Uncoupling The Soul - Wolf's Log

[Waynish]

I definitely agree. However, without a true scientific understanding of consciousness and the ability to prove this “hard problem”, it continually leaves room for highly religious, spiritual, or otherwise superstitious individuals to introduce all sorts of speculation on the matter of consciousness.

I like Jacque Fresco’s take on things, in which all things which aren’t functionally useful and overly whimsical are discarded as a waste of time. Poets, gurus, religion, etc… which focuses on unverifiable speculative nonsense is ultimately wasteful and harmful when there are repeatable, verifiable means by which we can understand and influence our reality. Without a scientific understanding of our world, we’d still be engaging in all sorts of degenerate behavior.

Congratulations on the biochemical degree. Have you entered the workforce?

Why are spiritual people speculators and people who identify as "scientific people" non-speculators? And doesn't a "scientific understanding" create a contradiction in terms to some degree considering "understanding" is a product of consciousness while "scientific" is merely refers to a method? So "scientific understanding" would mean ideas that are absent anything but that which is a part or product of the scientific process... I could continue, but those that get it will see what I mean.

 

[Waynish]

Is consciousness not biochemical in nature and subject to material constraints?

It is not. Biochemical in nature by definition means biological chemicals or chemicals - which are material. While consciousness (especially soul), by definition, is non-material. Can you measure biochemical reactions in lab experiments? Yes. Can you measure the soul in lab experiments? No.

 

[Wolf]

I definitely agree. However, without a true scientific understanding of consciousness and the ability to prove this “hard problem”, it continually leaves room for highly religious, spiritual, or otherwise superstitious individuals to introduce all sorts of speculation on the matter of consciousness.

I like Jacque Fresco’s take on things, in which all things which aren’t functionally useful and overly whimsical are discarded as a waste of time. Poets, gurus, religion, etc… which focuses on unverifiable speculative nonsense is ultimately wasteful and harmful when there are repeatable, verifiable means by which we can understand and influence our reality. Without a scientific understanding of our world, we’d still be engaging in all sorts of degenerate behavior.

Congratulations on the biochemical degree. Have you entered the workforce?

I have. Corporate double speak is nonsensical but it is what it is. It seems even if I went into a true biochemical process engineer role I would still be subject to the nonsense and waste of corporations. Best to just have money in my pocket and a smile on my face I suppose.

 

[Wolf]

Health wise it seems the inhibition of serotonin is way more critical than any dopamine boosting. The BCAA protocol with 500mg of tyrosine and some natural(artificial) light for 30 min prior to BCAA leads to a nice motivation/confidence boost that lasts most of the day. Fatigue at the end of the day is more pronounced, but it is of the "I'm sleepy because I worked hard" sort of tired and not the overworked tired. If that makes any sense.. I really need to work on getting in more tonifying foods in.

My aversion to caffeine previously seems to be a marker of poor liver health as that has improved dramatically with introducing small amounts of caffeine and improving my liver's ability to hold sugars. Sitting down for years and staring at books and suffering seems to be the cause.. The famotidine I take as an antacid at 10mg/day and 20mg/night seems to have helped with that... Famotidine Increases Glycogen, Improves Glucose Metabolism

Beyond that, it seems much of the motivation I possess is reactionary in nature. In response to a stressor or challenge I will actively seek to overcome it, but with no stressors or challenges skills atrophy. The only novel motivation boosting protocol seems to be very low dose ondansetron alongside progesterone so the QT interval isn't whacky. 5HT3C is a cruel mistress. Perhaps isolating myself from TV and other distractions and diet changes per Travis' recommendation some time ago would do me some good.

 

[Wolf]

Update: Health continues to improve even more with continued monitoring. It seems the famotidine was causing some constipation which in turn led to some endotoxin overloading. I also got my appendix removed which seems to have massively helped many aspects of my health. Chronic appendicitis can apparently suck. Currently down to 10 mg/night of Famotidine alongside some Zinc Carnosine in the hopes it relieves this GERD(which I believe is due to constipation/slow bowels). Additionally, application of small amounts of preg/andro/prog daily(2/1/2 drops) and some NDT(3 drops currently, adding 1 per week) and some tocopherols(5 drops and staying there consistently). In the realm of normal supplements, on and off 325mg aspiring split into two daily doses and 100-500mg niacinamide depending on how I'm feeling. I'm loading up on fat solubles via liver(A), thorne K2/D3(K/D), and magic tocopherol liquid. I am also independently supplementing some policosanol since it seems to help generalized energy.

