initial (before colitis induction) colon protein synthesis can be related to our previous study in which we showed that P30 diet improved (when compared to the P14 diet) the colonic mucosal healing process by accelerating inflammation resolution, increasing epithelial repair, reducing permeability, and inducing epithelial hyperproliferation [14]. This suggests that the P30 diet, by furnishing an increased amount of amino acids, helps in the restoration of the colon epithelium, thus explaining the less active protein synthesis at this site. However, the relative amount of amino acids that is devoted to the restoration of the colonic epithelium remains to be determined when compared to other amino acid-consuming processes involved in inflammation. We previously showed that a specific mixture of amino acids given to rats after colitis induction was able to improve the colon regeneration/re-epithelialization, and this amelioration was found to coincide with a reduction of the stimulated protein synthesis rate in the colon when compared to control animals not receiving the amino acid mixture [23]. In sharp contrast, by further increasing the protein content in the diet (P53), we did not observe in this study any effect on the colon protein synthesis rate when compared to the P14 diet. This result can be ascribed to the deleterious effects of the P53 diet on the disease activity index, both in intensity and duration after a DSS challenge [14]. The reasons that would explain how a very high-protein diet consumption, although furnishing more amino acids is counterproductive after colitis induction, are not clear. One possibility is that by increasing the protein content in the diet, a larger amount of the dietary and endogenous protein escapes digestion in the small intestine, and thus reaches the large intestine. As a consequence, the microbiota produces an increased amount of amino acid-derived metabolites, some of which (hydrogen sulphide, ammonium, p-cresol) being known to be deleterious for the colonic epithelial cells, notably in terms of energy metabolism [24]."

"In conclusion, our study highlights the severe impact of acute colonic inflammation not only on the metabolism of proteins in the splanchnic area, but also in the peripheral tissues. The ability of the P30 diet to restore a normal protein synthesis in the colon may correspond to its documented beneficial effect on mucosal healing. In addition, the recovery of the initial protein synthesis rate in the various tissues in the period of time following colitis induction appears to be modulated by the amount of protein in the diet, with the P30 diet being more effective than the P53 diet."

Programmers may use code editors for general purposes and some people are fond of the basic notepad with the default font.

If your writing involves reflecting on what you just wrote, monospaced fonts can be an issue. However, the split screen with the goofy font for editing and a live preview with a readable font perhaps addresses this.

Learnability in Information Design

"Text can be presented in a monospaced font or a proportional font; extensive research has demonstrated that a proportional font is more readable than a monospaced font [4]."

User Interface Design For Programmers

"You may have noticed that almost every edit box on the Macintosh uses a fat, wide, bold font called Chicago which looks kind of ugly and distresses graphic designers to no end. Graphic designers (unlike UI designers) have been taught that thin, variable spaced fonts are more gracious, look better, and are easier to read. All this is true. But graphic designers learned their skills on paper, not on the screen. When you need to edit text, monospace has a major advantage over variable spaced fonts: it’s easier to see and select narrow letters like “l” and “i”. I learned this lesson after watching a sixty year old man in a usability test painfully trying to edit the name of his street, which was something like Fillmore Street. We were using 8 point Arial, so the edit box looked like this:"

"Notice that the I and the Ls are literally one pixel wide. The difference between a lower case I and a lower case L is literally one pixel. (Similarly, it is almost impossible to see the difference between “RN” and “M” in lower case, so this edit box might actually say Fillrnore.)"

"There are very few people who would notice if they mistyped Flilmore or Fiilmore or Fillrnore, and even if they did, they would have a heck of a time trying to use the mouse to select the offending letter and correct it. In fact, they would even have a hard time using the blinking cursor, which is two pixels wide, to select a single letter. Look how much easier it would have been if we had used a fat font (shown here with Courier Bold)"

"Fine, OK, so it takes up more space and doesn’t look as cool to your graphic designers. Deal with it! It’s much easier to use; it even feels better to use because as the user types, they get sharp, clear text, and it’s so much easier to edit."

From Monospace to Duospace: In Search of the ideal writing font

"In contrast to proportional fonts that communicate “this is almost done” monospace fonts suggest “this text is work in progress.” It is the more honest typographic choice for a text that is not ready to publish."

"The typographic rawness of a monospace font tells the writer: “This is not about how it looks, but what it says. Say what you mean and worry about the style later.” Proportional fonts suggest “This is as good as done” and stand in an intimidating contrast to a raw draft."

"Proportional fonts are optimized for high reading speed. That makes them the perfect choice for reading. Good writing, on the other hand, is measured, reflected, slow. It takes one step at a time. In a monospace font every letter, every number, every punctuation mark and every space takes the same visual space, which slows us down. And, for writing that’s a good thing."

"Proportional fonts save space. They suggest that you “hurry up and fill the page.” Monospaced fonts, on the other hand, feel more productive. Every typed letter translates into a homogenous visual progress in writing. It is both more relaxing to write at a slower pace and more satisfying as the progress is more tangible."

"Programmers use monospaced fonts for their indentation and because it allows them to spot typos. In a perfectly regular horizontal and vertical raster, letters and words become easily discernible: A typical proportional font comes with word spaces as wide as an i. Monospace fonts come with rather large word spaces. This makes it easier to discern each word and letter."

"Designers have pointed out that, with all the structural benefits that may or may not come from using a monospace font when writing, there are typographical compromises in typewriter fonts that are mere mechanical constraints that can and should be overcome. Due to the way mechanical typewriters worked, using the same horizontal space for each letter was inevitable at the time."

