Posts made by CrumblingCookie

@marmalade_cat said:

I'm wondering how one determines that thiamine is being excreted in urine?

I guess because thiamin has a very distinctive taste and smell?

The intramuscular route can be also dirt-cheap with 5-10 weeks of thiamin vials, syringes, needles, alcohol wipes going for $30, tops. What's really pricey is the oral benfothiamin form (or the Allithiamin/TTFD - glutathion needed to tackle the mercaptan group of this form).
But those forms are not neccessary as the same effects can be achieved by using four to five times as much ordinary Thiamin-HCl and every 5h in order to maintain maximum levels. There had been a global backlog for thiamin powder in recent years with really difficult availability. Don't know how that is going currently. I expect bulkpowders would carry thiamin-HCl in their store.
It's well worth looking into, imo.

@Insomniac said:

"During the nearly 160 years covered by the analysis, the average oral temperature gradually fell by more than one degree. As a result, the new normal seems closer to 97.5˚ F."

Thank you for sharing this impressive marker of doom and gloom.
Overall metabolic decline across the board.
Is it just PUFA? Is it an altered setpoint of carbohydrate/caloric malnutrition? Is it electromagnetic interference of physiological cellular functioning? Is it a (low-key) chronic disease state?

It boggles my mind how much heat is still being irradiated by healthy infants and children. They are like little power plants in comparison to adult life.

Reminds me of another publication on breathing frequency I had seen recently. Nowadays the PR reference range starts at >12/minute and lower PRs are simply being ignored and deemed impossible. Whereas back 100 years ago or so the average was somewhere between 6-10/minute (vaguely remembered).
I reckon PR and temperature are probably not directly related with each other, though, i.e., low PR can present with low temps, too.

@pabloag10
You may want to look into taking serious amounts of dextrose throughout the day to fuel the non-adrenergic energy supply.
With such a low body weight, maybe sufficient glucose could even put any supplemental thyroid hormone needs aside.
Low serum sodium and serume chloride is a bit odd. Raises questions about kidney functions or abuse of laxatives.
You may also want to totally abstain from the vit D mania.

Thanks for your reports coming in, everyone.

@Ecstatic_Hamster said in Glucose loading cures everything?:

I think Dr. Stephens’ brain theory is sorta wrong, but they do call dementia type 3 diabetes. I think this dextrose works because without the fructose, it can efficiently stop excessive lipolysis and kickstart oxphos.

I also reckon that ultimately a lot is going to be mediated through liver energy metabolism. Which, not least through biliary functioning, duodenal microbiome and barrier integrity and non-translocation of pathogens, toxins and LPS, is directly related to brain inflammation and functioning.

This brief little comment also stuck with me and I am now looking into extra CoQ10 and (tauro)ursodeoxycholicacid:

@LetTheRedeemed said in "Glucose Loading" protocol, a la Dr Stephens - A Critique:

Honestly, if one's liver function is so compromised they need to avoid fructose, [...]

@gentlepotato said in Glucose loading cures everything?:

it's very strong, and the smell reminds me of perfumed soap. There's a similar aftertaste

I had experienced and reported something similar already. You can try to keep the bag wide open for a few days (and put it into other containers) and see if some of those solvents dissipate. Some of them will. But as you can even taste them it's likely some (or all) will remain.
+1 on S.Holme's suggestion of not buying dextrose in cardboard boxes or paper bags anymore. (As also for many other foods' packagings, indeed)

Thank you everyone for the initiated discourse so far.

@Sugarnotsnow said:

So would the pasteurization of juice create oxythiamine?

The same question occured to me as well!
I don't know the answer. So far all I know on this is what is written in the papers above.

@mostlylurking said:

I wondered why Dr Costantini warned against taking oral thiamine hcl doses with "sour" liquids; now I know. Water only, never juices. Costantini also advised taking thiamine at least 30 minutes away from eating food. Perhaps this is because eating food would trigger the release of stomach acid? Makes sense to me.

The thiamin only converts to oxythiamine in sour and hot conditions. In their experiments above, sour conditions at 37°C didn't create oxythiamine.
Wrt to these recommendations I assume Costantini is wary of the substantial acidity of large amounts of thiamin-hydrochloride itself. Larges doses of thiamin-HCl with sour juices or on an empty stomach would be harsher, especially to sensitive people. It's also not a nice taste to burp up the sour taste of thiamin.