As far as my previous TTFD supplementation goes I have backed off as it seems to cause issues after a few weeks that I never got from pure B1. Perhaps some glutathione related issue per Paradoxical Reactions With TTFD: The Glutathione Connection - Hormones Matter

'
For TTFD to “release” its thiamine, its disulfide bond must gain electrons from another donor molecule. In chemical terms, this process is referred to as reduction. Once this reduction occurs, thiamine is freed and can then go on to participate in cellular biochemical reactions.
Of the few molecules which have been shown to reduce TTFD, glutathione performs this function most effectively. As the cell’s primary antioxidant, glutathione is responsible for donating electrons to neutralize reactive oxygen species, and can either be found in its reduced form or its oxidized form. Once a reduced glutathione molecule (GSH) has donated its electron, it bridges with another to molecule to form oxidized glutathione (GSSG). GSSG is then recycled back to two GSH molecules through accepting electrons from NADPH via the enzyme glutathione reductase (vitamin B2 as FAD dependent).
When TTFD enters cells, GSH in red blood cells chemically reduces TTFD via a process called “disulfide exchange” (presumably using a protein called glutaredoxin). Reduced glutathione becomes oxidized glutathione and TTFD “releases” thiamine to producing free thiamine inside the cell with an extra TFD mercaptan group left over.
The initial phase of processing TTFD requires that cells have enough reduced glutathione. Furthermore, the more GSH you have – the faster the rate of this reaction. So in simple terms, to obtain thiamine from TTFD the cells “use up” their reduced glutathione.
I recently had correspondence with one individual who only gained tolerance of TTFD after supplementing with 200mcg of selenium in the form of sodium selenite. Selenium supplementation in different forms has been shown to increase red blood cell GSH levels by up to 35%. This is thought to occur due to selenium’s ability increase glutathione synthesis through upregulating the enzyme gamma-glutamylcysteine synthetase. I suspect that poor glutathione status might be one of the reasons for benefit from selenium.
Having enough glutathione is clearly very important, but recycling it is also essential to maintain a pool of glutathione in its reduced form. Unfortunately TTFD can place a burden on this system, and this was demonstrated in one old study from Japan which showed that TTFD administration rapidly lowered red blood cell GSH. Interestingly enough, that same experiment showed that GSH levels were restored within 5-10 minutes. This restoration was accomplished by the vitamin B2 (as FAD)-dependent enzyme glutathione reductase, which donates electrons to GSSG with the reducing power of NADPH to recycle it back to two GSH.
What this basically means is that cells require a robust antioxidant system to properly process TTFD and return back to their original state. First, cells need enough of the antioxidant GSH to cleave thiamine. Second, cells also need to be able to recycle the oxidized glutathione back to its reduced state.

Immediately, we see two potential issues that could arise from TTFD supplementation which might provide a better understanding of why some people may not tolerate this molecule.
In someone who has poor glutathione (GSH) status, they might theoretically be less able to cleave thiamine from TTFD. There are many reasons why someone may have poor glutathione status:

• Low precursors (cysteine, glutamate, glycine)
• Chronic oxidative burden and/or inflammation
• Deficiencies in the nutrients required to generate, process, or utilize glutathione (B6 or selenium)

Alternatively, an individual may have enough resources to make glutathione, but if they cannot recycle it through the necessary machinery (i.e glutathione reductase), then taking a substance which depletes their GSH (like TTFD) might further contribute towards their oxidative burden.
A total and/or functional riboflavin deficiency is the probably the most common culprit responsible for poor glutathione reductase activity. The glutathione reductase enzyme also requires adequate reducing power from NADPH to drive the enzymatic reaction. NADPH is derived from niacin (vitamin B3) and is generated in the pentose phosphate pathway which, ironically, requires the thiamine-dependent enzyme transketolase.
In the context of poor enzyme activity, without the reducing powder to drive GSSG back to GSH, the oxidized form of glutathione can theoretically drift towards the path of generating a free radical called the glutathione radical. This alone could further contributes to oxidative stress and cell damage.
Below is a hypothetical scenario to demonstrate my point:

1. An individual suffers from long-term thiamine deficiency and has suboptimal riboflavin status
2. Thiamine deficiency leads to lower activity of transketolase
3. Low transketolase activity produces a lack of NADPH
4. A lack of NADPH and a lack of FAD means that glutathione reductase is unable to efficiently recycle glutathione, which produces an imbalance between reduced/oxidized glutathione.
5. Intracellular GSH is further lowered by taking high dose TTFD, and there is not enough enzyme activity to recycle it back
6. Oxidative stress is made worse

In the above scenario, taking a high dose of TTFD may not be appropriate. Rather, restoring NADPH levels through supplementing with ordinary thiamine and supporting the glutathione system via other measures might be advised before starting with TTFD. Optimal riboflavin status is also necessary for the above processes to run smoothly.
Older research in Japan showed that TTFD supplementation could lead to a secondary B2 deficiency through increased urinary excretion. The increased need for glutathione reductase could at least also contribute to this effect. When taking TTFD, it has downstream effects on other nutrients. Hence, these supporting nutrients should also be taken in conjunction when someone is supplementing TTFD in high doses.