Making Code Beautiful With Type

Gain the Upper Hand with Good Typography

"Times New Roman was invented in the early 20th century for the Times of London and quickly gained traction among newspaper publishers. The Times commissioned it as an intentionally narrow font to fit more text per line and to enable quick reading.[6] Even from the beginning, it was criticized as unappealing to the eye."

"For all its ubiquity in self-published documents, when was the last time you saw Times New Roman in a book? Maybe never. Fonts used in professionally published books are comparably easier to read. This visual appeal, in turn, fosters comprehension and retention.[7]"

Are you able to access the archived forum pages on the Internet Archive?

"This URL has been excluded from the Wayback Machine."

"No URL has been captured for this URL prefix [raypeatforum.com/*]."

Have you ever seen one of those videos where a dog barks at something and the companion brushes it off, as if it was an overreaction to nothing? These authors are good storytellers and have a luring speech, making them prone to influence. Once you realize how they operate, the pattern becomes obvious and it's natural to be compelled to alert others, pointing out why it's worth being watchful with them. It's somewhat revolting to spot the same people, employing similar methods, fooling over and over again.

Either way, if you would like to help, consider placing junk in the Junkyard next time. It warns readers while reminding them that they can eventually find valuable stuff.

Otherwise, you can lead by example and ignore my posts. I've been making this easier in no longer tagging or quoting you, as it can be the case that the message won't resonate while you continue to admit that false information is not much of a concern.

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

So do you think there are any cases where restriction could be helpful?

I’ve read your article on daily excretion rates and it seems you said hepatic stores of 30ug/g is what the body wants as after that point it tends to dramatically increase the disposal of retinol.

Do you think restriction for a short while could be useful followed by introduction of retinol back into the diet with other things that may prop up the metabolism to help utilise it. It seems a lot of these low A people can’t go too long on it and end up resorting to eggs. I personally tried Low A for about a month now and each time I restrict to much I feel what I can only describe as though I am becoming dumber, I lose inspiration for life and just drift. Then as soon as I eat some cheese and or eggs I feel my gusto coming back again…

Is restoring thyroid function the best way to deal with this and some sort of mild restriction?

However going low A brought some relief in terms of anxiety and other problems like that but if I go to long I feel mentally impaired.

Just to clarify, the expert here is Kvothe. It's why I tried to get him to embark on a project for mentorship.

Yes, moderating any "nutrient" makes sense if it's doing more harm than good, but calls for alternative means to increase the tolerance to normal instead of finding comfort in labeling it as a toxin, as the poison A crowd do.

I don't know what you consider a short period, but to get to the therapeutic range, people need to be extreme and consistent. A month of restriction won't get you any lasting result and it's preferable to skip it.

If the issue is immunological, focusing on adequate metabolic rate (and the nourishment needed to sustain it) probably won't be enough. Compromised barrier integrity and disturbed gut composition can be the underlying problems.

Shared on the Garrey Pith Forum, but worth reposting here:

Kinetic Analysis Shows that Vitamin A Disposal Rate in Humans Is Positively Correlated with Vitamin A Stores

"Previous studies have demonstrated that serum retinol is the main determinant of VA disposal rate in rats with low to moderate VA intake (16), whereas VA status affected disposal rate in rats with higher liver stores (15). Our results appear to support those observed in rats with high liver VA stores (15) by showing that the model-predicted VA disposal rate was strongly correlated to VA total traced mass in Chinese (Fig. 3 A), U.S. (Fig. 3 B), and all subjects (Fig. 4 A). Moreover, when we compared VA disposal rate to serum retinol concentrations in all subjects, we observed that retinol concentrations were correlated with VA disposal rate (Fig. 4 B, C), indicating that serum retinol also contributes to whole-body VA disposal as previously reported (16)."

"[..]differences in VA nutriture will lead to changes in VA kinetics that will alter VA disposal rate to either conserve VA (VA deficiency) or prevent excessive accumulation of VA (VA sufficiency) even when VA levels are adequate."

When readers object the needless sexuality featured on every opportunity, he's being targeted by puritanical homophobes. An overproud homosexual is just as annoying as a bragging heterosexual, and neither of them need to praise their orientation in a health book.

The extravagance manifests on the cover too:

Stacked in phallus shape, with a peculiar opening on top, some stuff dripping of it, two elements on each side of the base, surrounded by a red color and next to 'F*CK'? Where is the editor?

I know that some of the experiments in his writings are valuable, if only they weren't accompanied by the distorted explanations in ruling tone. Readers shouldn't worry about extracting them; he can't mind. More so because a lot of protocols are borrowed from others. "I do it all the time, yet you're not allowed"? Sharing only the experiments through paraphrasing would expose people to the good while sparing them of the bad. We're dealing with an exceptional case.

A reader:

"Some of these claims are pretty out there and while I'm not wholly doubting you I consider myself an honest skeptic. Is there any chance you can share some of the resources that lead you to these conclusions so I can read myself?"

Bombastic Nathan:

"No I am not going to take time from my busy day to provide you with references. If you want to know any additional or supporting/contradictory information you can do that yourself. It's a good practice to get into anyway, if your aim is really to be healthy."

Since we can't have access to the consulting material, to help understand what leads to outrageous conclusions, we need demonstration.

Why content with curing cancers in front of us?

Invite hyperphosphatemics to show that it's nothing but an oleic acid deficiency and cure the condition with olive oil, or preferably the purified fatty acid. What about those with stubborn weight gain? I bet that they would be into trying cilantro to chelate the causative excess iron.

