@CrumblingCookie
Thank you for the information. It was interesting to read of ACh being a possible factor. My first thought was to attempt to get this with food; or as @zorba990 mentions, pantothenic acid or pantethine forms of vitamin B5. But, the last 15 years has all but put me off of all supplements. I simply can't take them without adverse effects. So, for now, this ACh experiment will have to wait. Though I will make note of it.

@GRay said in mk4 dosing?:

Basically, I need to supplement with 1000mg Ca, and I generally use grassfed living bone from ancestral, or cheese or a combo of the two.

Are you in France or US? if the latter where do you get your mk4?

Ok, right.
Remind we better absorb 4 x 250 mg Ca element than 2 x 500 mg when taking a supplement.
I live in Belgium. My MK4 comes from iherb.com in USA. Could be bought in France:
Thorn Research, liquid. Not cheap but high dose and proportionally not expensive if used as I do: 1 drop at breakfast, with minimum 25 g fat, most of the time. Otherwise, to be taken at another meal (14 - 25 - 35 g threshold).
I protect my bottle from light.

Advise: I 'd take potassium bicarbonate powder, as well as potassium citrate. Alternate.
Mine come from France, la Compagnie du bicarbonate. I buy it in one Kg (2 pounds). - 1 kg potassium bicarbonate. 1 dose 3.2 g
1 kg sodium bicarbonate (NaHCO₃)
I use NaHCO₃ in 2 ways: 1. To get rid of toxins from my fruits (pH 8.5 => 1 big tsp in water). (study, not from a post on internet) 😉 2. when I make a cure with 2 g NaHCO₃ to reset Th1 >< Th2.

@GRay Increasing testosterone is anything but straightforward

@CrumblingCookie
very helpful. Thank you.

@BroJonas I know the symptoms of the two overlap a lot but they map perfectly to my increase and decrease of thyroid dosage

Endotoxins sources when eating starch?
Short answer:
LPS toxins don’t come from starch from itself but are the result of died gram-negative bacteria (killed by the milieu or arrived at the end of their life).
Developed theory
Endotoxins, specifically lipopolysaccharides (LPS) from Gram-negative bacteria, can be a concern when eating starch, but the primary source is not the starch itself. While some LPS may be present in food, including those containing starch, the major source of endotoxins in the body is from the bacteria that naturally inhabit the gut. Starch, especially resistant starch, can influence the gut microbiome and potentially impact the amount of LPS produced and absorbed.
Endotoxins from Gut Bacteria
Gram-negative bacteria, which are a normal part of the gut flora, have LPS in their outer membrane. When these bacteria die or their cell walls are disrupted, they release LPS into the gut. Some LPS can be absorbed into the bloodstream from the gut, potentially contributing to inflammation. (…)

In essence, while starch itself isn't a direct source of endotoxins, its impact on the gut microbiome can influence the amount of endotoxins produced and absorbed, with resistant starch potentially playing a beneficial role in mitigating the effects of LPS if, and only if, there is no stagnation of the feces (optimal transit, with a functional MMC), the liver isn’t overburdened (neutralization of side-effects), the way-out is free …
Note: The kind of stuff used in the 2 studies is deprived of fiber. An isolated “nutrient”.
Potatoes induce a higher insulin reaction than sugar cane. When I eat 2 medium potatoes, I mix them with butter, one egg and pieces of broccoli or some frozen spinach. (+ a calcium source to neutralize the very high source of oxalates from spinach: 660 mg for 100 gr spinach).
The capacity of the body is 50 mg oxalate/d. 150 - 200 mg if not every day.

@sunsunsun Russia had McDonalds

d04cdd50-c252-4b7d-8fb0-5a758869d508-image.png

@Corngold go to Spain or western Canada for a vacation xD

or le south de Francé

@yerrag 100%!