It is therefore possible that the glutathione-depleting effect of TTFD could be responsible for some of the side effects associated with supplementation. This is probably most applicable in individuals with poor glutathione recycling and underlying oxidative stress. Therefore, nutrient therapies that may support this initial phase of TTFD metabolism include:

• Selenium (improve GSH levels)
• Riboflavin (improve GSSG-GSH recycling)
• Niacin (increase NADPH)
• Ordinary thiamine (increase NAPH via PPP)
• NAC, glycine and/or glutathione TAKEN HOURS AWAY from TTFD (GSH precursors)

The above is just for my own reference really. Making another independent post seems painful. I recently picked up a different Selenium(SelenoExcell) and it seems night and day better for me than the L-Selenomethionine I've tried in the past. I do plan on taking TTFD again but for right now it appears that my body is releasing some PUFAS into circulation(feeling shitty and not really too full alongside adrenaline symptoms) and/or estrogen(puffiness, emotional, etc.) which is cyclically combatted by myself. I view this as a pretty good outcome and its indicative of releasing tissue stores. I view this in much the same way Ray viewed his addition of coconut oil to his diet:

Although I had stopped using the unsaturated seed oils years ago, and supposed that I wasn't heavily saturated with toxic unsaturated fat, when I first used coconut oil I saw an immediate response, that convinced me my metabolism was chronically inhibited by something that was easily alleviated by "dilution" or molecular competition. I had put a tablespoonful of coconut oil on some rice I had for supper, and half an hour later while I was reading, I noticed I was breathing more deeply than normal. I saw that my skin was pink, and I found that my pulse was faster than normal--about 98, I think. After an hour or two, my pulse and breathing returned to normal. Every day for a couple of weeks I noticed the same response while I was digesting a small amount of coconut oil, but gradually it didn't happen any more, and I increased my daily consumption of the oil to about an ounce. I kept eating the same foods as before (including a quart of ice cream every day), except that I added about 200 or 250 calories per day as coconut oil. Apparently the metabolic surges that happened at first were an indication that my body was compensating for an anti-thyroid substance by producing more thyroid hormone; when the coconut oil relieved the inhibition, I experienced a moment of slight hyperthyroidism, but after a time the inhibitor became less effective, and my body adjusted by producing slightly less thyroid hormone. But over the next few months, I saw that my weight was slowly and consistently decreasing. It had been steady at 185 pounds for 25 years, but over a period of six months it dropped to about 175 pounds. I found that eating more coconut oil lowered my weight another few pounds, and eating less caused it to increase.

Of course in my case I'm releasing nonsense into my body then upping X,Y,Z to get rid of it but all the same.

 

[Wolf]

Note on what seems to be erection type sides that are common here: For both famotidine and the topical stack for boosting androgens common here I experienced some erection quality issues resolved by taking some Kyowa L-Citrulline. 3g was sufficient before the act alongside an odd 30-40 min for it to begin taking effect. It seems my prior experience was confounded by taking Swanson's Goat Weed complex pretty consistently around that time along with consistent pre workout blends containing dopaminergics and citrulline. Supplement is linked below on the off chance they ever remove it from circulation and one[Me] has to blend it from some herbs.

Supplement Facts​

Serving Size 2 Capsules

Servings Per Container 60

Amount Per Serving	% Daily Value
Horny Goat Weed Extract (Epimedium spp.) (aerial parts) (standardized to 10% icariins) 500 mg	*
Tribulus terrestris Extract (fruit) (standardized to 45% saponins) 300 mg	*
Maca (Lepidium meyenii) (root) 250 mg	*
Mucuna pruriens (seed) 36 mg	*

Famotidine Link:

Famotidine Is A Powerful Scavenger Of Nitric Oxide (NO)

This is probably one of the main reasons behind famotidine's healing of GI / liver damage, and protection from cancer. It could be a good alternative to methylene blue (MB) for NO scavenging purposes as the doses of MB required to scavenge NO are in the tens of milligrams per dose...

raypeatforum.com

Beyond that, 1 drop andro, 2 drops progestene, 2 drops preg, and 2 drops pan mirror my old regimen with 2 more drops preg thrown in. I'll likely get some bloods done here soon just to verify that feeling much better isn't some sort of cursed placebo effect.

 

[Wolf]

Began using Bas Rutten's O2 trainer about a week ago on my workout days. At the end of a session it is quite different than at the beginning so my breathing muscles are being used(obviously) and I am noting a net increase in body temp of something like 0.1-0.5F for an odd two hours afterwards(random variability???) if I use it post workout. I am at the 01 and 05 settings and plan on slowly but surely getting down to 01 and 02. The included blocker type piece is really just a flap and did not work at all to stop air flow so I defaulted to 01 instead of that.
I may look into 3D printing or casting an elbow to increase resistance, but I'd need to find average breathing force then probably do some modeling if I wanted to be intense about it. Or just print and see subjectively instead of doing the MFRs work for them.

On another note, it seems I am getting the pansterone insomnia reported on here. Only real change to the protocol in the past couple days. It comes with massive energy increases and even cypro @ 1mg didn't do too much to help curb the energy. I'm gonna assume its maybe a one off thing and try again in a few days when I don't have work the next day. Perhaps enough preg is going down the dhea pathway with testicular administration and eating 2-3 raw egg yolks...

 

[Wolf]

It actually appears that I misspoke when it came to pointing the finger at DHEA. What’s more likely is some transient hyperthyroidism based on the dramatic increase in my resting heart rate(83bpm) and decrease in temp(97.2)(feeding/sick?)(crap thermometer?). Blood O2 at 97-100% so no concerns there. In any case I can wait it out and withhold all supplements for an odd day or two and see what happens. I definitely was a bit over eager this week and did not do my usual cycling. If it dies down then maybe I can titrate down the NDT, keep the Tocovit the same, and continue with the topicals. My body is producing plenty of heat as I was completely fine outside in a shirt with the temps below freezing. Fatty weight is continuing to drop and muscle should in theory come alongside that. Stronger in the gym compared to a few months ago and should be working at 20# weighted pullups here soon. For reference I can crank out 20 currently alongside 15 pistol squats RL and 13 LL.

