Posts made by Lejeboca

@TexugoDoMel said in Can PUFAs be absorbed through the skin?:

PRESS, M. (1974). CORRECTION OF ESSENTIAL FATTY-ACID DEFICIENCY IN MAN BY THE CUTANEOUS APPLICATION OF SUNFLOWER-SEED OIL. The Lancet, 303(7858), 597–599. doi:10.1016/s0140-6736(74)92653-1

OMG!
From this paper in Discussion: "It has been claimed that there is " immediate absorption " of E.F.A.s when applied to mammalian skin...It thus seems that linoleic acid is more efficiently utilised when applied to the skin than when given orally or intravenously. Rats fed linoleic acid oxidise about 60% immediately, presumably in the liver, so that one possible explanation for this greater efficiency would be if linoleic acid applied to the skin were incorporated directly into circulating lipoproteins without first going through the liver."

# Note on oil application method:
"sunflower-seed oil, whose fatty-acid composition is shown in table 11, was applied to the flexor surface of one forearm and rubbed in. About 230 mg. of oil, containing 120 mg. of linoleic acid, was applied daily throughout the experimental period."

This got me thinking that, since our endogenous CORT is "naturally" elevated in the morning, if we have an LPS-prone breakfast, then any existing inflammation will spike.
So

• rule #1, breakfast that is easy on digestion (Ray-Peat-right-again!)
  At breakfast time consider
• charcoal or anything digestion-promoting
• getting red/sun light at breakfast time to to decrease NO and other inflammatory cascade factors.

@yerrag said in Thymus health:

was it to calm the cytokine storm as a way to dampen Inflammation? I just know cortisone is used as an anti-inflammatory but don't know the mechanism.

Below is a study that considers the dual pro- and anti-inflammatory effects of cortisol under stress with respect to the time of introduction of immune challenge (LPS), It also notes the mechanism of upregulating TLRs, which recognize pathogen molecular patterns, in the brain and liver.

Prior exposure to glucocorticoids sensitizes the neuroinflammatory and peripheral inflammatory responses to E. coli lipopolysaccharide

Abstract

Acute and chronic stress has been found to sensitize or prime the neuroinflammatory response to both peripheral and central immunologic challenges. Several studies suggest that stress-induced sensitization of neuroinflammatory processes may be mediated by the glucocorticoid (GC) response to stress. GCs, under some conditions, exhibit pro-inflammatory properties, however whether GCs are sufficient to prime neuroinflammatory responses has not been systematically investigated. In the present investigation, we tested whether acute administration of exogenous GCs would be sufficient to reproduce the stress-induced sensitization of neuroinflammatory responses under a number of different timing relationships between GC administration and immune challenge (lipopolysaccharide; LPS). We demonstrate here that GCs potentiate both the peripheral (liver) and central (hippocampus) pro-inflammatory response (e.g. TNFα, IL-1β, IL-6) to a peripheral immune challenge (LPS) if GCs are administered prior (2 and 24 h) to challenge. Prior exposure (24 h) to GCs also potentiated the pro-inflammatory response of hippocampal microglia to LPS ex vivo. In contrast, when GCs are administered after (1 h) a peripheral immune challenge, GCs suppress the pro-inflammatory response to LPS in both liver and hippocampus. GCs also up-regulated microglial activation markers including Toll-like Receptor 2. The present data suggest that the temporal relationship between GC treatment and immune challenge may be an important factor determining whether GCs exhibit pro- or anti-inflammatory properties.

Although the study considered a pretty high dose of cortisol (CORT), smaller (and chronic) doses would have a similar effect, in its nature, *the authors fixed the measurements at 4h of LPS introduction.

A dose of CORT was chosen that had previously been determined to mimic the plasma CORT profile produced by an acute stressor (a session of 80–100 inescapable tailshocks) (Fleshner et al., 1995). We had found that this acute stressor potentiates the neural and peripheral inflammatory responses to LPS administered 1–4 days later (Johnson et al., 2002).

@b1 said in Boron supplements:

I cant find any borax supplements unless you mean the cleaning / slime making stuff

Indeed, to second @noseleather borax 'for cleaning' is good stuff. (modulo 'slime making' probably .lol)

Anecdotally, I add Borax powder to wash my linens (and light-colored clothes). This is my only 'supplement' with Borax. Idealabs hair tests showed a good load of boron. This was my only change in boron consumption. (I used to and I do eat quite a bit of raisins too.)

05/2024 -- Hair                                   05/2023 -- Hair 

@Mauritio
Travis also spoke about boron as a 'natural fluoride's antidote' :

"This [catechol‐O‐methyltransferase] enzyme can be safely inhibited with epicatechin gallate, found in high concentrations in green tea. However, green tea also has fluoride; this fact would make me add fluoride's natural antidote—boron—to the tea."