@yerrag
If I read your thoughts correctly, your worries about thiamin turning to oxythiamine in acidic body conditions are the same as mostlylurking's. So far that seems unlikely to happen at body temperature - at least by the chemical processes identified. And importantly, it was observed that more thiamin did overcome the impairments.
But a sole dietary origin of oxythiamin is still a hypothesis.
Maybe there's more to it. As mostlylurking is hinting at. It's all still speculative with not much data.

If indeed certain microbes (in the human guts) were able to produce oxythiamine, there could be contradicting good and bad systemic effects at the same time. The research above only measured the rise of thiamin-dependent enzyme acitivities in blood or serum: It's possible that (in bacteriologically predisposed people) the guts would get thrashed and confound expectations of a systemic net benefit.

Experience update:
13 weeks into dextrose now (3 months). At c. 70grs (8-9 tbsps) 5 times/day.

@CrumblingCookie said:

I am thinking that a lot of the supplements and supposed remedies I had been taking over the years were all in wain. Especially, I am thinking many (the potentially most beneficial of them) exacerbated the glucose deficiency dilemma. Consequently, I am thinking that now that I am providing sufficient glucose, I may need to rewind and redo/retry all the "good" supplements because only now they become both able to be used and necessary as cofactors for every cellular and organ function.
I a way, this would mean back to square one and a reevaluation of all supplements and remedies I know since long ago and which I had previously used and discarded.

Along the thoughts above and my observations that I've been feeling the needs for a certain minimum of mainly extra b1 and b6 (and even extra methylfolate after not having eaten veggies for a couple of days),
I was wondering whether I could benefit from some ω-3 fatty acids to supply a maybe increased nervous system regeneration by the glucose fuelling, as perhaps my body can't keep up with the needed FA conversions or is too inhibited in doing so by stored ω-6 AA and LA.
So, mere speculation, followed by trial.
And error.

I was taking a mere 3grs or even only 2grs of a high quality non-rancid cod oil ω-3 and became super cold, freezing, dumbed down in all senses and thinking for over half a day afterwards. Repeatedly.
This is a super sensitive reaction to PUFAs. It made me pay more attention to the effects of any sunflower oil (ω-6 LA!) ingredients in foods like frozen potato fries or little waffles.
Those showed the same effects but in a more sneaky, much less obvious and more delayed way.
I can't say whether the glucose protocol has heightened my PUFA sensitivity itself or my awareness to its effects. Just want to share this info.

Since I've been reacting well to drinking H202, especially at night before going to bed for less miserable and deeper sleep, I've been thinking:
I am providing all the fuel (glucose) and the means to get it into the cells (potassium, chloride) and process it (b vitamins + very little vit c).
Yet, still, the cellular energy metabolism capacity is remaining very low.
I am still hoping that somehow, over time, this will sort itself out.
As many others in their respective conditions, however, I am having doubts about the glucose fuelling being sufficient all by its own.
H202 improves things for a while for me. Maybe that's in part through overcoming the incapacitated peroxisomes in thyroid follicles.
So, two weeks ago, I've started taking T4+T3 every morning.

(Btw, while reading some of the previous posts about the always resurging doubts of progress I remembered DS said, very early on in one of his presentations, that it is very easy and almost typical for many of his patients to not see and recognize their various improvements since their changes are so subtle and marginally slow that they only became obvious to the observer and the patients themselves when he kept asking them about the occurence and severity of their prior symptoms or compared their original testing with later ones).

*crosslink to PUFA experiences thread ->https://bioenergetic.forum/topic/2714/share-your-pufa-story**

@bigpeeter

The above listing does not tell anything about the concentration / content of the vitamins.

Commonly, vitamin B1 hydrochloride is being offered at 50mg/mL and rarely at 100mg/mL solutions.
For your 0.5mL I would therefore assume that it was 25-50mg of thiamin-HCl.
To compare it's fair to multiply the injected amount by 70-140 for an equivalent oral weekly dose. That's Antonio Costantini's guideline and checks out (100mg injection 1x/2x weekly -> ~ 2g oral thiamin daily). These 25-50mg therefore correspond to about 500mg of B1 per day.