General cognition is improving as well, but I attribute that to the cholinergic effects of thiamin. Its helpful for this Masters Program I'm in alongside all the other odds and ends.

Amazingly I no longer have GERD type symptoms at this higher bpm and slightly decreased temp. And that’s with eating acidic foods. That’s my only complaint nowadays sans appendix in any case.

 

[Wolf]

I am actually still pretty solidly warm(98.7), oxygenated(99%), and beating(75-85). This is post break from supplements so perhaps my metabolism just needed a kick in the **** for a few weeks. GERD is essentially gone and definitely has a postural component, gotta make sure I don't bend forward and create pressure where there should be none.
The O2 trainer continues to kick my **** and is equivalent to the belly breathing plus weights I did years ago sans the inconvenience. I'm assuming that this new setpoint for my metabolism is indicative of not really needing a lot of these odds and ends so I'm going pretty barebones with only shilajit in my water sparingly(250mg Primavie/day/>=90oz), niacinamide @ 100mg 1-3x/day, and perhaps a baby aspirin. I'm also working in some citrulline as it seems to counteract the blood flow issues with all of these NO reducing supps. Plus having more energy to crank out reps = more muscle mass = burning the odds and ends that accumulated while suffering through my engineering program. What would be funny is if the O2 trainer is solely responsible for this new set point and those supplements were for naught. Guess we'll see.
I will say that it was 1,000% worth it to go through that period of stress for school. For example, it appeared my Pansterone hadn't dissolved and it was pretty easy to reason I could sonicate the bottle for 5 min at ~90F to completely get it into the solution evenly and lo and behold that happened. I attribute this lack of dissolution to some of the good/bad effects I had when I started incorporating transdermal dhea.
Before working out it has rather dramatic effects and I can actually recall that's what I did back when I was doing trades hell + farmer walks.

https://journals.physiology.org/doi/full/10.1152/ajpendo.00100.2006

Strangely enough there's a massive increase in Estrogen/DHEAS/IGF and T(in women), but that does not match my experience back when I was going through the protocol. I believe its highly likely there's the lower dose I used(5mg oral or 2mg transdermal on and off) coupled with other nonsense like high mushroom intake, egg yolks, etc etc.

Age-Dependent 100-300% Increase in Testosterone With 50mg of DHEA the Night Before HIIT Training. But is it Still Side Effect Free & Ergogenic When Taken Chronically?

Don't be fooled: DHEA won't allow you to train forever day in and day out and still make progress. The most recent study does however add weight to previous results which already suggested that it could have its merits especially when we are talking about intense training sessions like HIIT at...

suppversity.blogspot.com

I really wish they would replicate these studies but with 5, 10, and 15mg doses of dhea.

 

[Wolf]

O2 Trainer working well every other day. Added a band that wraps around the lower abdomen to further potentiate the "belly" breathing with the drawback that now there's a consistent constricting force. Breathes in(expanded abdomen) occur at a faster rate than breathes out doing this which is ok for the time being. Trying to get the sensation back more than anything and the bands help me to focus on the correct musculature. Can do the 04 now without much of an issue but will likely stay at the 05.
Metabolic set point is still going strong, still nice and warm and energetic on my work in office days where I withhold nearly all supplements.

 

[Wolf]

Tocovit dosing: 2 drop
Assuming 1 drop = 750/25 IU = 30 IU
2 drops = 60 IU which equals ~60mg*0.6mg/g PUFA^-1 = 100g PUFA per day that I can "safely" combat. This is assuming an IU is a mg, but the calculation always confuses me. Worst case its actually 60IU*0.67mg/IU = 40.2mg. 40.2mg * 0.6 mg alpaTE/g ^-1 PUFA = 67g PUFA. This is moreso a maintenance dose and I'll likely pulse dose every now and then to saturate my stores over time.

Below is a post from the Tocovit posting:

I don't think there are any significant amounts of tocotrienols. The breakdown is roughly 60% alpha tocopherol, 20% delta tocopherol, 10% gamma tocopherol and 10% beta tocopherol. I will post a more specific analysis in the original post when I get the formal paperwork from the vendor.

