@Hando-Jin said in Just like SSRI “antidepressants”, talk therapy likely no better than placebo:

You just sit there and they hum and haw and write something down. Who knows what they are writing when they are the only ones allowed to see it.

R.D. Laing supposedly used and promoted lsd to help de-stress patients. I think it's proven LSD helps people socialize and feel social unity (it does). He also went on walks with them or had casual conversations. His books are worth taking a look at. He was I think as much against the new pharmaceutical approach as he was against mainstream psychotherapy. "Sane person in an insane world," I think was one of his lines about "mental illness." Because environment is a huge factor; every mind is within a body, every body within a community or space, so those connective areas need to be healed. (not sure if Peat mentioned Laing but I feel like he might have, it was pretty revolutionary stuff in the 60s-80s apparently).

@Mauritio XD

@LucH - Thanks again for sharing all of the detailed information from your forum. It is a great resource.

@LucH said in Endotoxin/LPS causes Alzheimer’s, insoluble fiber (carrot salad?) may prevent/treat:

How relevant are these elements to facilitate the elimination of LPS endotoxins after taking antibiotics or chemotherapy?

Every little bit helps.

I consider endotoxins to be an issue with aging and I have not thought about it much beyond that. There are no antibiotics or chemotherapy on my horizon.

Effects of Aging on Endotoxin Tolerance Induced by Lipopolysaccharides Derived from Porphyromonas gingivalis and Escherichia coli 2012
9a6bf360-092a-4e3f-8c92-fbc0372b8908-image.png

Aging Accelerates Endotoxin-Induced Thrombosis (2002)

49a08f3d-6131-4ea9-aa25-2beed872ae34-image.png

Impairments of intestinal arginine and NO metabolisms trigger aging-associated intestinal barrier dysfunction and `inflammaging
cbef08bc-1b87-4887-865b-d9086cb3a586-image.png

@jamezb46 Sounds good 👍🏻

@haidut said in Intermittent fasting causes hair loss by increasing lipolysis and fatty acid oxidation:

https://www.medicalnewstoday.com/articles/intermittent-fasting-may-slow-hair-growth-study

Not readable without giving total access to tracking and advertisers. Limited access not functional.
When I'm not allowed to see the whole study and where it comes from, I have it thrown away. Vertical classification (=> trash bin).

@CrumblingCookie aspirin is le good

@haidut Throwback to this classic thread: The Progesterone-like Action Of Testosterone And Other Androgens

@bot-mod said in Vaccines:

Fascinating specimen.

IMG_20250417_200610.jpg

"Autistic people contribute every day to our nation’s greatness."

How interesting.

I didn't hear anything wrong in Rob's comments personally. Toxicity could mean a lot of things.

@Corngold

Also going to link from this discussion on "high fat diet" https://bioenergetic.forum/topic/3990/high-fat-diet-triggers-memory-decline-within-days

Similar pattern as this study "Impact of a high-fat diet on the fatty acid composition of the retina" defines "high fat diet" as basically >60% mufa/pufa.

https://sci-hub.se/10.1016/j.exer.2020.108059

Mice in the chow diet had 10% fat, of which 47% was pufa and 30% was mufa, so almost 80% unsaturated fat. Mice in the high fat diet had roughly 30% sfa, 30% mufa, 30% pufa, also a majority unsaturated fat.

Conclusion:

In conclusion, the relative proportion of PUFAs, including essential fatty acids incorporated in the retina are modified by the consumption of a HFD, without impacting the amounts of the two major retinal LCPUFAs, AA and DHA. However, chronic exposure to a HFD led to several alterations among retinal SFAs, MUFAs and Pls, that could have deleterious consequences on retinal physiology.

So, once again, it seems that PUFA is the "good" fat, but "high fat diets" are bad.

It's reassuring to remember Ray's wisdom when reading through these types of papers with a sense of irony:

Retinal phospholipids also contain saturated FAs (SFAs, ~42% of total phospholipids in human) and monounsaturated FAs (MUFAs, ~19% of total phospholipids in human) (Acar et al., 2012). To our knowledge, no function that would be specific to the retina has been described for SFAs. Interestingly, a role of MUFAs in the visual cycle has been reported (Semenova and Converse, 2003; Xue et al., 2004).
MUFAs, and particularly palmitoleic acid (C16:1n-7), could also play a role in the protection of the retina from environmental stress (Gutierrez et al., 2016).

I mean, how does something that makes up 42% of the fat content of the retina serve "no function" ?

I also wonder about the Ling cell membrane ideas. Saturated fat seems to be the nebulous "other" here. Is its role being deliberately lied about?

And heres the AI offering a little help:

Functional Roles
Rhodopsin stabilization

SFAs and cholesterol interact with rhodopsin, stabilizing its inactive state in photoreceptor membranes.

Excessive SFA intake (e.g., from high saturated-fat diets) may rigidify membranes, impairing rhodopsin activation and phototransduction.

Membrane integrity

SFAs reduce oxidative vulnerability compared to PUFAs, as their single bonds are less prone to peroxidation.

In dietary studies, high SFA/cholesterol intake decreases retinal PUFA levels, altering membrane composition and potentially disrupting visual function.

Dietary and Pathological Implications
High-SFA diets: Linked to reduced retinal DHA content and increased risk of age-related macular degeneration (AMD).

Developmental roles: During retinal maturation, SFAs dominate early but are gradually replaced by PUFAs (e.g., DHA) to optimize photoreceptor flexibility and signaling.

Balance with Unsaturated Fats
While SFAs provide structural stability, excessive levels compromise the retina’s reliance on PUFA-driven fluidity, which is essential for:

Photoreceptor disk renewal

Efficient rhodopsin conformational changes

Antioxidant defense coordination (via PUFA-derived signaling).

