Posts made by CrumblingCookie

@yerrag said:

Use of natural substances available in nature that are known for their antifungal properties may help as a start. Taking turpentine orally, for example. This would help change the microbiome towards a dominance by bacteria instead of fungal forms.

When you said turpentine, did you only think of its antifungal properties or of more?

I've been harboring some aversion to turpentine and didn't try it as intended. A few days ago, however, I started 4-5 times daily 4-5 drops of aforementioned monoterpenes (from peppermint oil) and whilst it's ached a little inititally and especially when taken without any dextrose (it's recommened to be taken with sugar, just as turpentine) its effects are remarkably beneficial and remarkably quickly so.
I've tried to find associations of turpentines/terpenes with intestinal mucosa.

And couldn't find much, really. From a bit of crossreading, however, it appears to be the case that turpentine AT LOW DOSES, but not at large doses (opposite effects!), exhibits trophic effects on the intestinal mucosa and villous length and proliferation by releasing cytokines (and perhaps improved microcirculation).
It helps to maintain villous lenghts during a couple of days of starvation/fasting (I hadn't known that villous atrophy sets in so quickly from a "use it or lose it" point).

So overall, low but not high doses of turpentine seems to stimulate the intestinal mucosa, and sort of imitate a well-functioning microbiome--brush border interaction in the absence of a proper microbiome?
Or maybe it reinstates the proper microbiome by putting right the brush border functionings? It's difficult so say with these reciprocities.

@war4512 Good replies!

@zaaku said in How did you treat your NAFLD and how long did it take?:

[Consider three to four times as much daily choline.]
Is this recommendation from personal experimentation or from a study?

Own experimentations after having read the available studies. The RDIs and AIs for choline are lamentable.

@CrumblingCookie said in B12:

Without choline, supplementation of B vitamins eventually leads to liver damage (Biskind).

https://pubmed.ncbi.nlm.nih.gov/16273261/
Benjamin Y Lee, Krishna Yanamandra, Joseph A Bocchini Jr
Department of Pediatrics, Louisiana State University Health Sciences Center

Abstract

Based solely on clinical clues from a malnourished population, thiamin alone was intentionally and successfully injected to human cases with some tumors or masses. Two cases of submandibular gland cyst and 13 out of 15 cases of Baker's cyst were cured without recurrence for several decades. In a case with pathology-confirmed osteosarcoma, subcutaneous perfusion of thiamin HCl 300 once only reduced its circumference from 30 to 20 cm, equivalent to a reduction of 50-75% in volume, within 2 days.
Current concepts on the role of thiamin in carcinogenesis are controversial. Some authors claimed that thiamin supported high rate of tumor cell survival, proliferation and chemotherapy resistance and suggested anti-thiamin therapy for cancer. On the other hand, some investigators have reported evidence of prevention of several varieties of cancers by dietary thiamin. A limited number of animal studies revealed evident relationship between thiamin deficiency and cancer development. Therefore, further study on the mechanism switching thiamin between cancer supporter and suppressor is needed.

@zaaku said in How did you treat your NAFLD and how long did it take?:

I was consuming 500mg choline via eggs and milk, but added an extra egg 2 days ago to reach 700mg choline per day.

Consider three to four times as much daily choline.

Consider TUDCA and monoterpenes and CoQ10.
Consider a cholagogic of your choice like sylibine, chlorogenic acid (coffee), coffeine, emodine, artichoke leaf extract, gold coin grass, liquorice.

@zaaku said in How did you treat your NAFLD and how long did it take?:

increased my T3 dose to 20-25mcg almost 3 weeks ago which has led to a decrease in appetite.

Consider the possibly detrimental and exacerbarting impact of additional T3 on an already burdened liver.