Based on:
Relationship between vitamin E requirement and polyunsaturated fatty acid intake in man: a review - PubMed

Spoiler: Abstract

Vitamin E is the general term for all tocopherols and tocotrienols, of which alpha-tocopherol is the natural and biologically most active form. Although gamma-tocopherol makes a significant contribution to the vitamin E CONTENT in foods, it is less effective in animal and human tissues, where alpha-tocopherol is the most effective chain-breaking lipid-soluble antioxidant. The antioxidant function of vitamin E is critical for the prevention of oxidation of tissue PUFA. Animal experiments have shown that increasing the degree of dietary fatty acid unsaturation increases the peroxidizability of the lipids and reduces the time required to develop symptoms of vitamin E deficiency. From these experiments, relative amounts of vitamin E required to protect the various fatty acids from being peroxidized, could be estimated. Since systematic studies on the vitamin E requirement in relation to PUFA consumption have not been performed in man, recommendations for vitamin E intake are based on animal experiments and human food intake data. An intake of 0.6 mg alpha-tocopherol equivalents per gram linoleic acid is generally seen as adequate for human adults. The minimum vitamin E requirement at consumption of fatty acids with a higher degree of unsaturation can be calculated by a formula, which takes into account the peroxidizability of unsaturated fatty acids and is based on the results of animal experiments. There are, however, no clear data on the vitamin E requirement of humans consuming the more unsaturated fatty acids as for instance EPA (20:5, n-3) and DHA (22:6, n-3). Studies investigating the effects of EPA and DHA supplementation have shown an increase in lipid peroxidation, although amounts of vitamin E were present that are considered adequate in relation to the calculated oxidative potential of these fatty acids. Furthermore, a calculation of the vitamin E requirement, using recent nutritional intake data, shows that a reduction in total fat intake with a concomitant increase in PUFA consumption, including EPA and DHA, will result in an increased amount of vitamin E required. In addition, the methods used in previous studies investigating vitamin E requirement and PUFA consumption (for instance erythrocyte hemolysis), and the techniques used to assess lipid peroxidation (e.g. MDA analysis), may be unsuitable to establish a quantitative relation between vitamin E intake and consumption of highly unsaturated fatty acids. Therefore, further studies are required to establish the vitamin E requirement when the intake of longer-chain, more-unsaturated fatty acids is increased. For this purpose it is necessary to use functional techniques based on the measurement of lipid peroxidation in vivo. Until these data are available, the widely used ratio of at least 0.6 mg alpha-TE/g PUFA is suggested. Higher levels may be necessary, however, for fats that are rich in fatty acids containing more than two double bonds.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594047/

Spoiler: Abstract

Vitamin E (α-tocopherol) is recognised as a key essential lipophilic antioxidant in humans protecting lipoproteins, PUFA, cellular and intra-cellular membranes from damage. The aim of this review was to evaluate the relevant published data about vitamin E requirements in relation to dietary PUFA intake. Evidence in animals and humans indicates a minimal basal requirement of 4–5 mg/d of RRR-α-tocopherol when the diet is very low in PUFA. The vitamin E requirement will increase with an increase in PUFA consumption and with the degree of unsaturation of the PUFA in the diet. The vitamin E requirement related to dietary linoleic acid, which is globally the major dietary PUFA in humans, was calculated to be 0·4–0·6 mg of RRR-α-tocopherol/g of linoleic acid. Animal studies show that for fatty acids with a higher degree of unsaturation, the vitamin E requirement increases almost linearly with the degree of unsaturation of the PUFA in the relative ratios of 0·3, 2, 3, 4, 5 and 6 for mono-, di-, tri-, tetra-, penta- and hexaenoic fatty acids, respectively. Assuming a typical intake of dietary PUFA, a vitamin E requirement ranging from 12 to 20 mg of RRR-α-tocopherol/d can be calculated. A number of guidelines recommend to increase PUFA intake as they have well-established health benefits. It will be prudent to assure an adequate vitamin E intake to match the increased PUFA intake, especially as vitamin E intake is already below recommendations in many populations worldwide.

https://ods.od.nih.gov/factsheets/VitaminE-HealthProfessional/#:~:text=To%20convert%20from%20IU%20to,0.45%20mg%20of%20alpha%2Dtocopherol.

Spoiler: Base info

To convert from IU to mg: 1 IU of the natural form is equivalent to 0.67 mg of alpha-tocopherol. 1 IU of the synthetic form is equivalent to 0.45 mg of alpha-tocopherol.

 

[Wolf]

Well, seems I don't need to worry about the odd 1-2g of Beta-Alanine I occasionally throw in when I'm working towards "fat loss"/endurance:

24-Week β-alanine ingestion does not affect muscle taurine or clinical blood parameters in healthy males​