He decided that yogurts are a "SHIT THAT GAVE YOU THE CANCER FROM WHICH YOU DIE IN 15 YEARS". If this earnest phrasing was all that I had available, I wouldn't need much more to form an opinion about the author.

And how difficult is it to do the basic?

Yogurt consumption and risk of mortality from all causes, CVD and cancer: a comprehensive systematic review and dose–response meta-analysis of cohort studies

"Summarising earlier cohort studies, we found an inverse association between yogurt consumption and risk of all-cause and CVD mortality; however, there was no significant association between yogurt consumption and risk of cancer mortality."

This guy tells people to avoid creatine supplements under the argument that it's a source of phosphate, that will cause premature aging. He then realized that creatine monohydrate doesn't contain phosphate, proceeding to claim that it should be avoided because it raises its intracelullar level.

Consider these two options to form ATP:

• ADP + Phosphocreatine ⇄ ATP + Creatine
• ADP + Pi + H+ ⇄ ATP + H2O

A typical use of ATP (↵) will release phosphate (Pi).

If ATP is regenerated from ADP with a phosphate group from phosphocreatine (↱), we're left with plain, dephosphorylated creatine.

What returns a phosphate to creatine is the reverse reaction on top (↰), yielding also ADP. To derive considerable amounts of ATP for this creatine phosphorylation, free phosphate is put to use in the habitual reaction with ADP (↳).

In other words, doing and undoing something gets you back to the starting place. With a stable concentration of creatine in cells, free phosphate must eventually be consumed. Otherwise, what will phosphorylate considerable amounts of creatine? I think that the main source of ATP would be what's produced in the respiratory complexes in mitochondria rather than the portion that's formed from incorporating the phosphate from other molecules (without involving free phosphate).

Creatine increases the capacity of regeneration. Even if free phosphate wasn't consumed at one point, what would be better, its temporary increase or a shortage of ATP? Ask athletes their opinion.

Also, request these athletes to list their favorite supplements and I bet that creatine will often be mentioned. They know from practice that it's safe and effective at maintaining tissues energized in times of stress, with applications in disease: possibly the audience that this individual speaks to. Here's the intestine of someone being aged by creatine:

• Dietary Creatine as a Possible Novel Treatment for Crohn’s Ileitis

Or he thinks that the skin doesn't age along with the intestines?

It's years of stumbling upon opinionated content.

He established that coconut fat is not optimal because of its uniqueness: it depletes poison A from the body. The dude has the Garrey Smeat Forum membership eager to volunteer for this one.

I think that it's about time for him to get practical to substantiate the fantastic claims, and we have a series of them in every curative article.

'It's a charlatan, but at least credits Ray.' In response to a perception that mentioning Ray somehow excuses quackery, it's the opposite: it degrades an author to be associated with charlatans.

And before he plays the oppressed victim, he's welcome to arrive here and elaborate on why I'm glad to recommend authors in reach, such as Alex Yartsev, Medicosis, Travis, Terma, and others—in this thread alone we had Brianna and Mike—but not a handful that include him and professor Garrett. Is it because of his skin color? Yet, we also have white and privileged in the respectable group. Sexual preferences? But Terma told us once that he's a "gigantic faggot". Religion? Most of us are devoted to Raypeatism. What differentiates one group from the other?

I've made my points. It's up to his readers to approach and promote the content as they prefer.

Now it's time to credit everyone else. For an author that prides himself on being well-read, why it doesn't show in his writings? He admitted somewhere to not care about referencing and (when asked) refuses in bitter tone to provide the sources behind his opinions and trials. I take that he's fine with people doing the same to him.

In his case in specific, readers should feel free to share with others experiments found in his materials without mentioning the source, as he would be in a complicated position to complain.

Porcine bile acids promote the utilization of fat and vitamin A under low-fat diets

"Hens were randomly divided into five treatment groups with six replicates of 15 birds per replicate. The five treatment groups were fed with: corn soybean meal diets supplemented with 0, 30, 60, 90, and 120 mg/kg porcine BAs, respectively. No extra fat was added to the basic diet (crude fat was 3.23%). The whole experimental period was 84 days, and the pre-feeding period was 7 days."

"The porcine BAs are composed of the following components: 7.99% of hyocholic acid, 19.65% of chenodeoxycholic acid, and 70.88% of hyodeoxycholic acid."

"In vivo, different kinds of fat-soluble vitamins are absorbed at different sites. For example, vitamin A is mainly absorbed in the proximal intestine, while vitamin D is absorbed in the median intestine and vitamin E is absorbed in the distal intestine (49). The preferential absorption of vitamin A competes against the absorption of other fat-soluble vitamins (49)."

"[..]supplementation of BAs in the diet of laying hens resulted in an increase in the content of vitamin A in the liver ["by 60-75%"], while vitamin D and E did not change significantly in the in vivo experiments."

"The present study concluded that BAs promoted the absorption of vitamin A by promoting the absorption of fat even under low-fat diets, thereupon improving the reproduction and health of model animals."