No clues are given to how much 5-MTHF is in that 0.5mL.
1mL of methy-B12 has usually 500-1000mcg.

To start this off here's some fringe knowledge for the curious and especially for a chronic kidney disease (CKD) relation:

Don't cook your thiamin supplements (who would do that?) or thiamin-rich foods in acidic conditions or it will turn into oxythiamine. Especially not when having impairments in renal clearance.

Didn't we learn that keeping acidic cooking conditions would be great because that drastically avoids the synthesis of huge amounts of Advanced Glycation End products from sugars with fats and proteins? Bummer.

On the bright side, simply providing more supplementary thiamin counteracts the effects of oxythiamine from cooked foods.

On the sad side, foods naturally high in thiamin could actually have negative effects on crucial thiamin-dependent bodily enzymes if they've been cooked in acidic conditions.

And processed/cooked foods which are already borderline low in thiamin could not simply be "thiamin-neutral" but extra negative in their effects on thiamin-dependent enzyme functioning.
It's yet another reason to avoid processed foods but to do home cooking from original ingredients.

Although the rate and the necessary conditions for such conversion is not yet known in practical detail, the results of impeded enzyme functions and high levels of circulating oxythiamine however was shown. What they experimentally studied (no in-between values): 0.06% of thiamin converted to oxythiamin in acidic conditions over 1 hour. A 500-fold dose of thiamin freed the transkelotase from inhibitory oxythiamin. "Standard Dietary Recommendations" for thiamin seem grossly insufficient in CKD in light of theses findings and about 30mg thiamin daily are fine.

For the future, it would be good to know what the oxythiamine/thiamin ratios of such causative foods really are, i.e. how little dietary oxythiamin counteracts what amount of dietary thiamin!
And what usual renal clearance and serum levels can be expected for oxythiamine in people with healthy kidneys - is it an accumulation specific to chronic kidney diseases (who, along with diabetics, additionally show impaired thiamin transporters) or could it also occur in various other populations (e.g. in those who get served a lot of canned fruit: caring homes, hospitals)?

Also, poultry could be a general source for an anti-thiamin by itself if they've been fed with amprolium in their standard chick feed mixes against intestinal protozoa. But if that amprolium accumulates in chicken meat to an extent that is harmful to humans, imagine the corresponding metabolic quality of life (and quality of meat!) of those chickens. Analytics by the food industry would be great to find out about that.

@mostlylurking said in Ideas for getting more CO2 into your everyday routine:

@CrumblingCookie
You might find the article at this link of interest: https://portlandpress.com/bioscirep/article/38/1/BSR20171148/57181/Thiamine-and-selected-thiamine-antivitamins

My question is this: are these thiamine anti-vitamins created naturally in the body? Or are these strictly lab creations made for experimentation or for pharmaceutical purposes and do not occur in nature so can be patented?

@mostlylurking
They write about purely synthetic thiamin derivates which are being used in lab testing (to create functional thiamin deficiency) and for some medical uses.
However, there's one derivative which stands out:

"recent research of Zhang et al. [132] indicates that we can be exposed to trace amounts of thiamine antimetabolites like oxythiamine as a result of thiamine transformation through cooking under acidic con ditions at 100◦C. That kind of contamination may cause undesirable effects on our metabolism (e.g. transketolase inhibition in dialyzed patients with end-stage renal disease). Poultry fed with amprolium as a means of preventing coccidiosis as well as post-production impurities from poultry farms may be also potential sources of thiamine an timetabolites contamination. From this point of view, there is a need for intensive development of new methods for the measurements of thiamine antimetabolites in food, feedstocks, and environment in order to constant monitoring of the level of contamination and prediction of the possible effects of thiamine antimetabolits pollution for people health"

Zang et al. [132] is to be found here:
https://www.kidney-international.org/article/S0085-2538(16)30057-6/fulltext

"Decreased transketolase activity is an unexplained characteristic of patients with end-stage renal disease and is linked to impaired metabolic and immune function. Here we describe the discovery of a link to impaired functional activity of thiamine pyrophosphate cofactor through the presence, accumulation, and pyrophosphorylation of the thiamine antimetabolite oxythiamine in renal failure. Plasma oxythiamine was significantly increased by 4-fold in patients receiving continuous ambulatory peritoneal dialysis and 15-fold in patients receiving hemodialysis immediately before the dialysis session"

"Oxythiamine is likely of dietary origin through cooking of acidic thiamine-containing foods. Experimentally, trace levels of oxythiamine were not formed from thiamine degradation under physiologic conditions but rather under acidic conditions at 100°C. Thus, monitoring of the plasma oxythiamine concentration in renal failure and implementation of high-dose thiamine supplements to counter it may help improve the clinical outcome of patients with renal failure."