Spoiler: Abstract

Abstract​

Purpose: To investigate the effects of chronic beta-alanine (BA) supplementation on muscle taurine content, blood clinical markers and sensory side-effects.
Methods: Twenty-five healthy male participants (age 27 ± 4 years, height 1.75 ± 0.09 m, body mass 78.9 ± 11.7 kg) were supplemented with 6.4 g day-1 of sustained-release BA (N = 16; CarnoSyn™, NAI, USA) or placebo (PL; N = 9; maltodextrin) for 24 weeks. Resting muscle biopsies of the m. vastus lateralis were taken at 0, 12 and 24 weeks and analysed for taurine content (BA, N = 12; PL, N = 6) using high-performance liquid chromatography. Resting venous blood samples were taken every 4 weeks and analysed for markers of renal, hepatic and muscle function (BA, N = 15; PL, N = 8; aspartate transaminase; alanine aminotransferase; alkaline phosphatase; lactate dehydrogenase; albumin; globulin; creatinine; estimated glomerular filtration rate and creatine kinase).
Results: There was a significant main effect of group (p = 0.04) on muscle taurine, with overall lower values in PL, although there was no main effect of time or interaction effect (both p > 0.05) and no differences between specific timepoints (week 0, BA: 33.67 ± 8.18 mmol kg-1 dm, PL: 27.75 ± 4.86 mmol kg-1 dm; week 12, BA: 35.93 ± 8.79 mmol kg-1 dm, PL: 27.67 ± 4.75 mmol kg-1 dm; week 24, BA: 35.42 ± 6.16 mmol kg-1 dm, PL: 31.99 ± 5.60 mmol kg-1 dm). There was no effect of treatment, time or any interaction effects on any blood marker (all p > 0.05) and no self-reported side-effects in these participants throughout the study.
Conclusions: The current study showed that 24 weeks of BA supplementation at 6.4 g day-1 did not significantly affect muscle taurine content, clinical markers of renal, hepatic and muscle function, nor did it result in chronic sensory side-effects, in healthy individuals. Since athletes are likely to engage in chronic supplementation, these data provide important evidence to suggest that supplementation with BA at these doses for up to 24 weeks is safe for healthy individuals.

Summary
β-Alanine in blood-plasma when administered as A) histidine dipeptides (equivalent to 40 mg · kg−1 bwt of β-alanine) in chicken broth, or B) 10, C) 20 and D) 40 mg · kg−1 bwt β-alanine (CarnoSyn™, NAI, USA), peaked at 428 ± SE 66, 47 ± 13, 374 ± 68 and 833 ± 43 µM. Concentrations regained baseline at 2 h. Carnosine was not detected in plasma with A) although traces of this and anserine were found in urine. Loss of β-alanine in urine with B) to D) was <5%. Plasma taurine was increased by β-alanine ingestion but this did not result in any increased loss via urine. Pharmacodynamics were further investigated with 3 × B) per day given for 15 d. Dietary supplementation with I) 3.2 and II) 6.4 g · d−1 β-alanine (as multiple doses of 400 or 800 mg) or III) L-carnosine (isomolar to II) for 4 w resulted in significant increases in muscle carnosine estimated at 42.1, 64.2 and 65.8%

So I'm good from 0-40mg/kg BW it would appear chronically up to ~4g per day. In the main study its pretty interesting to see the plasma taurine levels following the 0, 3 and 6h intakes of 10mg/kg BW beta alanine.

Spoiler: Image

Taurine:

Beta Alanine:

I: 800 mg of b-alanine was given 4 times per day (approximately 9 am,12 am, 3 pm and 6 pm) to give an average daily dose of 3.2 g and total 4 week dose of 89.6 g

II: used a more frequent dosage strategy in order to increase the dose but not to exceed 800 mg in any one dose. In week 1 subjects consumed 800, 400, 400, 400, 800, 400, 400 and 400 mg at 9, 10, 11 and 12 am, and, 3, 4, 5, and 6 pm to give an average daily dose of 4 g. In week 2 the 11 am and 5 pm doses were increased to 800 mg; in week 3 the 10 am and 4 pm doses were similarly increased and in week 4 also the 12 am and 6 pm doses. Thus in week 4 the average daily dose was 6.4 g. The total dose over the 4 weeks was 145.6 g.

III: subjects ingested L-carnosine using a dosing strategy identical to II) and where each individual dose was approximately isomolar with respect to b-alanine. Thus where 400 and 800 mg of b-alanine were given in II), 1000 and 2000 mg of L-carnosine were given in III). The total given over the 4 weeks was 364 g of L-carnosine correspondingto 143.3 g of b-alanine.

IV:subjects were given capsules containing maltodextrin to match thoseof II) and at the same frequency as given also in III).

Main takeaway:

Increases in b-alanine in plasma were associated with increases in the plasma taurine concentration. b-Alanine shares the same transporter as taurine, a b-sulfonic amino acid, and acts as an antagonist of taurine uptake into tissues. Three to 4 weeks administration of b-alanine (3% in the drinking water) has been shown to halve the taurine content of myocardium and skeletal muscle of rats (Alloet al., 1997; Harada et al., 1988; Mozaffari et al., 1986; Dawson et al., 2002) whilst 22 mmol kg1 bwt administered twice per day for 5 days decreased the taurine concentration in both muscle and brain of chickens (Tomonagaet al., 2005). However, the amounts of b-alanine given in these studies are typically more than 100 times higherthan the doses used in the present investigation, which were based on amounts obtained from the diet. Thus 22 mmol kg1 bwt would correspond to 156,000 mg inan 80 kg individual whereas the highest single dose usedin the investigation of 4 weeks supplementation (study 3)was 800 mg b-alanine. This corresponds to approximately10 mg kg1 bwt (0.112 mmol kg1 bwt), and is the amount in dipeptide form in 100 g of whale beef or 150 gturkey breast meat (Abe, 2000), and 100 g north-Atlantic sea-prawns (unpublished observations). Despite the increase in plasma taurine following 10–40 mg kg1 bwt b-alanine, no significant loss of taurine was detected in urine. Four weeks of b-alanine supplementation in the freeform, or as L-carnosine, did not result in any change in themuscle content. However, this does not preclude the possibility of selective taurine loss in one or other muscle fibretype, given that type I muscle fibres contain higher concentrations than type II (Harris et al., 1998).