#toxicbileapocalypse

@T-3 said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

I support Amazoniac's criticism of Hatch's (or anyone's) exaggerated claims, which, as Amazonic pointed out, reveals Hatch's less-than-competent knowledge about underlying mechanisms regarding the multiple ways in which glucose oxidation and cellular respiration may become deranged. The writers I would trust the most would emulate Ray, acknowledging gaps in his/our knowledge about multiple mechanisms relevant to bioenergetics, etc. I also support S.Holmes's interest in self experimentation and openness to learning from writers whose style isn't necessarily our most preferred (emulating Ray). I see no conflict between these two positions of (i) holding Hatch and others to high critical standards while (ii) being open to benefiting from advice they have given that might work for some of us (depending, of course, on context) even though Hatch’s understanding of cellular respiration is obviously incomplete. Even those like S.Holmes who say they don’t care about understanding the underlying mechanism correctly will benefit from much higher-quality insights/coaching/advice generated from those of us who are interested. It’s reasonable to learn empirically (by induction or, in Hatch’s case, even by incorrectly understood theory) that something “works” without understanding the mechanism explaining why the advice has worked. My main point is that we are joint stakeholders (disliking Blackrock’s use of the word): (i) those who want to understand mechanisms, critiquing and vetting Hatch and others and (ii) those who just want to know where to find high-quality advice or even speculative hypotheses that could prompt useful self experimentation. The vetting and critiques by the Amnizoniacs of the world exert adaptive pressure that should improve the performance of and our curation of advice givers. This includes all of us posting on this board, generating potentially useful speculative hypotheses for us to consider experimenting on ourselves with. I am hoping that both rigorous vetting/critiquing and clear/honest reporting from self-experimentation flourish and multiply on this board.

I have doubts if commentaries put any pressure on self-absorbed authors, they might play victims of persecution and believe that the world is not prepared for their brilliance yet.

What's cool about this kind of personality is that their lack of respect for any law makes them good a proposing new models, their creativity is allowed to flourish because nothing holds it back.

But if bombastic Nathan has found 'THE CURE FOR CANCER' through acidified silicic acid, what is he waiting to prove it? Get here and invite volunteers dealing with cancer to participate and document it.

• Group U: tartaric acid* in water
• Group S: tartaric acid* in water + silicic acid

U and S for 'unsealed' and 'sealed'. Both followed by a carbohydrate.

*It seems a better alternative to others acids to reduce confounders in acidification.

The Fate of Tartaric Acid in the Human Body

"The experiments demonstrate that tartaric acid (sodium tartrate) is not burned in the human body. When injected intramuscularly it reappears almost quantitatively in the urine within 10 hours, the major portion being excreted within the first 4 hours. Apparently the human body can neither oxidize nor otherwise transform this acid."

"When taken by mouth, only about 20 per cent of ingested tartrate is eliminated in the urine. At no time in the course of investigations have any traces of tartrate taken by mouth been demonstrated in the feces. It has long been known that tartaric acid is destroyed by fungi and by certain bacteria. Pasteur (11) in 1860, treated a mixture of d- and I-tartaric acid with the mold, Penicillium glaucum, and found that the d-tartaric acid was destroyed by this organism. Maassen (12) in 1896 found that twenty-three varieties of bacteria were able to destroy tartaric acid, among those being the Bacillus pyocyaneus, the Friedlander bacillus, the typhoid bacillus, the Bacterium enteritidis of Gaertner, and the Bacillus coli. Underhill et al. (10) found that tartaric acid is destroyed by fecal material. It is therefore probable that the portion of tartaric acid given by mouth which fails to appear in the urine (80 per cent) is destroyed in the intestinal tract by bacterial action. 20 per cent or less is absorbed before it is subjected to the destructive action of the intestinal bacteria, and is excreted in the urine. The experiments of Pickens and Hetler (13) are in accord with these results. They gave large quantities of grape juice to their subjects and found that the urine was acid and not alkaline as might be expected from feeding of malic or citric acid. The excretion in the urine of a part of the tartaric acid present in the grape juice may account for their findings."

"With the doses employed in our observations on human beings, renal damage did not occur, and it is therefore possible to recover practically all of the injected tartrate in the urine and to demonstrate that none of this fruit acid is utilized by human beings."

Rehashed Max and Ray's strategies can't serve as a crutch, we're after the contrast above.

It wouldn't be ethical to involve people with elevated serum lactate to track the expected normalization, but compared with not taking the sealer, we can anticipate non-advanced cancers being cured, and perhaps a change in expired carbon dioxide.

He should join us to show that's it's not one more addition to the record of charlatanry.

@Mulloch94 said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@Amazoniac I think some people are having a hard time accessing the forum because Charlie is attempting to block VPN and Tor ip addresses, lol. But you can change servers and be viewing the site again without issue. Charlie doesn't realize we can bypass authoritarian censorship.

I've never understood why someone would want to try that "ad libitum" approach unless they're like anorexic and trying to gain weight. High carb, low fat, low protein results in weight loss because people are generally unaware just how many calories they've cut out. It's the lazy man's approach to calorie counting basically. Same thing with low carbers. All they realize is they've cut out 300 grams of sugar, they don't really consider the fact that's a 1,200 calorie reduction.

It ignores some of the more basic rudimentary principles about how adipose tissue is created in the first place. Fat is stored as such, eat too much you'll get fat. Glucose is burned and stored as glycogen until it's full, then it gets stored as fat. Protein will be used for repair and any extra will be converted to glucose and then fill glycogen until it's full, at which point it will be turned into fat, lol. Everything leads back to fat on your ass if you take in too much. I've never really considered this as controversial either. I don't think Ray did either. The only fringe takes I've seen disputing this type of stuff are the Gary Taubes's of the world who have these broscience opinions about insulin driving fat gain instead of simply eating too much.

Yeah I like Mike a lot, can't say I've watched many of his videos though. I saw the most recent one about vitamin A, and an older one where he and Danny was with like two other people and they were all talking and taking questions. Looked like a livestream thing or something. Kyle Mamounis was always my personal favorite, but he is quite elusive. Not making many posts. Usually a video like once a year, and here lately nothing at all really.

