Posts made by Mauritio

@DavidPS makes sense since it's so anti cortisol .

@Ecstatic_Hamster I've been wanting to try LDN for a long time . Is there anywhere we can read about people's experience with it ?

Peat has often talked how important thymus health is and how in old people the thymus is often non existent anymore due to stress.
Here's a few strategy's to fix it:

1. Vitamin B3 rescues thymus weight by increasing NAD+ and Sirt6. Also prevents hepatosteatosis.
   https://pubmed.ncbi.nlm.nih.gov/28536482/

2. The number of serotonin synthesizing cells in the thymus increased as we age. I wouldn't be surprised if there was a causative relationship here.
   https://pubmed.ncbi.nlm.nih.gov/19827686/

3. This study shows causative relationship on serotonin causing thymus involution.

"Administration of serotonin or 5-HTPH causes a marked reduction of the thymus weight. It is reasonable to postulate that the described effects result from the thymus involution..."
https://pubmed.ncbi.nlm.nih.gov/6967931/

4. T4 can stop thymus involution and be anabolic to it, even at old age.

"...thymuses from T(4)-treated aged mice revealed that the cortex was preferentially enlarged and repopulated with immature thymocytes. "https://pubmed.ncbi.nlm.nih.gov/16684146/

5. Zinc deficiency can cause thymus atrophy.
   https://pubmed.ncbi.nlm.nih.gov/20860857/

6. Spermidine and even more so Spermine stop glucocorticoid induced thymus apoptosis.
   https://pubmed.ncbi.nlm.nih.gov/1649056/

@LetTheRedeemed interesting . Did you notice any other effects from it ?

Azithromycin might have interesting anti-aging effects. It targets senescent cells very effectively and without targeting healthy cells. The effect is concentration dependant though .

"Azithromycin preferentially targets senescent cells, removing approximately 97% of them with great efficiency. This represents a near 25-fold reduction in senescent cells."

"Azithromycin, at 100 μM, had no effect on the viability of normal MRC-5 lung fibroblasts, but selectively killed only senescent MCR-5 fibroblasts."

"Neither drug showed any significant effects on viability at 50 μM, indicating that the effects we observed were concentration-dependent."

https://pmc.ncbi.nlm.nih.gov/articles/PMC6286845/

Another macrolide antibiotic Azithromycin also inhibits mTOR according to these studies:

https://pubmed.ncbi.nlm.nih.gov/34600916/
https://pubmed.ncbi.nlm.nih.gov/37633240/
https://pubmed.ncbi.nlm.nih.gov/30334401/

Although there is one study that said it didn't have an effect on mTOR:

https://pubmed.ncbi.nlm.nih.gov/39284999/e

In light of this thread, the findings of this old thread by haidut are even more interesting.

https://lowtoxinforum.com/threads/gut-bacteria-overgrowth-drives-cocaine-addiction-glycine-can-reverse-it.48285/

@yerrag
Yes, although this study shows rapamycin has thymus weight lowering effect in mice. Although there was clearly a dose dependant effect and the HEDs were like 15-60mg per day which is really high, so I'm not sure if there would be any such effect if you were to take just 1-5mg / week .
So the weekly dose of this study was about 30-100 times higher than what most humans take.

https://pmc.ncbi.nlm.nih.gov/articles/PMC9360838/

@yerrag definitely. I think it has benefits because of endotoxin reduction and reduction of toxic chemicals.
But the mTOR activation and high amounts of methionine and cysteine are definitely an issue.
Large amounts of gelatin might protect to some degree. But the studies on rapamycin and methionine restriction are so obvious and many that I don't think theres a way around this.
It always leads back to a high carb diet.

@Lejeboca said in Strong Sistas finally posted an interview with Dr. Ray Peat - The Basics Of Pro-Metabolic:

@yerrag said in Strong Sistas finally posted an interview with Dr. Ray Peat - The Basics Of Pro-Metabolic:

I've been wondering why in one of his last newsletters Ray would say that when the body is in the process of drawing calcium from the bones, in an osteoclastic process, it cannot be at the same time in a full optimal mitochondrial respiratory mode where among other things CO2 is being produced.

From this paper Calcium paradox disease: Calcium deficiency prompting secondary hyperparathyroidism and cellular calcium overload
in Page 7:

Mitochondria are conspicuously affected by
Ca overload [151]. These organelles have the capacity
to store significant amounts of Ca in the form of biologi-
cally inactive amorphous calcium phosphate, but when
their buffer capacity is overtaxed mitochondrian physi-
ology is disrupted with severe reduction of oxidative
phosphorylation, resulting in an ATP deficit that in turn
diminishes the effectiveness of the Ca pump with fur-
ther cellular Ca overload. Elevation of [Ca] stimulates
Ca-activated neutral protease [7,8] and phospholipases
[6], affecting the pathophysiological process of muscu-
lar dystrophy [152] and other diseases characterized by
cellular Ca dishomeostasis [146]

That sounds like a good answer to yerrags question above. We don't want intra-cellular calcium.