@LucH @Jakeandpace
That graph, whilst displaying B12+Folate+P5P as the most crucial, does not show B4.
B4 is choline. It's really unfortunate that B4 has been dropped from the "canonical" B vitamins.
In my view all good vitamin b complexes should build up on no less than 150-200mg of choline per dose.
Without choline, supplementation of B vitamins eventually leads to liver damage (Biskind).
It's also super important for the nerves and brain and all organelles as phospatidylcholine in the membranes. Which is a vital building block when stimulating cellular replication with B12 etc.
Choline can be converted to TMG=betaine for methylation purposes. But that's a one-way-pathway, i.e. supplying betaine (or methyl-B12) only spares some choline going into that route. Which is of limited use and perhaps even conflictive if increased methylation results in a metabolic boost (cave: or unfavorable epigenetic silencing) with which overall choline intakes are too low to keep up.

@Serotoninskeptic said:

He also gets jitters and anxiety from coffee which leads me to believe its a nutrient deficiency or thyroid issue. Any advice is appreciated.

He also reported getting cold extremities after drinking the coffee. This leads me to believe cortisol and/or adrenaline are chronically elevated.

Glucose loading cures everything?

@Jakeandpace

Don't neglect the P5P and perhaps give choline a try. Either citicoline or the common bitartrate three times a day?

@Peatful said:

It’s “suffocation” in many places where it is legal

Supposed to go fast
Supposed to…
And yet many have needlessly suffered
While family watched
Some wanting to reverse their decision

I feared it to be something along the line of ineffective executions of death penalty.

@Insomniac said:

This narrative is very useful for framing support for widespread euthanasia as loving and compassionate.

I agree with you there. It remains ambiguous.

@Peatful said:

Read the data on how it is done
What it looks like
The cost

Brutal and or cruel…

I haven't looked into that tbh. Is it just "cold" or brutal in many more ways?
If it were me I certainly wouldn't want to have it in a specified medical setting. I had seen lots of possible ways in the early days of internet and would want to choose my own way and moment.

@Peatful said:

I will leave it to you as to why one should care

It's sinister and my thoughts about it are ambiguous.

@Peatful said:

Rebranded eugenics

In the bigger picture I am very certain that we are not amidst any eugenics programme.
It's kakogenics. Or metriogenics to the lower end of such. You all know the playbooks.

In this sense and the commercial setup of the world MAID is like the ultimate discarding after having caused great demise upon a human being and leeched off all its commercial securities.

That said, to those who find themselves at the irreversible end of such willful malice,
or to those who find themselves at the end of otherwise greatly unfortunate fates...

I find this a classic example of misinterpretation of scientific studies.
And there are way too many to discuss each one of those in their wrong conclusions.

D3 metabolism in rodents is known to be crucially different from D3 metabolism in humans.
It's beyond poor science to even directly convert these rodent findings to human equivalent doses.

This just feels like science-spam.
The findings themselves and the priorly known implications of hypothyroidism may be valid.
The conclusions (and motives for funding such studies) with regard to "vitamin D prevents it" are not.

@Sam-Crow said in Methionine restriction shrinks tumors by ~90%.:

They used the exact same 'complete' tumor for comparison in pictures 2 & 3 but another one in picture 1. Why is that?

No, watch closely: They've used the very same complete tumor in all three pictures. But in the first picture it is turned by +90° clockwise and it looks fresher. So they probably did the methionine restriction first along with the control, then froze the control while they did the other two tests and took the complete control tumor back out for the later comparison photoshots.

@Mauritio said:

we need small and hydrophilic molecules for an anti-fungal effect

Im looking for anti-fungal candidates that fit the above category:

Encapsulated calciumhypochlorite granules ("Chloryte") may fit this bill for the upper GI and various deep tissues. It's rather rough and destructive and not a thing to do for more than two weeks at the very most, IMO.

@Mauritio said:

I took Haarlem oil daily for a while.
I believe it contains turpentine and sulfur. I got less and less of an effect as time went on so I stopped. But I recently reintroduced it and found that cycling it, seems to maintain its effects.