The problematic combination for someone prone to gain weight would be the diet abundant in fats along with carbohydrates that's promoted.

Every nutrient deserves to be moderated if it's causing issues without signs of improvement, and the person can try to improve its tolerance indirectly in the meantime.

Stubborn weight gain after persisting on such diet? No puzzle, this guy determined that the cause is excess iron and cilantro to chelate it should solve.

@T-3 said in Conditional problems with vitamin A: a place for sane discussions:

@Amazoniac
I hope others will contribute to this thread re absorption and clearance rates as well as mechanisms by which vit A may be poisonous/problematic. Are you personally limiting vit A intake at this time?

I’m not (yet). Given what’s going on at RPF, I have, if anything upped eggs/milk/pumpkin/etc in my diet over the last few months to celebrate high-metabolic-rate good health, Ray Peat style, as quiet dissent. Like Amazoniac, I think it’s good for us to remain open to new information as it arises, however, about any potential problems associated with excessive vit A intake.

Might I get your advice based on my brief personal history, which was unusually high-dose vit A for several reasons? Growing up in the 1970s, my mom became a health-food nut and both mom and dad took – and gave me as a child – a large volume of vitamin supplements. From the age of 3 onwards (maybe through puberty), I was encouraged to take a daily beta-carotene supplement. We drank lots of carrot juice. The soles of my feet had an orange tint, which my doc may have even commented on once. We kept up this extraordinarily high diet + supplement regimen until I was a teenager. I took a round or two of Accutane for acne as a 17 year old. Under lots of other stressors and chronic sleep deprivation, I was diagnosed as a type-1 diabetic at age 20, which ran in my half-Norwegian family. I would be a likely candidate to have had – and very likely still have – excessive vit A stored in liver, adipose and elsewhere. Do you think I should try the low vit-A diet? (I can’t believe I’m actually writing those words…!!!...rest assured, only as a speculative hypothesis and not a likely action plan.)

@T-3 said in Conditional problems with vitamin A: a place for sane discussions:

@T-3
Adding: I never had (and don't think I have at present) any vit A toxicity symptoms. The callouses on my feet and palms are probably a bit more "orange tinted" than most people's and my complexion is noticeably darker than either of my parents, but I also get a lot of healthy sun exposure. My default is skepticism toward the hypothesis that I suffer from vit A toxicity. Eating high-vit-A foods makes me feel good and I don't think I have any problems associated with those foods. Thus, I'd say that worrying about vit A intake would be creating a pseudo diet problem where none in fact exists. But I gather that Amazoniac has made this thread because he has some concerns about vit A in his own diet, or is that wrong?

The terms 'macabrotenoids' and 'poisonoids' are for fun. It used to be clear early on, but the poison A crowd took the confusion to proportions that may create doubt for some people on whether these are humorous or not.

You can find a report (on the main poison A thread of the Garrey Smeat Forum) from researchers who found that people with diabetes and hypothyroidism were groups that had unusually elevated stores of poisonol. What increases the metabolic rate tends to also increase the internal consumption of poison A, and reserves can be normalized this way rather than through restriction.

I think that the community has to separate excess poison A stores from its toxicity. Lumping them invariably together contributes to the pro-poison A and anti-poison A pro-life camps going on futile debates.

The person doesn't have to be overloaded with poison A in the body to experience toxicity problems, these can happen at low intakes when the metabolism of a substance is deranged or if its addition influences pathways that are maladjusted (⇈).

And we don't know when it's really a maladjustement, making avoidance risky. The elevation of poisonoids may be containing an infection or inhibiting cancer. If the immune system is suppressed, it can represent easing on a battle, forcing the body to find ways to internalize the problem and minimize the associated cost.

One of the sources of poison in the gut is what recirculates through bile, that may contribute to local problems as dietary poisons do, but what's framed as 'detoxification events' can be the body transitioning from aggressive mode to tolerance. Something of this nature would align with people suddenly being able to not overreact to foods that used to cause trouble.

In the previous post, the authors pointed out that inhibition of specific inflammatory proteins carries risks (despite improvements). I suppose that it's riskier to try to inhibit inflammation manipulating at a more basic level through poison A restriction.

Poison A deprivation is a desperate immunosuppressive measure and doesn't seem to apply to your case. And you already mentioned to respond well to contaminated foods. So, I wouldn't bother with it.

If the body has an overactive pathway, any fluctuation in the availability of a precursor can result in exaggerated formation of derivatives. An example of this would be someone with sarcoidosis, who may have a shock-like response to small amounts of venom D3 because of excess conversion to metabolites that are more active. It's toxicity at low doses without the person being overloaded with venom in the body. When someone treats it as rat poison, it can be that for this individual it's behaving as such: a poison to a rat. It's converted in excess, that would normally take much higher doses of the precursor to achieve the same effect. The poison A crowd tend to have poor tolerance to venom D3 as well, and exposure to toxins should be regulated as drugs.

Unrelated:

• Control by the brain of vitamin A homeostasis (it's not about the abdominal brain, but the intracranial one)

Trace Element Speciation in Food
↳ [54] Iron and Zinc Compounds in the Muscle Meats of Beef, Lamb, Pork and Chicken

"Figure 1 shows that the soluble zinc in all meats is distributed between five main components.

