@Mauritio im also interested. plus did you ever try out NMN for weight loss

Tumors partially destroyed with sound don't come back

https://www.sciencedaily.com/releases/2022/04/220418093955.htm?utm_source=dlvr.it&utm_medium=twitter

@DavidPS while he didn’t mention lactoferrin in the interview, I remember hearing Peat once say that an all milk diet would be sustainable for about a month before causing iron deficiency. Just another thing to think about in the role milk and its components seem to have on iron.

I’ve had pretty rough teeth my whole life despite following dentists recommendations as a child/teen. I have found a ton of relief in lactoferrin, (helps with tooth sensitivity, color, (from yellow to white) and translucence). The color of my teeth reminds me of rust, (which when diluted is more of a yellow-orange than red).

Another modality that has improved my teeth has been the work of Dr Manhart over at the Calcium Therapy Institute. His products combine calcium with zinc… And here we are again, zinc, iron. I wonder, if bones are holding iron instead of zinc what their appearance might be? Maybe yellowing from oxidized iron? How is the Calcium Therapy Institute able to recalcify teeth that have almost completely disintegrated, (they primarily focus on bacterial infections causing the decay-though this brings us back to iron potentially)?

Another thing I think about regularly is copper plumbing. All the water that touches our body lives/travels in copper. I don’t know one way or that other if this matters, but it’s just another drop in the bucket of “what the heck is going on with iron, zinc, and copper?” Is it possible we’d be better off with pex tubing? I recall another interview with Peat where he mentioned that the plastics used for pex were actually some of the safest. I have become fully convinced that environmental factors are possibly the most important to our health, but maybe they aren’t the ones commonly considered. People seem very worried about pollution, and sprawl, and things of this ilk, (which obviously have their own issues) but no one really talks about copper plumbing as potentially problematic. I have no evidence it is to be clear, it’s just something that pops in my head from time to time.

One final thing I consider is the number of times I heard Peat say that typically chelation is more deleterious than simply leaving it alone. This stops me from jumping on the HG7 bandwagon despite being interested. I sometimes wish Dr Peat was still with us, as l’d love to have his option on some of the newer modalities that pop up now and then. I also think that Peat tended to focus on simplicity over utility because of his understanding of the nature of those who are ill. It’s possible that a complex system like say HG7 could be beneficial, however Peat may have discounted it for its potential to harm, and the difficulty of adhering to it. This doesn’t mean however that something so complex is inherently non-beneficial.

@DavidPS

DavidPS said

Lithium has been known to benefit the brain. Small amount of lithium found in the water table had great benefit.
Excerpts from the study (main points): Here we show that endogenous lithium (Li) is dynamically regulated in the brain and contributes to cognitive preservation during ageing. Of the metals we analysed, Li was the only one that was significantly reduced in the brain in individuals with mild cognitive impairment (MCI), a precursor to AD. Li bioavailability was further reduced in AD by amyloid sequestration. Replacement therapy with lithium orotate, which is a Li salt with reduced amyloid binding, prevents pathological changes and memory loss in AD mouse models and ageing wild-type mice. These findings reveal physiological effects of endogenous Li in the brain and indicate that disruption of Li homeostasis may be an early event in the pathogenesis of AD. Li replacement with amyloid-evading salts is a potential approach to the prevention and treatment of AD.

Analyze
Yes, but …
The amount is so light that it’s hard to measure without an appropriate tool.
I’ve decided to make a search with LucH’s pendulum (1) when I saw last month an article in a medical review. 😉
We have to make a distinction between a pathology (AD) and cognitive preservation by anticipation.
First, note that the improvement has been obtained on mice. Not only, but well in the referenced study. The improvement observed in the axons is fine / real but there is no feedback on the long term. A mouse doesn’t talk and doesn’t feel good but shows an ability to target sth (behavior to recognize, to memorize a way to get a sweat).
The mouse acts in order to obtain a reward in the form of food or a punishment when it makes a mistake.

I explain the restriction:
Synaptic reuptake is a key process for regulating neurotransmitter concentration in the synapse. Lithium acts on this process to modulate neuronal activity.
How much lithium is found in brain axons and how much is sequestered by cortical amyloid plaques has been studied. It has been done with human beings. See further details on the link beneath.
For the other readers:
Overall, lithium readjusts the balances between excitatory and inhibitory neurotransmission, as well as between catecholamines and acetylcholine. It is the adjustment of these balances, rather than the isolated effect on a single neurotransmitter, that partly allows for the improvement and stabilization of mood. End of the parenthesis.