@Epik this guy gives a great answer at 51:22

Rapamycin dampens excessive sterile inflammation that is often present unnecessarily in old age.

While cortisol has a strong short term anti-inflammatory effect as well, it is disastrous for the body in the long run.

https://youtu.be/_vsNw-OCciU?si=0N8V-Bdlhelu7iUo

Rapamycin, fisetin and other anti-aging compounds (but not Metformin) help with stem cell formation .

https://pubmed.ncbi.nlm.nih.gov/21615676/

It increases dopamine .

"MPTP-induced reduction of dopamine contents in the striatum and hippocampal CA1 region was improved by nobiletin administration (50mg/kg i.p.). Acute intraperitoneal administration of nobiletin also enhanced dopamine release in striatum and hippocampal CA1,..."

https://pubmed.ncbi.nlm.nih.gov/24316474/

NOB could restore memory impairment via the improvement of neurogenesis by ameliorating neuroinflammation in the hippocampushttps:

//pmc.ncbi.nlm.nih.gov/articles/PMC10181043/

Nobiletin increases testosterone and lowers estrogen.

In this in vitro study nobiletin increases testosterone:

"Furthermore, we found that these compounds enhanced testosterone production via cyclic AMP (cAMP)/cAMP response element binding protein signalling. In particular, the compounds inhibited activation of phosphodiesterase and thereby increased production of cAMP. These findings support the possibility that K. parviflora extract, 5,7-dimethoxyflavone, and nobiletin may mitigate age-related disease and hypogonadism by enhancing testosterone production."

https://www.researchgate.net/publication/306926144_Effect_of_Kaempferia_parviflora_extract_and_its_polymethoxyflavonoid_components_on_testosterone_production_in_mouse_testis-derived_tumour_cells

Nobiletin lowers estrogen by inhibiting aromatase.
https://pubmed.ncbi.nlm.nih.gov/28177754/

Another take away from this interview was the exact mechanism by which calcium helps with heavy metal toxicity. It's about PTH, which makes the body retain heavy metals, so by consuming calcium (and thus lowering PTH) you stop accumulating heavy metals.

So by using that logic, Vitamin D and K should also be anti-heavy metal.

Another nutrient that keeps coming up when talking about heavy metals is selenium.
Not only does it protects from oxidative stress, caused by heavy metals, it also binds with heavy metals forming less toxic, more excretable -selenite molecules.

Here, selenium deficiency has been shown to double PTH levels:

"This group had a 2-fold increase in parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] in plasma."

https://pubmed.ncbi.nlm.nih.gov/11499879/

That is such an interesting comment on the benefits of blood donation.
Does anbody know more about that?

He talks about it at about 4:58

"Besides getting rid of the iron, as you start aging there are signals like exosomes or extra-cellular vesicles that carry information that excelerates aging and if you just get rid of those, you are tending to reverse the aging process"

From what Ive read these exosomes can carry inflammatory cytokines like TNFa or IL-6 and others. But they can also carry the so called senescence factors (SASP), which create a circle of contionous inflammation.

So in that sense donating blood works against senscent cells and inflammation, which are two main cotributors to the aging process.

@yerrag said in Glycine is an anti-biotic, restores sensitivity to antibiotics:

@Mauritio said in Glycine is an anti-biotic, restores sensitivity to antibiotics:

@yerrag This study suggests that lowers the GSH/GSSG ratio, causing oxidative stress in the cell.

"More specifically, in Vibrio alginolyticus and Escherichia coli, exogenous glycine promotes oxidation of GSH to GSH disulfide (GSSG), disrupts redox balance, increases oxidative stress and reduces membrane integrity, leading to increased binding of complement."
https://www.sciencedirect.com/science/article/pii/S2213231722002841

The body has the wisdom to know of using glycine to turn the redox ratio against pathogens to kill them by oxidative stress? Awesome. What part of the immune system is involved. eg white blood cells, peptides etc?

I guess it'd similar to how quinones work. They also have a pro-oxidant effect.

@Sunniva it's linked in the post you quoted

Does anybody know if these shielding devices actually work?
I read that they might also reflect the EMF back upwards which is bad as well.

https://defendershield.com/defenderpad-laptop-radiation-heat-shield?ref=emfa

I returned both of the above laptops and settled for a 16" Lenovo Chromebook.
It has higher EMF readings than my 14" Lenovo Chromebook, but it's stil ok .

Next step is to buy a e ink tablet and a protection device for the laptop .