"A possible source of oxythiamine found clinically is formation by high-temperature processing of thiamine-containing foods under acidic conditions, similar to but not as severe as conditions of oxythiamine synthesis.15,17 To model this, we incubated 1 μM thiamine in water, pH 7.0, at 37°C and 100°C, and in 100 mM acetic acid, pH 2.9, at 37°C and 100°C for 1 hour. Oxythiamine was detected only in thiamine solution heated at 100°C and pH 2.9. The concentration of oxythiamine formed was 0.56 ± 0.06 nM or 0.06% of thiamine. Similar conversion of dietary thiamine in cooking or commercial food processing with limited clearance over 2 to 3 days could explain the accumulation of oxythiamine to low nanomolar levels in ESRD patients."

"Examples of thiamine-containing foodstuffs with natural low pH are fruits and fruit juices; canned fruits are heated during commercial processing. Foods may also be made acidic by vinegar, lemon juice, and other acidic culinary additives.19 The use of vinegar in cooking has been proposed as beneficial in the diet of ESRD patients to decrease the potassium and magnesium content of vegetables22 and to decrease the formation of advanced glycation end products in foods.23 This requires reappraisal in light of the current studies."

"Given the requirement for acidic, high-temperature processing for oxythiamine formation, high-dose thiamine administered as a pharmaceutical at ambient temperature does not lead to oxythiamine formation. Supporting evidence for this is experimental and from clinical studies of renal failure with high-dose thiamine or related derivatives where transketolase activity was increased."

"The recommendation for patients with stages 3 to 5 CKD to take a supplement of the daily reference intake of 1.1 to 1.3 mg thiamine may be insufficient given the increased concentration of OTPP in renal failure. The remedy to the antimetabolite effects of oxythiamine accumulation is pharmaceutical doses of thiamine to produce increased TPP for OTPP displacement from transketolase. Thiamine (30–45 mg/day equivalent) in HD patients was studied and found to alleviate transketolase deficiency."

@mostlylurking said:

You stated: "What's known about the metabolites of thiamin in the human body and their pathways is quite murky."
"the metabolites of thiamin in the human body and their pathways" search results are extensive. Although complex, they seem pretty well defined to me.

I was hoping to discover something new which I might have missed before but unfortunately all I could spot in these links above is this properly poor

"Elimination: Thiamine is a water-soluble vitamin; excess thiamine is exerted in the urine."

but no info or consideration on anything about the metabolic breakdown of thiamin. Am I being selectively blind or were you under the assumption that excess thiamin is simply being renally exreted, 1:1, completely unaltered?

I shall kindly provide what I could unravel on thiamin and aminooxidases. I've had to dig really deep for it. All the more I could appreciate later and further findings on these:

NAKAMURA, T. (1960). INHIBITION OF D-AMINO ACID OXIDASE BY THIAMINE AND THIAMINE DIPHOSPHATE. THE JOURNAL OF VITAMINOLOGY, 6(2), 103–108. doi:10.5925/jnsv1954.6.103

Meltzer, H. Y. (1961). The effect of thiamine on monoamine oxidase. Biochemical Pharmacology, 7(3-4), 277–278. doi:10.1016/0006-2952(61)90095-8

"in thiamine-deficient rats, the MAO-activity of the brain and intestine is increased"

"These workers suggested that the increase might be related to the stress theory of Selye"

"in vivo, thiamine, which has a quaternary nitrogen in its thiazole moiety, is either itself an inhibitor of MAO, or more likely, is metabolized via a pathway which produces another quaternary nitrogen compound which is an inhibitor of MAO"

"The MAO-inhibition caused by this thiamine-like compound also might explain the hypotension and ganglionic blockade which thiamine produces in man and experimental animals; hypotension in man has been noted with the administration of inhibitors of MAO."