Anecdotally, I never experienced issues with beta-alanine previously, but I would cycle it alongside glycine and taurine depending on what sort of training I was doing. Regardless, its nice to know that if I stay within the confines of this study I should be ok. 1g each time and wait at least 2 hours or so. I do wonder if the cyclical increases of taurine in plasma reflect some sort of tissue release and if so does that same taurine make it back into the tissue. It doesn't seem to end up in the urine, but they didn't test fecal excretion so who knows. Numerically, it would appear that the taurine does in fact make it back in as Table 3 shows a 10% decrease that similarly occurred in placebo(IV). Maybe there's some sort of repartitioning of amino acid content in muscles.

 

[Wolf]

Exchange between @Travis and myself regarding his Formal Education Background and what I should do to maximize learning in my BioChemE degree.

Jul 27, 2018
Whats your educational background? You have a great ability to research and get to the core of the material that you read.

Jul 27, 2018
Chemistry.

Jul 27, 2018
Any studying tips You can offer?

Jul 27, 2018

Any studying tips You can offer?

Chemical engineers are the more serious intellectuals, and I believe dopamine and epinephrine are a prerequisite for that condition. Dopamine is very similar to catecholamines in structure, and I see it somewhat as a 'neuro-catecholamine.' Serotonin seems to get in the way of hard-headed thinking, yet it could actually be useful for creativity. Were there neurotransmitters corresponding to art and logic, I would guess they'd be serotonin and dopamine.

I still haven't done any L-tryptophan experiments so I am still somewhat uncertain about serotonin, but too much digestible protein leaves me with a reduced ability to concentrate. I think: (1) slower-digesting proteins are good, (2) exorphins should be avoided, and (3)the television should be defenestrated.

Nicotine has been shown to increase brain glucose flux by 30% in experiments, and acetylcholine antagonists—i.e. mecamylamine—reliably reduce it. Folate is indispensable for choline synthesis—for the methylation—although some of that can be dietary-derived.

There's quite a few things to consider, and even some fatty acids can be detrimental. The body synthesizes DHA (22∶6ω−3) from α-linolenic acid (18∶3ω−3), a unique functional membrane lipid irreplaceable by no other. Linoleic acid (18∶3ω−6) is also a substrate for Δ⁵-desaturase, an enzyme α-linolenic acid needs to use twice for its elongation–desaturation into DHA. Without enough DHA synthesized, the body will elongated and desaturate omega−6 fatty acids to maintain a constant unsaturation index in grey matter membranes. Osbond acid (22∶5ω−6) becomes the main offender in this location, a lipid that lacks DHA's unique ability to exclude cholesterol from the cell membrane. This sum of osbond acid and DHA always equal a constant range—between about 15–17% (grey matter)—yet the ratio between them is always associated with pathology. So besides avoiding omega−6 fatty acids on account of downstream 2-series prostaglandins and 4-series leukotrienes, they ought to be avoided with increased diligence because they induce a cascade of events leading to the disruption of the physicochemical properties of cell membranes.

An increased (22∶5ω−6)/(22∶6ω−3) ratio reduces brain myelination indirectly by increased the grey matter's affinity for cholesterol. Sterols are out of place in that location, so besides actively-reducing glucose flux they are made less-available for myelin where they belong.

Jul 27, 2018
Continue taking an maoi -b.
Switch to casein protein.
Avoid gluten as much as possible(exorphin), but what of milk?
Chuck the TV and social media.
Smoke or at least get nicotine gum.
Folate should be supplemented regularly in addition to other b.
Avoid omega 6 at all costs, what of omega 3?
I primarily consume saturated fats with negligible amounts of polyunsaturated fat. Nearly no monounsaturated fat.

Jul 31, 2018

Continue taking an maoi -b.
Switch to casein protein.
Avoid gluten as much as possible(exorphin), but what of milk?
Chuck the TV and social media.
Smoke or at least get nicotine gum.
Folate should be supplemented regularly in addition to other b.
Avoid omega 6 at all costs, what of omega 3?
I primarily consume saturated fats with negligible amounts of polyunsaturated fat. Nearly no monounsaturated fat.

There are reasons to suggest that goats' milk would be preferred.

Dec 4, 2018
Update: Increasing dopamine/epinephrine reliably increases logical thinking and helps me make sense of the math and understand it quickly.
Increasing serotonin helps wrap my mind around abstract concepts.
Work capacity and being able to actually sit down and do math has been greatly improved from back when I was in school. I can sit at a table and get through a 10 hr block of math with a lunch break.
Thanks for the previous chat, it really helped guide my dietary and supplement choices this semester.