Similar to what alot of the keto and carnivore ones thought about reducing/eliminating carbs, and later on realised their mistake(s) (e.g. Thomas Delauer, Mercola, Paul Saladino etc.), though I'm still waiting for Eric Berg to come to that realisation too 😉

Sounds very good. The parsley also has a decent amount of apigenin and is more than just for flavor.

Another idea would be to also use some ginger. Although raw ginger isn't to everybody's liking and I'm not sure the intense taste destroys the overall taste of the other ingredients.

@ThinPicking Thanks for weighing in

thyroid hormone is dosed and micrograms and iirc is sensitive to light

theres multiple posts on the reddit sub about experiencing problems by removing iodized salt from diet.
i used to use pickling salt, it’s idiotic to cook and season with except in soups where it totally dissolves. i actually got some sort of stomach issue that lasted weeks before it resolved from accidently swallowing a bunch of undissolved kosher salt crystas in my coffee. i actually almost threw up a couple times drinking the super concentrated undissolved pickling salt crystals in my milk too
i went back to iodized salt

search the reddit sub. theres one user that says they/them are allergic to seafood and that xer got suicidal after two months off iodized salt and it instantly resolved in two minutes after taking a bit of iodized salt in the middle of the night when xer was on auto pilot as if their body knew they needed it

@DakotaWorrell You will never, ever be able to "figure this out". We all have different diet histories, activity levels, etc.

I think that as long as you're staying well under known toxic doses, you feel good, and you have some degree of balance between nutrients that are known to interact (ex. vitamin d, k,a; phosphorous:calcium, protein:carbs), that's about the best you can do.

Lack of magnesium
How does a lack of magnesium induce a deficiency in mitochondrial energy at the end of the process?
I’ve been reading a RP letter recently and I wanted afterwards to go deeper in the PKC system (Protein Kinase C) to connect the dots. (1)
Nearly every reader here knows the impact of PUFA on metabolism. And the interdependence and the ripple effect between excess estrogens and adipocyte cells (though AA cascade when we are stressed).
When we have difficulty in maintaining an adequate energy production, whatever the cause may be (e.g. diabetes, hypothyroidism, colopathy, etc.), a deficit produces an alarm state, causing increased production of adrenalin and cortisol. (2) (Derived from the "fight-or-flight" response, a protective survival process). These stress hormones trigger the release of stored energy from the liver (glycogenolysis) and fat tissue (lipolysis). Thus, adrenalin mobilizes fat from storage, and these free fatty acids are often going to create a chronic problem.
Metabolic Shift
During stress, the hormones adrenaline (epinephrine) and cortisol shift the body's energy focus from glycolysis (using glucose for energy) towards lipolysis (breaking down stored fats for energy). However, reduced reliance on glycolysis is not completely shut down; its relative importance is diminished as the body prioritizes fat breakdown for energy. Big advantage of our specie on the animal reign (enable to quickly mobilize stored energy reserves for a long time).
Estrogen and PUFA activate the PKC system
I cite RP:
“Estrogen and the polyunsaturated fatty acids (PUFA), linoleic and linolenic acid, alike activate the protein kinase C (PKC) system of cellular activation. Many of the functions of PUFA are similar to the functions of estrogen (e.g., antagonism to thyroid function, promotion of age pigment/lipofuscin), so this information showing that they both act similarly on the same basic regulatory pathway is important.
Estrogen increases secretion of growth hormone (GH; it's closely associated with prolactin, also increased by estrogen), and GH causes an increase in free fatty acids in the blood. Estrogen promotes iron retention, so it sets the stage for oxidative stress. At least in some systems, both estrogen and PUFA promote the entry of calcium into the cell.” (1)
In diabetes, there is a generalized excess activation of the PKC system (protein kinase C). (…)
Protein Kinase C system (PKC)
What is the role of PKC system and its impact on energy?
In short: PKC is a key player in cellular energy regulation, influencing mitochondrial function, energy sensing, neurotransmitter release, and other energy-related processes. By modulating these processes, PKC helps cells maintain energy balance and respond to changes in energy availability.
PKC is also intertwined with other energy-signaling processes (AMPK) and neurotransmitters.