This or these very potent MAO-inhibiting thiamin metabolites are not fully created two hours after injection, but gradually build up over a day or two or so:

"rats given 70 mg of thiamine per kg subcutaneously, and sacrificed after 2 hr, when thiamine pyrosphosphate levels in liver are elevated, showed no inhibition of the MAO activity of liver, brain, and intestine, as compared with untreated controls. However, this does not constitute a refutation of the proposed theory, if the rate of formation of the postulated thiamine metabolite proceeds maximally with the amount of thiamine provided by a normal diet."

"Although in higher animals most of the thiamine which is absorbed is excreted unchanged, the fate of the thiamine which is degraded is largely unknown."

"This action of thiamine is unrelated to its properties as a coenzyme.[4]"

@josh That's a good thing to read about you putting on (previously lacking) weight!
Yes, with thyroid hormones it's very important, too. Quite some people crash when starting thyroid and fall prey to abominable self-enriching creatures and their harmful, incomplete and misguided fables of adrenal fatigue allegedly brought about or amplified by thyroid hormone functions which makes them tenaciously believe in that they now require extra cortisone to metabolically cope.

@mostlylurking said:

Yes, other b's can get depleted. Anytime you improve oxidative metabolism, whether it's from supplementing thyroid hormones or from thiamine, the act of increasing/improving metabolism is naturally going to use up other nutrients faster. B2 is one to consider taking more of. A good b-complex in addition to high dose thiamine would be helpful.

@mostlylurking said:

I suspect this is because thiamine improves the conversion of blood glucose into cellular energy which would lower blood sugar which can wake you up.

Humans have no thiaminase to break down thiamin. What's known about the metabolites of thiamin in the human body and their pathways is quite murky.
They are very strong inhibitors of MAO and other aminoxidases, especially in the ganglia. This (also) happens through displacement of enzymatic flavoproteins (made from vitamin B2, which is crucial but of which very little (not even double-digit mg/day) is needed).
Much stronger than rasagiline, selegiline.
The MAO-inhibiting metabolites of thiamin are also very long lasting in the human body, as their effects wear on for two to three weeks, easily. Although once a week as per Constatini really maintains the maximum plateau.
This MAO-inhibition, beside the positive metabolic effects of active thiamin itself, is the main reason for Constatini's high-dose-thiamin protocol working so well.
Since thiamin and its metabolites also effect MAO-A it can cause strong diarrhea.
Now, this is not only because of flavoprotein displacement in various aminooxidases, though, but to a far extent due to the lack of available glucose which in turn raises stress and adrenergic hormone actions and serotonin at tissue levels.
It's important to generously supply glucose through carbohydrates or dextrose with HDT (high dose thiamin).
AFAIK this immediate glucose context about HDT has not been put forth appropriately to its crucial significance anywhere. Not by Constatini, not by Lonsdale at hormonesmatter, not by Georgi nor at the lowtoxinforum.

@ricksaban
Try get your hands on H202 3%, acid-free if possible, and put it on repeatedly with a Q-tip. It should reduce the swelling and make a dry scab.

@S-Holmes:

Yes, Mercola's daily dosing recommendation is absolutely a lot (c. 250-500grs/day).
However, I reckon it ought to be the most detrimental to teeth to drink that an ounce at a time (= 1/2-1 tbsp or c. 4-8 grs), or even 'sipping' it continuosly throughout the day!
Mercola's still worried about any insuline spikes, though, and for these reasons recommends such i.v.-style dosing. I don't think he has met with DS yet. Or maybe he has but treads carefully wrt what he presents since BG/insuline spikes are the first and decisive thought most people get scared of.

I still find 2-hourly dosing much more reliably comfortable than longer periods. Although it's greatly convenient to have had enough dextrose to last 4-5hrs, such long times between servings do not always work or suffice IME.

@GreekDemiGod said in Personal Log - Digestion, energy, vitality:

I also have a deviated septum and one of my nostrils clogged, which is affecting my sleep.
Today I woke up feeling better, had 3 bowel movements by 12PM. Quit starch for a few days.
And I’m breathing better today.