-- https://lowtoxinforum.com/threads/caffeine-and-progression-of-parkinson-disease-a-deleterious-interaction-with-creatine.7841/post-301043

@Mauritio said in Just 1 minute of red light is effective:

Just one minute in the morning was enough to improve eye health in a study . It only worked in the morning as far as I remember. There seems to be something about red light in the morning being very healthy

Some time ago, I posted about it on RPF here.

Below is that post screenshot as I don't know whether the link is generally usable.

@LetTheRedeemed , Ray recommends gelatin to be about 1/3 of the total amount of protein since gelatin is missing essential amino acids.
For me, the ratio has to be even lower, of about 1/4, not produce negative effects such as brittle nails and hair.

@DavidPS , the main takeaway from the paper in the OP is that sometimes you absolutely want to suppress NO (and iNOS) and sometimes you might not want to do so. The former is broadly true for autoimmune conditions and the latter is for true infections, esp. those with which the body has to deal with whatever means it can.

Thanks for the article Inducible Nitric Oxide Synthase: Regulation, Structure, and Inhibition (2020) !
It will take me some time to digest its 45 pages . The abstract, however, already points to the dichotomy, "both the dual modalities of iNOS and NO in disease states (i.e., protective vs. harmful effects)" indeed.

@happyhanneke said in I need x-rays:

I've been consuming gelatin and a carrot salad for a long time now. I'm also taking aspirin and cynomel.

To start with, I'd stop these substances, unless they are vitally needed for you.
Firstly, to start with a clean slate, and maybe add those gradually as needed.
Secondly, depending on the ratios of gelatin to other proteins, the amount of carrot salad, aspirin and cynomel doses, these substances may not be benign (!).

@happyhanneke , I agree with @LetTheRedeemed that this could be dealt with without x-rays.
I'd try to rule out hypotheses one by one: Do something for arthritis for a week, if helps continue (adjust), If not move on to another hypothesis for another week. This algorithm, of course, assumes that you research precise remedies for specific hypotheses and not throw a kitchen sink on each (because with a kitchen-sink approach, it will be hard to differentiate what works.)

@DavidPS , thanks!
The links to the book that I found via the rpf search
( http://krishikosh.egranth.ac.in/bitstream/1/2027529/1/HS1519.pdf )
didn't work for me [Site not accessible] .
But I managed to get a copy via scihub. Use 0046410236 in the search field. [This is book's ISBN.]
The annas-archive site worked for the books too,

Also, for laughs, check out Let's Eat Right to Keep Fit
Reviewed by: Robert E Shank >

@Mauritio said in Strong Sistas finally posted an interview with Dr. Ray Peat - The Basics Of Pro-Metabolic:

So by using that logic, Vitamin D and K should also be anti-heavy metal.

Re: Vitamin D -- No.
It facilitates the absorption of heavy metals from the gut.
Confirmed myself by idealab's multiple hair and nail analyses.
I have several posts on this as well as some reference research on the formally known as RPF.

@yerrag said in Strong Sistas finally posted an interview with Dr. Ray Peat - The Basics Of Pro-Metabolic:

I've been wondering why in one of his last newsletters Ray would say that when the body is in the process of drawing calcium from the bones, in an osteoclastic process, it cannot be at the same time in a full optimal mitochondrial respiratory mode where among other things CO2 is being produced.

From this paper Calcium paradox disease: Calcium deficiency prompting secondary hyperparathyroidism and cellular calcium overload
in Page 7:

Mitochondria are conspicuously affected by
Ca overload [151]. These organelles have the capacity
to store significant amounts of Ca in the form of biologi-
cally inactive amorphous calcium phosphate, but when
their buffer capacity is overtaxed mitochondrian physi-
ology is disrupted with severe reduction of oxidative
phosphorylation, resulting in an ATP deficit that in turn
diminishes the effectiveness of the Ca pump with fur-
ther cellular Ca overload. Elevation of [Ca] stimulates
Ca-activated neutral protease [7,8] and phospholipases
[6], affecting the pathophysiological process of muscu-
lar dystrophy [152] and other diseases characterized by
cellular Ca dishomeostasis [146]

@diomedes , I assume your morning coffee is before ~10am. This is the time until cortisol, the "waking hormone" is still high, so it may counteract the coffee "sleepiness" effect, which is possibly due to some theobromine in coffee.

There is much less theobromine in tea or mate. Try them if you'd like to stay awake in the afternoon

@LetTheRedeemed said in Reversal of hair loss in Mice with “sugar gel”:

EDIT: "it increases NO [nitric oxide is bad for metabolism] so according to danny roddy it is le bad." - sneedful
Any references indicating this to be true or false would be appreciated.