Dose range
The effective dose range for lithium is relatively narrow, and exceeding it can lead to adverse effects. The specific mechanisms by which lithium exerts its effects on the brain are still under investigation (…). In case of supplementation, toxic effects are to be expected, such as concentration problems, but not only that.
Plasma concentration is reached within 2 to 4 hours after oral administration of a supplement. (1) The plasma half-life is approximately 24 hours. Equilibrium is reached between the 5th and 8th day. More quickly if the kidneys' elimination capacity is reduced. Be careful, apprentice chemists, especially in the case of insufficient sodium intake.

Final thought:
Yes, Li is a cofactor in the absorption of certain vitamins, helps the body produce serotonin, supports the transmission of neural messages and much more.
But I’d rather try to get my Li through food, provided you don’t suffer from intolerance, as there is a lot of Li in milk, cheese, eggs and sea food or liver (chicken or beef).
Not yet official, but lithium is gradually being considered an essential trace element, with a recommended daily intake of 1 mg for a 70 kg adult. (2)
Studies also suggest that lithium's effectiveness depends on the availability of other minerals and works synergistically with them to maximize its effectiveness on mood, longevity, and cognitive support. (3)
In another human study, a daily microdose of just 300 mcg of lithium was found to significantly reduce age-related cognitive decline just three months after starting a lithium supplement. (4)
NB1: Alzheimer is a complex pathology. We need to act in many directions.
In short: exercise (mental and physical), K2 MK4, tocos, iodine and other well-known ones. For another article. 😉
NB2: I won’t trust a labo when they say lithium orotate could do the job. (5) Low supplementation (e.g., 5 to 20 mg/day of lithium orotate) may produce transient or subtle effects, but does not guarantee stable maintenance of brain levels.

Sources & references

My article on lithium
https://mirzoune-ciboulette.forumactif.org/t2124-le-lithium-ameliore-l-humeur-optimise-les-cellules-souches-la-longevite-et-plus-encore#30285 Lithium: occurrence, dietary intakes, nutritional essentiality. J Am Coll Nutr, 2002) DOI: 10.1080/07315724.2002.10719188 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443601/ https://pubmed.ncbi.nlm.nih.gov/22746245/ Une supplémentation faible (ex : 5 à 20 mg/jour de lithium orotate) peut produire des effets transitoires ou subtils, mais ne garantit pas un maintien stable des niveaux dans le cerveau (cf. étude Human brain 7Li-MRI: 10 à 60 µM, stable après 2-4 semaines).
Human brain 7Li-MRI following low-dose lithium dietary supplementation in healthy participants - ScienceDirect 2024

@LucH - thanks for your analysis. I tend to underthink some of these studies and often I do not make connections to other studies.

I stopped eating grapefruit moths ago but I had not given a second thought to eating mandarin oranges. I am goig to rethink my dietary sources of Vitami C.

@lobotomize-me said in Random, interesting studies:

@Mauritio

Sodium butyrate increases seratonin

: Peripheral (gut) serotonin: In vitro and in vivo studies show that butyrate stimulates tryptophan hydroxylase‑1 (TPH1), the rate‑limiting enzyme for serotonin synthesis in intestinal enterochromaffin cells. Low concentrations of sodium butyrate (0.5–1 mM) increased TPH1 mRNA expression in human EC cells by 2.5–3.5‑fold; high concentrations (>2 mM) suppressed TPH1. A review notes that butyrate in the gut lumen can activate a zinc‑finger transcription factor (ZBP‑89) and stimulate serotonin production in enterochromaffin cells.