You may want to know that there is the "one-airway-theory" or something called like this. Essentially, it says all your mucosa are connected. Bad digestion causes asthma and bronchitis and vice versa. Intestinal inflammation causes inflammated sinus mucosa and vice versa.
That being known, it's still possible that your demigod facial features were prevented from fully developing and your septum was caught in too little space for its original design because of underdevelopment of the width and length of your maxilla. In which case, confirm whether your swallowing technique is right and proper (no touching of the teeth with your tongue, ever) or invest in (dynamic) orthodontics and logopedics lessons first, before any nasal surgery. And ascertain that your surgeon will definitely stitch back any cartilage as reinforcement on the opposite side of where he/she removed it from instead of discarding it. This will of course transform a 15-20 minutes surgery into a thorough c. 1.5hrs surgery.

Mercola seems to start dipping his toes into glucose, as per his latest article:

"So how can you begin implementing this approach? If you have severely compromised gut health, start with pure sugar water. This is a temporary measure to jumpstart the healing process. Mix one-half pound, up to a full pound, of pure dextrose (glucose) into a half gallon of water and sip it slowly all day. Don't drink more than an ounce at a time to avoid spiking your insulin.

Once your gut health has improved, you can switch your primary carb source to whole foods. More than likely, you'll also need to eat more frequently than you're used to during this transition to avoid hypoglycemia. Eating every three to four hours, with snacks throughout the day, is crucial when relying on simple carbs for energy.

As your mitochondrial energy production continues to improve and your gut starts to heal, you will begin the transition back to complex carbs. This is a slow and steady process — don't rush it."

@haidut
Interesting. I looked for success markers along the stated timeframe of 6 months in the study's full text but the authors did not disclose any details.
Would be great to contact them and ask if anybody here would be so forthcoming?
As in: How was the success measured and did those measures improve gradually or was it switch-like at about 6 months or earlier?

Has anybody looked into this 2021 study from Hungary below?

Post Orgasmic Illness Syndrome (POIS) and Delayed Onset Muscle Soreness (DOMS): Do They Have Anything in Common?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8392034/

They argue for a complex system of energy depletion, mitochondria dysfunction and also a polyamine depletion (by expulsion) for the crucial spermidine levels in neurons in combination with odd stress signalling patterns. There could be a unique case for spermidine supplementation.
And the participation of a long-term manifestation of changes in the endocannabinoid and opioid system.
And much more.
For some odd reason there even seems to be succesful, positive interaction between hCG injections and spermidine and POIS?

By the authors' establishing ties of a common multifactorial pathogenesis between POIS and delayed onset muscle soreness I wonder whether either of these two are 'special' manifestations of a general CFS, mitochondrial, energy, neuronal, autonomic dysfunction.

I just put this here for your appreciation. 5th day lecture GA 177:

"We should not fool ourselves, for we are faced with a quite specific movement. At the Council of Constantinople it was decreed that the spirit did not exist; it was dogmatically stated that the human being consisted only of body and soul, and it was heresy to speak of a human spirit. In the same way attempts will be made to decree the soul, the inner life, as nonexistent.

The time will come — and it may not be far off — when quite different tendencies will come up at a congress like the one held in 1912 and people will say: It is pathological for people to even think in terms of spirit and soul. ‘Sound’ people will speak of nothing but the body. It will be considered a sign of illness for anyone to arrive at the idea of any such thing as a spirit or a soul. People who think like that will be considered to be sick and — you can be quite sure of it — a medicine will be found for this. At Constantinople the spirit was made non-existent. The soul will be made non-existent with the aid of a drug. Taking a ‘sound point of view’, people will invent a vaccine to influence the organism as early as possible, preferably as soon as it is born, so that this human body never even gets the idea that there is a soul and a spirit.

The two philosophies of life will be in complete opposition. One movement will need to reflect how concepts and ideas may be developed to meet the reality of soul and spirit. The others, the heirs of modern materialism, will look for the vaccine to make the body ‘healthy’, that is, makes its constitution such that this body no longer talks of such rubbish as soul and spirit, but takes a ‘sound’ view of the forces which live in engines and in chemistry and let planets and suns arise from nebulae in the cosmos. Materialistic physicians will be asked to drive the souls out of humanity.

People who think that playful ideas will help them to look ahead to the future are very much mistaken. We need serious, thorough, profound ideas to look ahead to the future. The sciences of humanities are not a game, nor just a theory; they are a true duty towards the development of humanity."