This review warns against high doses of D-ribose:
https://www.spandidos-publications.com/10.3892/etm.2021.9927

"In addition, high D-ribose concentrations may also cause chronic diabetes complications by other means. D-ribose may glycosylate insulin to form ribosyl insulin, activate Caspase-9 and -3/-7, trigger transcription factor NF-κB and produce intracellular reactive oxygen species (ROS) that may cause cytotoxic damage to the surrounding tissues and cells, eventually leading to the manifestation of chronic complications (63)."

So, I suppose, D-ribose may increase inducible NO (iNOS) by way of triggering NF-kappaB, which is a primary inflammatory response (see, e.g., pubmed here)

Personally, i will avoid supplementing with D-ribose due to a possible NF-kappaB trigger, even not being a diabetic.

Ethanol extract of propolis (EEP) inhibits nitric oxide synthase gene expression and enzyme activity

I long hoped there would be anything else but MBlue + Red Light to inhibit NO. And voilà: it's the caffeic acid phenethyl ester (CAPE), which is "identified as a major peak in the chromatogram of EEP".

From the abstract:
"EEP inhibited the iNOS promoter activity induced by LPS plus IFN-g through the NF-kB sites of the iNOS promoter. In addition, EEP directly interfered with the catalytic activity of murine recombinant iNOS enzyme. These results suggest that EEP may exert its anti-inflammatory effect by inhibiting the iNOS gene expression via action on the NF-kB sites in the iNOS promoter AND by directly inhibiting the catalytic activity of iNOS."
[emphasis mine.]

Preparation of extract from the paper:

Coarsely powdered propolis (100 g) was extracted with 10 volumes of 95% ethanol for 2 weeks. The ethanol extract was filtered, evaporated, and lyophilized to give the dry ethanol extract (33.3 g).

In Anti-inflammatory Effect of Propolis through Inhibition of Nitric Oxide Production on Carrageenin-Induced Mouse Paw Edema, even smaller amounts of extract were successfully used:

Because lyophilized ethanol extract of propolis used in the present study is equivalent to 18.5 mg propolis per 100 ml, 16) 1: 1000 and 1: 100 dilutions of propolis correspond to 1.85 and 18.5 mg/kg, respectively. Therefore, the propolis used in the present study was 5.4—54 times more potent than that reported by Borrelli et al. ... though there was a difference between mouse and rat.

@Mauritio
As a rule of thumb, you need more quantity of a plant as food than as an extract to achieve the same effects.
What horseradish you eat as food is on the order of grams for a single serving, I imagine, while 1-3 drops contain less than a milligram of the plant matter.

With extracts, it is easier to gauge the dosage too.

I, personally, like alcohol extracts because they are stored for a long time and are always on hand. A 30ml bottle would last for 8 months to a year in the dosage as above.

Cross-linking here my post about horseradish inhibiting tumor-cell proliferation which I posed in the Cancer tread here:

https://bioenergetic.forum/post/24447

Again small doses of extract components seemed to be used.

Stumbled on this one from references in links in the Horseradish thread but didn't read beyond the abstract.

Tumor cell proliferation and cyclooxygenase inhibitory constituents in horseradish (Armoracia rusticana) and Wasabi (Wasabia japonica)

Abstract

Cyclooxygenase and human tumor cell growth inhibitory extracts of horseradish (Armoracia rusticana) and wasabi (Wasabia japonica) rhizomes upon purification yielded active compounds 1-3 from horseradish and 4 and 5 from wasabi rhizomes. Spectroscopic analyses confirmed the identities of these active compounds as plastoquinone-9 (1), 6-O-acyl-beta-d-glucosyl-beta-sitosterol (2), 1,2-dilinolenoyl-3-galactosylglycerol (3), linolenoyloleoyl-3-beta-galactosylglycerol (4), and 1,2-dipalmitoyl-3-beta-galactosylglycerol (5). 3-Acyl-sitosterols, sinigrin, gluconasturtiin, and phosphatidylcholines isolated from horseradish and alpha-tocopherol and ubiquinone-10 from wasabi rhizomes isolated were inactive in our assays. At a concentration of 60 microg/mL, compounds 1 and 2 selectively inhibited COX-1 enzyme by 28 and 32%, respectively. Compounds 3, 4, and 5 gave 75, 42, and 47% inhibition of COX-1 enzyme, respectively, at a concentration of 250 microg/mL. In a dose response study, compound 3 inhibited the proliferation of colon cancer cells (HCT-116) by 21.9, 42.9, 51.2, and 68.4% and lung cancer cells (NCI-H460) by 30, 39, 44, and 71% at concentrations of 7.5, 15, 30, and 60 microg/mL, respectively. At a concentration of 60 microg/mL, compound 4 inhibited the growth of colon, lung, and stomach cancer cells by 28, 17, and 44%, respectively. This is the first report of the COX-1 enzyme and cancer cell growth inhibitory monogalactosyl diacylglycerides from wasabi and horseradish rhizomes.

@Amazoniac Thanks!
It is on my reading list now! Main goal not to side-track