Central (brain) serotonin: In mice exposed to chronic unpredictable stress, sodium butyrate treatment alleviated depression‑like behaviours and increased brain serotonin (5‑HT) concentration and brain‑derived neurotrophic factor (BDNF) levels. A gene‑expression study in rats showed that sodium‑butyrate‑induced HDAC inhibition downregulated the 5‑HT₂A receptor in the brain and another study reported up‑regulation of 5‑HT₁A receptor mRNA when sodium butyrate was combined with estrogen therapy (data from behavioural tests) – suggesting receptor‑level modulation rather than direct synthesis of serotonin

SB prevented behavioural deficit made by CUMS
by raising seratonin and BDNF
https://pubmed.ncbi.nlm.nih.gov/26957230/

Increase seratonin under stress:
https://pubmed.ncbi.nlm.nih.gov/18817816/

https://pmc.ncbi.nlm.nih.gov/articles/PMC4396604/

"When mice were treated with antibiotics to deplete gut microbiota, serotonin levels dropped significantly.

Recolonization of the microbiota or administration of SCFAs restored normal 5-HT levels in the colon"

This means sodium butyrate could be the pathway, gut bacteria use to trigger serotonin production⬇️

https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2022.1035538/full

@Mauritio

So many studies, great!
Is this one been posted yet? (L. Reuteri as the sole factor in obesity?!)

Microbial Reprogramming Inhibits Western Diet-Associated Obesity
https://pmc.ncbi.nlm.nih.gov/articles/PMC3707834/

I am debating between going all the way with a yoghurt maker or just eating kefir, Sauerkraut and so on every day…

@pittybitty said in The artificial/accelerated aging effects of ultra-filtered sunlight:

Full spectrum light bulbs (aka grow lights) are quite easy to get

I find it easier to get sunlight than grow bulbs. 😉

Sunlight is much more intense than the light emanating from the bulbs. Grow lights are typically positioned very close the plants to get the best results.

The image in Fgure 4(d) posted above shows how rapidly the incandescent light fades from it source. I would expect the same from grow lights.
https://en.wikipedia.org/wiki/Radiant_intensity

Winndow pane glass filters the portion of sunlight that the body uses to make vitamin D. If you go outside for 10-20 minuts during the day you can make enough vitamin D.

The manufacturers of e-glass are charging a hefty premium for this specialty glass. I would expect that home buliders would not want to build using this glass.

@Mauritio said in Sirtuins, Klotho and Ray Peat:

Im courios what you guys think of that ?
@DavidPS I've seen you post about sirtuins from time to time.

I try not to overthink the effects of sirtuins. My posts about sirtuins have mostly been to support the effects of healthy foods. Here are my posts from the RPF.

https://lowtoxinforum.com/search/2681847/?q=sirtuins&c[users]=David+PS&o=relevance

Dr. Peat's quote about sirtuins needs to read in context. It may have been written many years ago. In addition, it does not distinguish which of the numbered sirtuins applies.

If Peat says sirtuins are bad because they block p53, the context matters here aw well.

Peatbot: P53 is a well-known tumor suppressor protein that plays a critical role in regulating the cell cycle and preventing cancer. It is often referred to as the "guardian of the genome" because of its role in maintaining genomic stability by preventing mutations. When p53 is functioning properly, it can help protect against cancer by repairing DNA or initiating apoptosis (programmed cell death) if the DNA damage is irreparable. However, mutations in the p53 gene can lead to a loss of its tumor-suppressing functions, which can contribute to the development of cancer.

C16.:0 Palmitic acid
C18:0 Stearic acid
C12:0 lauric acid or
C4:0 butyric acid or
C6:0 Caproic acid

Note: Some people could have allergy problem with stearic acid when suffering from leaky gut or border bross inflamed (stomach). When consumed on a regular base, from supplements, e.g.

It depends on the amount and the frequency. As a whole food or re-combined as a soluble vehicle when adding e.g. essential oils.
When you take it with food and not directly injected in the blood (fatty muscle leg or arm), is quite different.
I haven't the answer.
Edit: If you meant "does the mixture change the assimilation" when fluid, no. Up to 10 carbons, direct assimilation from the liver to the muscles (or in the Krebs cycle) (portal vein). Between 12-14, +/ half and half (half with VLDL and LDL vehicle). Higher carbon chains with these two last conveyors.

From ChatGPT (confirmation asked):
MCT oil is indeed utilized by muscles for energy, not just for the Krebs cycle in the liver. While MCTs are readily metabolized in the liver and can be converted into ketone bodies, they are also transported to other tissues, including muscles, where they can be directly used as fuel. This direct utilization contributes to muscle energy production and can potentially enhance muscle function and growth.