• The first zinc peak corresponds to the exclusion volume of the column (molecular weight approximately 130 000) and therefore represents high molecular weight zinc. The zinc in this peak is possibly associated with a-macroglobulin which has a molecular weight of 820 000 and is known to account for one-third of all plasma zinc.[30]

• Zinc peak II eluted in the same volume as the reference protein, transferrin, at a molecular weight of 76 000. Transferrin is known to bind a small amount of plasma zinc.[30]

• The third zinc peak is very large and eluted at a molecular weight of approximately 65 000. Some, if not all, of the zinc in this peak is probably bound to albumin (molecular weight 67 000). Albumin is one of the sarcoplasmic proteins of meat[31] and is the predominant form of zinc in plasma.[30]

• Zinc peak IV is also large and eluted at a molecular weight of approximately 35 000. This peak probably consists of the zinc metallo-enzyme carbonic anhydrase which has the same molecular weight, is a major soluble form of zinc in liver,[32] and accounts for nearly all the zinc found in erythrocytes.[30]

• The fifth zinc peak eluted in a volume corresponding to low molecular weight compounds (< 12 000). The fractions from zinc peak Vb reacted with ninhydrin which suggests that this peak consists of zinc bound to amino acids.[19] Fractions from peak Va showed no reaction with ninhydrin and therefore probably consist of zinc bound to small peptides."

@Mulloch94 said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@S-Holmes Well I don't believed I used the word unsuccessful, sorry if I made you insinuate that. I guess success needs to be put in relative terms to the goals at hand. All I was trying to get across is this dude applied the lack of portion control principle, said a big "F#$%k you" to CICO and the law of thermodynamics, and proceeded to swell up like a balloon. He did cite Nathan in numerous places, so he made it obvious he was greatly influenced by him. To what degree he applied those principles beyond a general lack of portion control is something I don't know. But you see this trend on several less established log entries on that forum over the years. People disregarding CICO, believe they need to eat more and more foods, then start complaining about weight gain. I don't know what degree Nathan's influence is personally responsible for this held belief, but undoubtedly it's influenced some of them. He was a presence on that forum for a stent of time.

I'm having issues accessing the forum lately, but found this example right on the first page of results in the searchable archive:

"I think Nathan Hatch makes some outlandish claims. He claims to have sat around all day at a computer while eating his high everything diet and all he did was gain muscle and lose fat. I call bull**** on this. I tried doing things his way for about 6 months several years ago and all I did was get fat and my fasting blood sugar went into the pre-diabetic range. I think his claims are ridiculous. My diet now is similar in some ways, but much lower in fat and protein. I'm at about 70 g of protein, as much sugar as I want, a little starch, and 80ish grams of fat. I have eaten this way for over a year now and have lost about 10 pounds rather than gaining weight and my metabolism has kicked it up a notch or two. I feel much younger and healthier than I have in 15 years. I did not feel this way at all trying Hatch's way of just eating everything ad libitum."

@Mulloch94 said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@Amazoniac said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

Sate and Garrett are similarly immoderate and pushy. It's not my intention to sort charlatans here, rank us as you prefer, but it's difficult to discriminate which of us is worse.

That's fair, I didn't mean to imply Hatch should be softly scrutinized by comparison to others. In my opinion what makes him less dangerous is his ideas are, quite frankly, less popular with people. Charlatans become more dangerous when they start gaining a following.

I agree.

If anyone is looking for assistance, Mike Fave offers the same type of service. He's also familiar with Ray's work, but is competent, careful as a health communicator, and doesn't treat the audience as fools.

@Mulloch94 said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@Amazoniac Speaking only for myself here...but I would be all for an open forum discussion about "poison A" with normal rational thinking people. It's still a position I profoundly disagree with obviously, but their theories on vitamin A is not what I find cringy. It's this weird religious cult they wrap all this shit up into. And the otherwise authoritarian censorship the ensues when someone isn't drinking that flavor koolaid. I'm also not thrilled about the forum adopting this premium payment thing, but that can take a backseat to the more glaring issues for now.

I don't think Hatch is right either, but in the grand scheme of things he much more rational in that his ideas are on the open market, free to accept or deny with no herd mentality or cult-like personas shoving it down people's throats. But yes, people should be VERY careful about incorporating his ideas, lol.

Sate and Garrett are similarly immoderate and pushy. It's not my intention to sort charlatans here, rank us as you prefer, but it's difficult to discriminate which of us is worse.

@S-Holmes said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@Amazoniac LOL. We (husband and I) tried the "poison A" restriction about 5 years ago. We were happy to leave that one behind. No improvements were noted.

The point is that improvements on any protocol don't found them.

@S-Holmes said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@Amazoniac I would actually like to hear from more people who have tried some of the things Nathan recommends and whether they did or did not see improvement on them. So far, I'm seeing some good results and not restricting any food groups, just finding healthier ways to combine and prepare food. As a LONG TIME Dr. Peat follower (I bought all of his books and subscribed to his newsletter back in the day) Nathan seems to be providing the things I need to go to the next level. AND he still uses Dr. Peat's guidelines, and more importantly, gives Dr. Peat credit for saving his life. (He and I have a lot in common.)

I get it if you don't like him. He and I are light years apart politically and maybe even religiously, but I take what I can use and leave the rest. I hope others will give his work a chance. What is there to lose...seriously?

I'm interested in knowing what's working as well, which is why it seemed sound to not dismiss the experiences of people who reported improvements from restricting poison A.

What bothers is the serial misinterpretations communicated as official declarations, but you already mentioned to not care about this aspect. Not sure where to go from here.