Also, any Church-affiliated Christians will always find reasons to deny and begrime Rudolf Steiner's thinkings and serious spirituality (intrinsic duplicities and superficialities aside), for it is not theirs to meddle with the dangers of the spiritual world but to rely on Christ or their instituted churchmen/bishop/exorcist or occultist/confusionist/extortionist to stand and act as a trustworthy gatekeeper between the realms in order to keep them safe and provide guidance.
Which is quite an example of self-imposed mental immaturity. Very anti-enlightenment.
Which can be alright, even a wise necessity for those who are otherwise unprepared.
Even in the best circumstances, however, it can also make you think of the story of Saruman when it comes to the middlemen being relied upon over time.

Also, by papal bull, both the corporal human being as well as the human soul are claimed by the pope, his puppeteers and shadowmen. So any Church-affiliated Christians really must not lay claim to either of these two but be content with their ascribed personae.

Have fun with this info.

@Ben
Are you experienced in being able to discern whether that much glucose fed your infections or whether it acted directly immunostimulatory on your preexisting infection levels?
Either way there'd be more immune activity involved, but the first would be bad whereas the latter - if kept in a sensible and safe range - could be regarded as a necessary evil to go through?

@S-Holmes
That was a suprisingly easy fix for you to simply dilute your glucose in more water! I wonder, are you perhaps generally prone to not drinking sufficiently every day?

For a couple of days I thought I could lower my dextrose servings to 50grs (down from 80-100) as an effect of the H202. That was wrong and much too low, I noticed. 70grs work well, though.
A few times I've now blended my dextrose serving with the diluted H202 in distilled water and must say: That's refreshing! Takes away the slight "taste" of the H202 and it feels like an enhanced way to take glucose. Curiously, so far, it even completely removed every hint of nausea by the H202. They don't seem to react with each other and by what I've read all the H202 IVs are usually being done in glucose solutions.

@GlucoseOrBust
Any news on the effects of your megaservings?

@S-Holmes
Good news! So you just pushed past your previous subjective nausea thresold?

Here's the concept of my dextrose troubleshooting guide with no claim to universal validity:

Situation: 
Can't increase serving size because of nausea or GI upset or terrible taste

Solution:
• Impure production batch/brand of dextrose. Switch to other brand.
• More time needed at the previous serving size and smaller increments because of a (still) very low rate of glucose utilization. 
• Improve cellular glucose uptake: Potassium, chloride, taurine. 
• Just push past and substantially increase the serving size because it's normal to have your upper bowels rearranged in the beginning as they gradually get access to glucose and start to function.

Situation: 
Dextrose not working sufficiently with cravings for more dextrose right after a serving. 

Solution:
• Improve glucose utilization (citric acid cycle): 
* Add thiamin +-10mg and pyridoxin 0.5-1mg, biotin +-50mcg, niacin(amide) +-10mg and riboflavin +-4mg. 
* Add magnesium if your levels are known to be low becaus lack of Mg can be a limiting cofactor for shifting the electrons in the citric acid cycle.  

Situation:
Dextrose not working sufficiently with servings sizes already very high and no cravings for more dextrose.

Solution:
• Do not undereat. Maintain a daily diet of basic foods for a sane amount of macro- (protein, calcium) and micronutrients. 
• Improve tissue and/or cellular oxygenation:
* (Light exercise, light walking in fresh air)
* (Lymphatic massage)
* (Vibration plate)
* Use H202: Orally every day. Intravenously. Baths. 

Any one adaptation can raise the need for one of the other.

@Bling5
Starches need way more digestive power and functioning which one may have lost below a point that is needed. The full reasoning of why starches don't work nearly as well lie, however, still in the mist.
All what is known and said is that at some point (about 6 months in or later, or gradually sooner), eating starches and eating generally enough becomes self-sufficient again.
So nobody's planning to continue drinking glucose until the end of her or his life, yet.
Sugar=Sucrose/Glucose-Fructose is not the same at all.
Honey (Glucose, Fructose, +stuff) is not the same either and the higher the fructose content of the type of honey the worse it is. I had eaten kilograms of honey before doing glucose. As in a lb jar per day, up to half a jar at a time. I had done that because it sort of kept me afloat but at the same time the fructose was super stressful and counteracting.