@LucH @wrl thanks for the interestng links.

Prebiotics Improve Blood Pressure Control by Modulating Gut Microbiome Composition and Function: A Systematic Review and Meta-Analysis (2025)

Results: Of the 3010 records screened, nineteen studies met the inclusion criteria (seven human, twelve animal). A random-effects meta-analysis was conducted on six human trials reporting post-intervention BP values. Prebiotics were the primary intervention. In hypertensive cohorts, prebiotics significantly reduced SBP (−8.5 mmHg; 95% CI: −13.9, −3.1) and DBP (−5.2 mmHg; 95% CI: −8.5, −2.0). A pooled analysis of hypertensive and non-hypertensive patients showed non-significant reductions in SBP (−4.5 mmHg; 95% CI: −9.3, 0.3) and DBP (−2.5 mmHg; 95% CI: −5.4, 0.4). Animal studies consistently showed BP-lowering effects across diverse etiologies. Prebiotic interventions restored bacterial genera known to metabolize DFs to SCFAs (e.g., Bifidobacteria, Akkermansia, and Coprococcus) and increased SCFA levels. Mechanistically, SCFAs act along gut–organ axes to modulate immune, vascular, and neurohormonal pathways involved in BP regulation.

110ba5d4-966b-4f7d-a2cb-6f51cf377aa4-image.png

Hi,
In my research on the effects of phytotherapy against inflammation in order to relieve pain, I found this. Boswellic acid from boswellia serrata is effective against these “agents”:
Board:
Tableau docx partiel.jpg
So effective against these agents.
Abréviations:
RA = Rhumatisme arthritique / Rheumatoid Polyarthritis (often calle « PR », in French)
PGE = Prostaglandines.
IL-1B = cytokine, mediator involved in particular in RA (destruction of cartilage/synovium).
TNF-a = facteur de nécrose tumorale alpha (cytokine, messenger involved in the inflammatory process).
MMP = matrice métalloprotéinase (MMP stands for enzymes that selectively hydrolyze peptide bonds and degrade structural proteins; they play a crucial role in the breakdown of joint tissues).
NF-kB = facteur nucléaire-kappa B (controls many genes involved in inflammation).
PLA2 = Phospholipase A2.
NO = monoxyde d’azote synthase (=>inhibited nitric oxide production).
LPS = Lipo-polysaccharides (immune reaction induced by an excess of bacterial residues destroyed by macrophages).
AO = anti-oxydant.
(x) => (moderate effectiveness) (if into brackets)
X? => A single source found. NB: Unchecked boxes only indicate that I have not found any "reliable studies" mentioning this action. We will complete this later, if possible...

See this post, on my forum, for analyze and comments:

Understanding the inflammatory response (AA cascade). Substances naturelles anti-douleur. Tableau
https://mirzoune-ciboulette.forumactif.org/t266-substances-naturelles-anti-douleur-tableau#15733
(update 04/2020) :
Comment: I’d combine Boswellia with Celadrin to target as much possible the other factors. These molecules only acts on inflammation, not on the pain.
Celadrin is a brand name and is made of “unsaponifiables”, often coming from of avocado and soy.
Lubricates joints. 350 mg 3X/jr.
Comment:
Don’t forget these molecules have to be taken in staples, with recovery periods, not to weaken the detox pathway Cyp450 (accumulation of toxins could happen, otherwise). So pause every 6 weeks, according to your feelings, as well.
Some substances have an impact on platelet aggregation, as well. E.g. curcumin and aspirin (white willow bark). Not Celadrin.
The body is able to manage and fight against pain, if not overburden. Need to be covered against oxidation, to preserve homeostasis (interaction). B6 PLP could be useful too but mind the side effects when overload. I associate 100 mg of each B1, B2, B3 niacinamide, B6 PLP + 500 mg TMG, but only 5 days a week, for 3 weeks. Then 2 weeks stop (to avoid problem with GABA when excess B6).

@Milk-Destroyer - Evidently, the study has its limitations.

Ideas like these keep disseminating:

"Each cell can only oxidize one substrate at a time."

"We know that both glucose and fats can't be metabolized at the same time."