Turpentine (or more generally monoterpenes) reduce hepatic cholesterol synthesis, thereby reducing the cholesterol-saturation of bile which is then able to gradually dissolve cholesterol "plaque" or even proper stones along the bile ducts and in the gall bladder. That improves the biliary milieu along with better biliary flow. It's a very long-term process, however. It takes several months of taking monoterpenes ("Rawachol" capsules or tincture is an OTC product) 2-3 times daily. Tudca or Udca works well together with monoterpenes.

@Mauritio said:

I'm not sure how the treatment should look.
Increasing transit speed and frequently emptying the gallbladder by eating fiber, using specific supplements like FXR-agonists

Tudca and Udca also reduce the same enzyme of hepatic cholesterol synthesis, while additionally altering the bile acids composition towards being much more hydrophilic and less sticky, and also increasing the bile salt export pump for an in overall much greater bile flow (less stasis).
I'd rather use those daily instead of doing any more gall bladder flushes ever again (which only work in a very mechanical and macroscopic way).

@yerrag
Sorry to read that you crashed into excessive MB MAO-inhibition and agitation, anxiety.
3x32mg = 96mg of MB in one day after already 48mg the day before and some the day before is really much.
It'd be easiest if some of the caused anxiety and insomnia were caused by low-BG and some dextrose could help.
I know fresh ginger, ginger juice or oily ginger extract are anti-serotonine at high doses. They'll block CYP3A4, though, so not a sustainable thing to do.

Not sure whether your CO hypothesis holds up after a trial with this much MB. Do you think your current extrapolations are becoming too far stretched? Perhaps very limited in their practical extent, even if theoretically true?

@yerrag said:

After breakfast I'll decide on the dosage I likely would do a 3 x 20mg for the day.

The wanted benefits should be felt very quickly, IIRC within 1 hour. If 20mg in the morning works well, maybe 15mg 8hrs later is also already enough. If the 20mg didn't bring any benefits but no bad feelings either, I myself would take try another 20mg already one hour after the first dose.
If up to 1mg/kg bodyweight within a couple of hours brings no relief I'd dimiss it and look elsewhere and keep MB in the cupboard for an acute urgent situation of ischemia.
I think MB is a very powerful and important instrument acutely.
I don't think it generally changes chronic conditions once it's out of the system again (after a few days). I won't take it again without carbs or glucose / on an empty stomach because of the glucose drop.

I also just remembered that Methylene Blue as a phenothiazine complexes with B2 and leads to higher excretion so it's important to not become deplete in B2 while "binging" MB. Vitamin B2 also acts as an important redox agent.

@yerrag said:

I don't have a hydrogen machine, though I admit I also am skeptical of hydrogen machines.

That's okay. Maybe careful inhalation of H202 solution (stabilizer-free) could also help the impaired alveoli? Either with a spray bottle or nebulizer or a vaporizer, humidifier for the whole room over night at about max. 1%.

@yerrag said:

As how would more oxygen work when the lung is watery and can't take in oxygen in normal amounts.

Have you looked into uses of molecular hydrogen gas?
Especially within recent years it has shown to be very effective in pulmonary conditions. By reducing the inflammation at the alveoli level the actual gas exchange is re-enabled. I.e., giving O2 in increasing gradients in pulmonary conditions often only increases the stress and doesn't get through to the bloodstream whilst there's more and more water filling the lungs.
The molecular hydrogen however (added to normal air, or as H2+O2, or as Brown's gas from a wet cell catalyst comprising H2+O2+plasma H2) soothes and allows for O2 to get in and CO and whatnot to get out.
I can confirm it increases SpO2 and capillary perfusion within moments. It's also a sort of a nutrient feeding right into these ATP nanomotors (ATP synthase?). And it's somewhat immunoinhibitive to an uncertain practical extent, decreasing NETs and citrullination and by antagonising TLR4 also the beta defensins/innate immunity and of course the ROS by neutralizing the hydroxyl radical (HO) in particular.
Overall the best effects of molecular hydrogen arise not from continuous but from intermittent use.