Giving credit is an obligation and Sate is not exemplary at it. Forgetting on occasion can happen, but how do you explain the extensive list of claims in his writings and the near-absent attributions? It's all BS, that is, butt-sourced? As for Ray, let's not discard the possibility that there can be more to mentioning him than gratitude, it can be in part for the community appeal.

If I'm not mistaken, you're dealing with a coach that advised an overweight person to ingest a stick of butter a day, who later complained of problems.

Nonetheless, the borrowing of experiments is not the central issue, it's the attached explanations, that deserve to be approached with suspicion and verified.

@S-Holmes said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@Amazoniac TBH, I don't really care (that much) HOW something works...only whether or not it DOES work. I've only just started the protocols so less than a week in and so far, following his suggestions, I have stubborn skin lesions on my arms (I've had for years) clearing up. As per his suggestions, I'm using silicic acid, sodium acetate, sodium citrate, having tannin and beta carotene with every meal, and eating more fruits and vegetables. I'm excited to get to the chapter on bread. I mostly make my own but I know preparation of grains is important and I've neglected that for too long.

@S-Holmes said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@S-Holmes I should also add that my energy levels and overall sense of well being have improved considerably.

We might as well argue that some people experience similar improvements in restricting poison A and find relief from an exclusion protocol, but does this give the protocolist a free pass to be sloppy and spread confusion?

Authors such as Sate and Garrett are at the root of distorted ideas that plague alternative health circles and sidetrack people from getting to the crux of issues with clarity.

We are witnessing the consequences in real time of what this type of personality can do to communities when they take the lead and find advocates who behave in hypocritical manner to promote their madness, only going by own immediate experiences and not minding the rest.

We had three separate threads on the Garrey Pith Forum dedicated to Sate's hyperphosphatemia cure. Sensationalism sells.

@S-Holmes said in BIOHACKING by Nathan Hatch, "F*** Portion Control":

@Amazoniac Actually, that was one thing that impressed me. He said by having the digital version we would get updates and corrections because he's certain he isn't right about everything and will let us know when changes are made. I don't sense any ego in his work.

No ego? Good one. Just the title of the article in question is enough to refute the impression:

• I SOLVED THE WARBURG EFFECT (A THE CURE FOR CANCER)

It's somewhat irresponsible of him to not curb the grandiose, in special when dealing with cancer. And it wouldn't be difficult:

• Silicon in mitochondria: effects on cellular respiration with relevance for cancer metabolism [if it wasn't junk]

To put into perspective, check these out:

• Metabolism of ketonic acids in animal tissues
• The role of citric acid in intermediate metabolism
  in animal tissues
• The formation of citric and α-ketoglutaric acids in the mammalian body

Despite the composure, they're Hans Krebs' original works on the TCA cycle.

• I HAVE WORKED OUT THE CITRIC ACID CYCLE, EVERYBODY (THE CURE FOR METABOLIC CONFUSION WORLDWIDE)

For more information:

• The Intermediary Stages in the Biological Oxidation of Carbohydrate
• Energy Transformations in Living Matter

On-topic, TCA cycle seems a preferable term to Krebs cycle for being more meaningful and (as suggested elsewhere) it would otherwise be unfair to him: Hans is responsible for discovering the ornithine and glyoxylate cycles too. Krebs cycle.. but which of them?

Back to our curer, he wrote:

"As would be expected cancer cells consume a great deal of nutrition but produce very little energy, and through further research and experimentation I became satisfied this is the case, as the Warburg Effect can only be explained by active leakage of electrons from mitochondria as opposed to the electron transport chain simply stopping as that would also stop the consumption of substrate, so the failure is in the mitochondrial transport chain such as the loss of insulating silicon would cause."

I often make mistakes, but Sate has his absurds marked by sloppiness and in authoritative tone. It's a problematic combination.

It seems that I get the rationale: for a given amount of 'substrate', if 'little energy' is being produced from it, what else could be happening if not electron leakage to explain the difference?

What about the partial oxidation of glucose that yields pyruvate and then lactate through lactate dehydrogenase (functioning as a pyruvate hydrogenase)?

Pyruvate
↳ Dehydrogenase (PDH): Pyruvate + NAD+ → Acetyl + (NADH + H+)
↳ Hydrogenase (LDH): Pyruvate + (NADH + H+) → Lactate + NAD+

It's the means to regenerate oxidized NAD to continue to oxidize more glucose as lactate is exported from the cell.

The electrons (e–) are omitted above, but we have:

           H+ (1 proton, 0 electrons) -- proton or hydron
 H+ + e– → H  (1 proton, 1 electron)  -- neutral hydrogen
H+ + 2e– → H– (1 proton, 2 electrons) -- hydride

NADH is the hydride donor:

• NADH ⇄ NAD+ + H–

And we have the typical extra proton next to NADH to indicate that electrons weren't extracted from molecules in excess of protons:

• NADH + H+ ⇄ NAD+ + (H– + H+)
• NADH + H+ ⇄ NAD+ + (2H)

It's simpler with FAD because it incorporates the two hydrogens, without leaving a lone proton:

• FADH2 ⇄ FAD + (2H)

You can find throughout Hans' publications the essence of reactions, with the two hydrogens being released from molecules at the levels where dehydrogenases occur.

Here's a neat diagram showing them:

The hydrogens (and their electrons) are accepted by pyruvate to become lactate:

• Pyruvate + 2H → Lactate

It's difficult to reconcile with the assertion that "the Warburg Effect can only be explained by active leakage of electrons from mitochondria". Electrons in this case didn't even reach the mitochondria to be "leaked".

Since lactate is a negatively-charged molecule that's often exported with an additional proton (H+) as the positively-charged counterpart..