 

[Wolf]

Down 6 odd lbs of fatty weight and continue to get stronger in pullups. 40# weighted are now possible at a BW of 245#. Still have an odd 20-30# to lose with an odd 20# of muscle to gain to get back to my working weight. Captains of Crush 2.5 closed as a working set with the CoC 2.0 closed cold(which slightly injured my hand, stupid). Grip is recovering much faster than anything else which is pretty nice. Working chia seeds in daily alongside the transdermals and recently TUDCA seems to keep everything moving along nicely. If motility slows down I can do some TTFD or go on a long walk which helps. Stools are hydrated(chia), well formed, and brown. Bristol Stool Scale of 4 if going when I feel the urge and not preoccupied, else 2/3 if I am running around working or deep in some sort of problem. A regular breakfast-lunch-dinner cycle seems to help alongside an odd TBSP chia with lunch and dinner. I skip breakfast as that is the most stressful part of my day and I'd rather not have a giant hydrated mass angry at me.

I once more experienced the "super sleep" I seem to encounter every time I get a rapid metabolic shift. Slept something like 12-16 hours back to back and woke up drenched in sweat twice. Lots of energy upon waking and more mind-muscle connection. It was only two days, when I was really sick it was something like two to four weeks and when I was recovering from lots of trades it would be something like 2 to 5 days in between jobs. The upside of office work is that if you manage your stress you don't really invite any catabolic influences like lugging 2x6s all day or breathing in god knows what.

Overall really happy with how this is playing out. Hoping to be at a good enough to suffer through some huge undertaking level within two months[05/01/2024] or so. Last time Peating intensely kept me going for about 1.5-2 years before a bout of the chronic appendicitis and school hell did me in.

 

[Wolf]

TUDCA notes:

Probably best to do 2tbsp chia:1 250mg cap of TUDCA to keep things moving and prevent excessive "soft" stools. At 1 tbsp:1 250mg cap of TUDCA stools are soft but ok. Smelly, but overall energy is going up and up and up. Elimination occurs pretty often and some skin stuff is clearing up. I suspect that whatever nonsense was populating my lower GI and causing the chronic appendicitis is being flushed out. Note that food is completely digested based on stool color and no evidence that raw food has made it down. I think my base dietary roughage was compensating for 1 cap of TUDCA per day, but at 3x250mg per day I was over and above that.

General:
Sweating more often and overall exchanging more heat and mass with my environment. I definitely note a greater benefit from 100mg of Niagen over 250mg of Niacinamide, but I think that might just be from chronic dosing and my blood sugar not dipping. Hoping to switch over eventually when I can find a reliable source of 100mg Niacinamide. B6 sublingually @ 6.25/12.5/25mg seems to put me in a high dopamine/adrenaline mode for an odd hour or two but chronically doing that I've noticed an improvement in dopaminergic function like motivation and grip strength. Biggest problem I'm noticing right now is a need to stretch out my muscles and being able to "focus" more and get more out of my grip. Will probably revisit Maxick's Muscle Control.

I do 1 drop of Tyromax, 2 drops of Tocovit, 1 drop andro, wait 30 min, 2 drops Pan, and 2 drops Prog before bed. I have MCT oil in my coffee alongside colostrum(~6g)[Symbiotics] and collagen(12g)[Great Lakes]. Beyond that everything else is kinda context dependent. If I'm working out more on a given day I'll up my casein protein, if its a "brain" day I'll throw in some b1, and if its a hell endurance workout sort of day I'll throw in some more beta alanine than I usually use. Beta alanine seems to be working since I can bike for a longer time at a lower rate of perceived exertion.

Will likely be getting blood work soon and will pick the brains of forum members soon.

Likely:
Cholesterol/Lipid
Testosterone
DHT
Prolactin
DHEA/DHEAS
Some estrogen markers, but I really would like to know which are the best to look at.
Prolactin

Previously I looked at a bunch of vitamins, T3/T4/TSH, and prolactin. Everything was pretty solid with prolactin being slightly higher than I would like.

 

[Wolf]

Throwing in Taurine for protein utilization on my "off" days @ 500mg Ajinomoto pharma grade.
TUDCA continues to be great on my off days and the 4 days on, 3 days off is great. By my 3rd day off I definitely notice being "slower" but I'm still very capable. No news is good news and my weight hasn't jumped on my off days this week. We'll see what UCP and cold exposure has in store for me.

 

[Wolf]

Taurine helps the protein utilization it would seem and CIT prevents any muscle catabolism.
TUDCA is pretty solid but I can only do 2 caps @250mg/cap before I get uncomfortable. I no longer have the 3rd day slowness so there's likely some storage going on of whatever magic Haidut cooked into his supps. I'm down 10 lbs from baseline, 4 net lbs since my Feb 17th post. So at an odd lb per week that's pretty nice. There's of course some offset with the muscle mass increase, but I'm past worrying about that. As long as my skin remains ok I could care less.
P5P has been amazing in the low and slow dosing and more likely than not contributes massively to the perceived increase in health.
Currently trying out the one a week fasting day with MCT/collagen/colostrum coffee in the morning, green tea in the afternoon, and an odd 200-400IU of Tocovit or NOWs awesome vit E supplement throughout the day. It worked last time pretty solidly and I dropped something like 25lbs of fatty mass over 2.5 months. I wasn't working out or doing anything else and the rebound occurred since I didn't really cement in any habits. This time I'm gonna try to work more stuff in as I am no longer doing things purely for the sake of maintaining my A average in chemE and living like an ascetic.
300mg NMN sucks and I dislike the effects compared to 100mg chronically.
/update