Lymphatic massage manuals or one of those "Chi machines" may be another idea to support lymphatic drainage, along with foot or full body baths with perhaps sodium hydrogen carbonate or hydrogen peroxide (to bring in more oxygen to bind with the CO (which also creates HO radicals so in a way it's an opposite approach to H2)) or magnesium chloride (the chloride for increasing renal excretions).

@hwisdom

Cynomel is produced by Sanofi-Aventis.
Thybon is produced by Sanofi-Aventis.
Do you think they produce different qualities in neighbouring countries?

@Ecstatic_Hamster said:

that is a huge dose of folate.

Mind-bogglingly huge!
From what I could read, neuropsychiatric improvements from restoring cerebral folate sufficiency is a veeeeeery slow and a gradual process.
In other cases where 15mg folic acid daily was used, improvements only became evident 9 months later. With further, significant improvements 18 months later. And things still improving 39 months later.
And many of those reported cases really weren't attributable to genetics but were all secondary due to long-standing "innocuous" conditions like poor diet, alcoholism, hepatic diseases.
Crazy.

For me, that's really essential to know that a finding of low serum folate does not become resolved after a few weeks of supplementation and a good follow-up serum folate lab. I've had some low serum levels stretched over several years in the past. Which I wrongly considered over and sufficiently dealt with.

The 3x 1mg folate makes me feel more sleepy - similiar to when I started (or raised) the glucose servings except now it's only in the mornings up to the early afternoons and not all day. Apart from that I notice no drawbacks.
Whereas without P5P and glucose I remember very well that any large amount of folate made me feel weirded-out and uncomfortably light-headed.

Overall, this fosters my suspected trajectory: That taking dextrose by itself is not enough to fix everything but that it is a crucial element to regeneration and also demands reevaluation of previously tried measures and supplements to finally unfurl their eluded benefits.

Since antibiotics wipe out the folate-producing intestinal bacteria, this post over in https://bioenergetic.forum/topic/2319/glucose-loading-cures-everything/669 also seems relevant to my issues here.
Seeing the reference for serum folate testing has been Lactobacillus casei, it seemed obvious that it cannot synthesize its own folate and I looked it up:

Folate Production by Probiotic Bacteria
"The sequenced strains of L. johnsonii, L. acidophilus, L. salivarius, L. brevis, L. casei, L. gasseri, L. rhamnosus, and L. crispatus lack the genes of DHPPP de novo biosynthetic pathway and also the gene encoding dihydropteroate synthase (EC 2.5.1.15), whereas they possess the genes for DHP transformation into DHF, THF, and THF-polyglutamate. Therefore, it is expected that these strains are auxotrophic for folates or DHP, and remain incapable of folate production even in the presence of pABA supplementation."

"The analysis of genome sequences for predictable metabolic pathways using KEGG database [46] suggests that the ability to synthesize pABA de novo is absent among all the sequenced members of the genus Lactobacillus (Table 1). In fact, the enzymes which are necessary for chorismate conversion into pABA are lacking. [...] Thus, it is expected that lactobacilli are generally unable to produce folate in the absence of pABA."

This means the very sought after L. acidophilus, L. salivarius, L. brevis, L. casei, L. rhamnosus cannot synthesize their own folate to feed themselves nor the human body, but are dependent on other (eradicated) bacteria to provide the initial precursors DHPPP and pABA.

Sort of a bummer then, to supplement such Lactobacilli, thought to be immensely valuable for health, after being nuked by antibiotics,
because without sufficient folate or folate precursors such lactobacilli 1) cannot thrive 2) use up what they can.
Sufficient oral folate supply therefore appears paramount for intestinal resettlement of lactobacilli, especially the most beneficial predominantly L-lactic acid producers instead of the unwanted predominantly D-lactic acid producers

This still leaves open the question of how any of the healthy folate-precursor-producing bacteria can come back in and join the scene.