PKC system in details
Here's a more detailed look at PKC's impact on energy:

Mitochondrial Function:
• PKC signaling can influence mitochondrial function by regulating enzymes involved in oxidative phosphorylation, the process by which mitochondria generate ATP.
• For example, PKC can regulate pyruvate dehydrogenase (PDH) and cytochrome c oxidase (Complex IV), which are critical for cellular energy production.
• PKC also plays a role in mitochondrial dynamics, which is important for maintaining healthy mitochondria and efficient energy production. Energy Sensing and Signaling:
• PKC can phosphorylate AMPK, an enzyme that is activated by cellular energy depletion.
• This phosphorylation can affect AMPK's activity, which in turn influences cellular processes that regulate energy balance.
• By interacting with AMPK, PKC can help cells respond to changes in energy levels and maintain homeostasis. Neurotransmitter Release and Energy:
• PKC is involved in regulating neurotransmitter release, which requires energy for the process of exocytosis (releasing neurotransmitters from vesicles).
• By modulating the proteins involved in synaptic vesicle exocytosis, PKC can impact the energy demands of neuronal signaling. Other Energy-Related Processes:
• PKC can influence various other cellular processes related to energy, such as the opening and closing of the mitochondrial permeability transition pore (MPTP), which affects mitochondrial function and energy production.
• PKC can also affect the activity of proteasomes, which are involved in protein degradation and cellular energy balance.
In summary: PKC is a key player in cellular energy regulation, influencing mitochondrial function, energy sensing, neurotransmitter release, and other energy-related processes. By modulating these processes, PKC helps cells maintain energy balance and respond to changes in energy availability.

Sources and References

Diabetes, scleroderma, oils and hormones”. 2006 raypeat.com The Role of Protein Kinase C During the Differentiation of Stem and Precursor Cells into Tissue Cells - doi: 10.3390/biomedicines12122735 Biomedicines 2024 AA cascade
Cascade AA Cox Lox P450 03.gif
The AA cascade explained when there is a discharge of FFA due to stress. We already know the deleterious effects of excess PUFA.
When you're stressed, your body releases certain hormones that trigger your cells to break down fats stored in the membranes. One of the fats released is called arachidonic acid (AA), which comes from a type of fat known as PUFA.
Once AA is free in the body, it acts like fuel for inflammation. It gets turned into other substances (prostaglandins) that tell the body to create swelling, pain, and heat — all part of the "inflammatory response." While this can be helpful short-term (like in healing), too much of it keeps the body in a state of constant low-level inflammation (especially from diets high in omega-6).
So, during stress, your body’s release of AA can make things worse if you already have a lot of these fats stored. That’s part of why people say excess PUFA can have harmful effects, especially over time.
Prostaglandins (PGE) and their link to excess omega-6 (ALA) in the AA cascade:
When we eat a lot of omega-6 fats — especially from things like seed, corn or soy oils — our bodies convert them into arachidonic acid (AA). This is especially true with a type of omega-6 fat called linoleic acid (LA, a type of omega-6) — not to be confused with alpha-linolenic acid (ALA, a type of omega-3).
Once there's a buildup of AA in our cells – we don't use / need much PUFA, stress can trigger the release of AA into the body. That’s where things take a turn: AA gets turned into compounds like prostaglandins (especially PGE2).
Prostaglandins (PGE) are like chemical messengers that tell the body to create inflammation. They're useful in small amounts for healing and repair, but when there’s too much AA around, you get too much PGE2, which causes chronic inflammation, swelling, and even pain.
This inflammation signals the body that something’s wrong — which ironically increases stress levels further. It becomes a vicious cycle:
More omega-6 → more AA → more PGE2 → more inflammation → more stress.
That’s one reason people are concerned about eating too much omega-6, especially from processed foods. It overloads this system and keeps your body in a kind of "fight mode" all the time.
Cascade AA & prostaglndines.jpg