Carbonic anhydrase IX and acid transport in cancer

..which contributes to the extracellular acidification of cancer, we have the equivalent of a glucose molecule leaving the cell:

• Glucose: C6H12O6
• 2×Lactate: C6H10O6
• 2×Lactic acid: C6H12O6

It's not that the elements of glucose are disappearing in enigmatic ways.

He went further: "the electron transport chain simply stopping [..] would also stop the consumption of substrate". A great deal of glucose is consumed in the cytosol at a high rate, without the need to involve the electron transport chain.

A gymnastic to make the claim reasonable would be to factor in anabolism and tie it in with glycolysis. After all, if glucose equivalents are exported from the cell as glucose is consumed, the cell will lack material to support growth.

Functional mitochondria of cancerous cells tend to be geared in favor of anabolism, and they adapt to find a way around metabolic steps that are inhibited, to redirect nutrients for synthesis. If a molecule has to undergo oxidation for this purpose, it may happen as far as needed to prepare it for anabolism.

Cancer Metabolism

"Although many cancer cells rely primarily on aerobic glycolysis for their energy, they still rely on mitochondria to produce precursors for fatty acid synthesis and other biosynthetic processes. How tumor cells with defective mitochondria produce the lipids necessary for proliferation has been unclear. Mullen et al. (2011) uncover new metabolic flexibility in cancer cells. Glutamine can drive citric acid cycle (CAC) reactions in reverse, such that reductive carboxylation yields acetyl-CoA for lipid synthesis. Glutamine-dependent reductive carboxylation has been recognized as a minor source of citrate in mammalian cells and as the major source of citrate and acetyl-CoA in P. falciparum, a parasite with limited respiration. By tracing the fate of carbons supplied to osteosarcoma cells by 13C-glucose or 13C-glutamine, the authors identify reductive carboxylation as the major source of [cytosolic] acetyl-CoA in ETC-deficient cancer cells. Although some tumors carry mutations in ETC components, oncogenic mutations are more commonly found in CAC enzymes like fumarate hydratase (FH). To test whether these types of mutations also favor glutamine-dependent reductive carboxylation, Mullen et al. (2011) examined the metabolism of renal tumor cells lacking FH activity. When cultured without glutamine, these cells stop proliferating. In the presence of glutamine, FH-deficient cells proliferate by employing both oxidative glutamine metabolism (a process well-known for replenishing CAC intermediates that are depleted under normal growth conditions) and reductive carboxylation of glutamine (contributing lipid building blocks). Despite the association between defective mitochondria and oncogenesis, this study highlights the central importance of mitochondria in cancer, even when they aren't generating ATP."

Both are cancerous.

• With intact respiration (left), glucose and glutamine can end up as citrate;
• With compromised electron transport chain (right), reflecting on a partial inhibition of the TCA cycle (that reinforces the inhibition of upstream pyruvate oxidation), glucose stays out of the mitochondria, that rely on glutamine through the reductive pathway in reverse to derive citrate.
  • The oxidation of ketoglutarate is not shown (clockwise), but it's possible for the cycle to be limited in addition to the metabolism of fumarate.

In either case, "consumption of substrate" continues to occur (glucose and glutamine are used up) to form new molecules rather than undergoing complete oxidation.

• Reductive carboxylation supports growth in tumour cells with defective mitochondria
• Pyruvate carboxylase is required for glutamine-independent growth of tumor cells

Sate also wrote that "cancer cells consume a great deal of nutrition but produce very little energy".

Targeting energy metabolism to eliminate cancer cells

"The inappropriate proliferation of cancer cells requires high energy, and the cells generate ATP to satisfy the biomass production. The enhanced glycolytic rate in cancer cells is required not only to meet the need for energy but also to maintain the level of glycolytic intermediates needed for biosynthesis of macromolecules. The biosynthetic activities required for proliferating cancer cells involve high rates of nucleotide synthesis, amino acid synthesis, and lipogenesis."

Another important piece shared in conversations with my masters:

Revisiting the Warburg effect: historical dogma versus current understanding

"Aerobic glycolysis has been described as an inefficient means of energy metabolism, since the net production is only 2 moles of ATP per glucose molecule, whereas the total yield is 32(−33) ATPs (Mookerjee et al. 2017) from the complete oxidation of 1 glucose molecule. However, the speed of the cytosolic ATP generation is approx. 100 times faster (range: 20–300 times) than in mitochondria (‘low yield, but high-speed ATP production’). ATP provision per unit time is higher than in oxidative glucose metabolism as long as an adequate glucose supply is maintained in the extracellular compartment (Vaupel et al. 2019). In cases of greatly increased ATP demand by cancer cells, aerobic glycolysis can rapidly increase while OxPhos remains quite constant due to the much faster ATP production through the Warburg effect."

ATP/glucose:

• Cytosol 2:30 Mitochondria
• Cytosol 1:15 Mitochondria

ATP/time:

• Cytosol 100:1 Mitochondria

Therefore, increasing reliance on glycolysis is more than enough to compensate through speed for the lower yield per glucose, and meet the high energetic needs of cancer cells. Considering that the body tries to maintain a steady level of glucose in the circulation (independent of carbohydrate ingestion), if greedy cancer cells have access, it's a problem. But nothing that 700 mg of silicic acid a day with tartaric acid for sealing up the mitochondria can't cure.

Charnathan concluded his article with:

"As I do not have access to scientific institutions that normally distribute such discoveries please share this information wherever and with whomever you can to document my work and help people suffering from cancer."

It's unbelievable.