Perhaps the reciprocal functions between the microbiome and the gut lining sets in here: Resettlement with lactobacilli will help restore the impaired mucosa and villi, which will then work better and stop leaking and allow for conditions favorable for strains of bacteria which produce the necessary precursors for the lactobacilli, reestablishing the circle?

@yerrag said:

I could find a lot of microscope eyepieces on sale online from online sites such as Temu, Aliexpress, Lazada, and Shopee, and I may just form a working microscope. And for the darkfield filter, I hope I can also buy it online and if not, it doesn't seem difficult to make one from online instructions.

That's great! I see lots of possible scenarios, like visualizing the effects on blood by having WiFi switched on vs switched off, after a meal which felt dodgy in comparison to after a meal which felt good, etc.

Update:

As I'm continueing with P5P 25mg with every glucose serving, I've come to notice a surge in folate requirements and have since added 3x 1mg methyl-folate every day.
(I've also come to notice a significant surge in daily protein cravings. Which seems fair given P5P's crucial role in protein tolerability and utilization).

I've found this 1976 bit of info.
These are some serious, real clinical findings from back then. Regarding the required doses there was certainly an issue from using folic acid (clogging up the pathways) instead of using folinic acid or folate.
Nevertheless, there may be a need to cast far aside the Peatarian cancer-focused condemnation of methyl groups and methylfolate when it comes to necessary restoration. There's probably implications of very high gradients being needed to pass the necessary amounts through an impaired intestinal barrier. Which seems to improve in a significant share of patients. Perhaps the others who missed out on improvements needed the glucose, B1 or P5P along with it?
The blood--brain-barrier appears to be narrowly focused on the cerebral folate receptor-a (FR-a) which can be inhibited from birth (genetically) or by autoimmune events. Depleted liver folate stores in chronic disease states, especially those of the liver, would be more widespread.

There's an under-appreciated link between folate and

1. carbohydrate tolerability,
2. unrecognized/atypical malabsorption by jejunal villous atrophy shown as a long-standing gastrointestinal disease usually only diagnosed as "functional", "psychosomatic", "spasmodic colitis", "irritable colon" or similar.
3. depression or an especially wide range of concurrently afflicting neuropsychiatric symptoms.

Folate deficiency and neurological disease
"The classical triad of steatorrhea, abnormal jejunal biopsy and abnormal d-xylose
absorption test (30) is replaced in our cases by another triad,
i.e. constipation, abnormal jejunal biopsy andabnormal d-xylose absorption (15, 23).
However, every patient met at least one of the criteria of disturbed
absorption. In 14 cases there-was a flat glucose and lactose
tolerance curve. In 6 patients on being treated for 6 months
with folic acid, the curves became normal. In three other
patients folate deficiency was accompanied by a glucose
tolerance curve suggestive of hyperactive hypoglycemia;
after 7 and 12 months of folic acid treatment the biological
syndrome of hyperactive hypoglycemia disappeared in two
of them, subsided in the remaining one. This possible cor-
relation between carbohydrate and folate metabolism seems
to be of special interest as a stimulus to further research,
In this respect a 42 year old woman with intolerance of
dietary carbohydrate and mild anemia has been reported as
having elevated urinary formiminoglutamate (FIGLU) ex-
cretion: she improved with combined folate therapy and a
reduction in dietary carbohydrate (31)"

"It is essential to stress that in all cases from this group
small amounts of folic acid (5 to 10 mg daily) were not
effective; only 30-40 mg of folic acid by mouth daily
(patients without jejunal atrophy) or 20-30 mg by mouth
and 15 mg parenterally daily in (15 patients with a subtotal
or partial jejunal atrophy) were effective. The first beneficial
therapeutical responses could be observed only after
treatment for three or four weeks in hospital, with regular
monitoring of plasma BIZ, hematologic parameters and
clinical reevaluation."