Some have embraced the notion that the body can't oxidize multiple substrates at the same time. Others have sophisticated this notion to argue that the body can use them in combination, as indicated by gas exchange tests, but only in separate tissues. However, both perspectives still share the premise that different substrates can't be oxidized together within the same cell. Despite the tendency for one substrate to prevail and outcompete the other, a cell can oxidize a mixture of substrates simultaneously. Inhibitions can also vary in degree of severity.

PDHc is the most interferred enzyme set:

Carbohydrate refeeding after a high-fat diet rapidly reverses the adaptive increase in human skeletal muscle PDH kinase activity

3a9a3a13-0f5c-4f6c-8679-07e5abb44add-image.png

Skeletal muscle fuel selection occurs at the mitochondrial level

2179642d-22e9-486e-88a9-91aa177369c8-image.png

Despite differences in practice, only in support that their simultaneous catabolism is possible:

Chronic hyperglycemia reduces substrate oxidation and impairs metabolic switching of human myotubes

82caedb1-fc8a-446e-9bf0-18a18c847c3b-image.png

Related to the topic, the TCA cycle serves for both catabolic and anabolic purposes, with part of metabolites being diverted and lost, needing replenishment. Common fatty acids can't replenish these losses because they yield acetyl-CoA (2C), which adds carbons in equivalence to what's eliminated in a TCA cycle 'turn' (−2C), making the oxidation of fatty acids dependent on other substrates. In contrast, glucose can generate oxaloacetate (4C) and refill the TCA cycle beyond oxidative losses.

When oxaloacetate (from glucose) and acetyl-CoA (from fatty acids) combine, the product is treated indiscriminately, and parts derived from glucose are eventually oxidized. This allows glucose to sustain fatty acid oxidation through a direct derivative or indirectly through glycerol, lactate, and related molecules. It's the idea behind Jorgito Campo de Rosas' saying that "fats burn in the fire/flame of carbohydrates", which appears to have some validity. The dependency seems to become evident when the need to synthesize glucose is high, drawing from oxaloacetate and preventing acetyl-CoA from entering the TCA cycle. Otherwise, we would have to rely on amino acids as an alternative for replenishment. Cancer cells can exploit this relationship (notably with glutamine, but also glucose) to favor biosynthesis while maintaining TCA cycle function.

He bases a whole segment on the following assertion:

"What's stopping ATP citrate lyase (ACL)? What's pulling the CoA out of the cytosol so that the ATP citrate lyase doesn't have the COA it needs? Well, when you burn fats or when when you are oxidizing fats, the fats have a CoA group added to them to make an fatty acyl–CoA and then they are brought in as a fatty acyl–CoA into the mitochondria through carnitine palmitoyl transferase 1 (CPT-1). This CoA is added to the fats in the cytosol of the cell. So, essentially, the fatty acid oxidation is depleting the cytosol of the CoA. So ATP citrate lyase is unable to take the citrate and convert it to acetyl-CoA by adding the CoA group because there aren't the CoA groups available."

He's relying on a image whose author omitted reactions and, for some reason, also brought 'Acetyl-CoA Synthetase' and acetyl-CoA to the picture.

23ddba67-0bac-4e0b-a043-d2bc7531b1a4-image.png

When long-chain fatty acids are imported, the CoA is left behind for reuse:

c293c30c-2c31-4dab-8bed-94bfce87495c-image.png

Therefore, CoA isn't being "pulled out of the cytosol" as stated, quite the opposite: one of the functions of carnitine is precisely to preserve the cytosolic and mitochondrial CoA pools relatively stable, accepting the acyl groups to free up CoA for other purposes in the compartment of origin.

What could be argued instead: in fatty acid overload, the rate of attachment exceeds the release, and this could deprive cytosolic enzymes of CoA. Alternatively, that CPT1 inhibition prevents the release of CoA. But these are different lines of argumentation.

Miguel is a positive addition to discussions and is of good service to others. It's only unexpected to come across issues of this kind in a pretentious material titled "masterclass". In decades of authoring and despite being knowledgeable, it's difficult to remember any piece published by Ray with connotations of expertise, setting people up to be schooled by a master.

It's also unexpected that the video reproduces "a bunch of graphics" from other sources without any crediting. Sometimes it's challenging to trace the origin of certain images online, but not a single attribution can be found within the video, its description or comments section. Moreover, when the material is largely scripted from someone else's work, it doesn't hurt to give it a shoutout.