Conclusion
SFAs in retinal phospholipids serve as structural stabilizers, but their benefits are context-dependent. Optimal retinal function requires a balance between SFA-mediated rigidity and PUFA-driven fluidity. Disruptions in this balance (e.g., from high saturated-fat diets) may contribute to degenerative diseases like AMD

Saffron can delay and treat macular degeneration (with no side effects).

abstract:
https://pubmed.ncbi.nlm.nih.gov/24819927/
full article:
https://sci-hub.se/10.1017/s0952523814000108

From the paper:

Chemically, saffron is known to contain more than 150 volatile and aroma-yielding
compounds and many non-volatile biologically active components, including carotenoids (zeaxanthin and crocetin) and various alphaand beta-carotenes. Its golden yellow-orange color comes from alpha-crocin, a water soluble beta-gentobiose (sugar) ester of crocetin. Its flavor arises from the glycoside picrocrocin, a molecule containing safranal and a carbohydrate. Its most potent antioxidant
ingredients appear to be crocin, and crocetin, a carotenoid dicarboxylic acid which forms the core of crocin. Several actions of
crocin on mammalian tissues have been reported including antiapoptotic activity and increased oxygen diffusivity (see Maccarone
et al., 2008 and Di Marco et al., 2013 ). Kanakis et al. ( 2007 )
showed that metabolites of saffron bind directly to DNA and induce
its partial conformation to beta-DNA, thereby protecting the cell
from damage. Saffron has been shown to have anti-infl ammatory
actions, including for example the inhibition of tissue necrosis
factor (Nam et al., 2010 ). Based on these observations, it is clear
that the saffron extract does not act as a simple antioxidant. The
peculiar characteristics of saffron components support the hypothesis that saffron has complex mechanisms of action ranging from
antioxidant activity to direct control of gene expression, as also
suggested by microarray experiments (Natoli et al., 2010 ).

I asked ai about saffron's role inhibiting lipid peroxidation:

Saffron inhibits lipid peroxidation through multiple mechanisms involving its bioactive compounds, particularly safranal and crocin, which counteract oxidative stress and protect cellular membranes.

Direct Antioxidant Activity
Free Radical Scavenging: Safranal, a key component of saffron, neutralizes reactive oxygen species (ROS) by donating hydrogen atoms or electrons, preventing ROS from initiating lipid peroxidation in polyunsaturated fatty acid (PUFA)-rich membranes. Its conjugated structure enables efficient quenching of singlet oxygen through energy transfer.

Enhancing Endogenous Antioxidants: Saffron increases levels of glutathione (GSH) and activity of antioxidant enzymes like superoxide dismutase (SOD) and catalase, which degrade peroxides and superoxides before they damage lipids.

Inhibition of Pro-Oxidant Pathways
Arachidonic Acid Metabolism: Saffron reduces malondialdehyde (MDA), a byproduct of lipid peroxidation, by suppressing arachidonic acid oxidation pathways in platelets and other tissues.

Enzyme Interactions: Molecular docking studies suggest safranal binds to enzymes like collagenase and hyaluronidase, potentially interfering with oxidative cascades that exacerbate lipid peroxidation.

Protection in Biological Systems
Neuroprotection: In animal models, saffron mitigates lipid peroxidation in brain tissues by restoring antioxidant enzyme activity and reducing MDA levels, critical in PUFA-rich neural membranes.

Platelet Membrane Stabilization: Saffron extract inhibits iron-ascorbate-induced lipid peroxidation in platelet membranes, preserving membrane integrity.

These mechanisms collectively highlight saffron’s role as a natural antioxidant, targeting both ROS and downstream peroxidation processes in lipid-rich environments.

Might be estrogenic

https://www.google.com/url?sa=t&source=web&rct=j&opi=89978449&url=https://pubmed.ncbi.nlm.nih.gov/34513331/&ved=2ahUKEwiisrat4tSMAxUewAIHHeTANO0QFnoECFEQAQ&usg=AOvVaw3GtS2so9cXbHJlzOKtETcO

https://www.google.com/url?sa=t&source=web&rct=j&opi=89978449&url=https://pubmed.ncbi.nlm.nih.gov/35267929/&ved=2ahUKEwiisrat4tSMAxUewAIHHeTANO0QFnoECEkQAQ&usg=AOvVaw2S_OChJ53PYXOk2OqA2ECW

Very interesting new study on protein restriction in humans.
They looked at high carb,low protein and high fat low protein .

What they found:

Low protein (8%) :

Increases metabolism by about 20%

Does NOT matter if you do high carb, low protein or high fat low protein. Both increase metabolism by 20%

When high protein diet resumes, meatbolism and FGF21 goes down

Quickly increases FGF21.
63% within 90 minutes of a low P-meal

Increases metabolic rate after only 3h

No muscle loss after 5 weeks of low protein

No change in free T3 and noradrenaline

Insulin sensitivity seems to be equal on high carb and high fat diet

Electron transport chain proteins and OXPHOS proteins were upregulated, while ATP synthase was downregulated, suggesting a "wasting"/ uncoupling of energy.
Although UCPs were not upregulated.
All of this downstream from FGF21 upregulation. FGF21-KO mice did not show changes in ETC and OXPHOS proteins.

Limitations/Remarks:

The high fat diet was not a ketogenic diet. It still contained 40% carbs!

The high carb diet was not a low fat diet. Still contained 21% fat.

So maybe the results would have been even better with a high carb, low protein, low fat diet. Leveraging the randle cycle.

Other studies showed that the deciding amino acids are methionne and cysteine (and maybe Tryptophan)
The absolute amount of methionine was very different on high carb (~2.5g) vs. the high fat diet (~1g) . Making the comparison less fair.

In any case it seems clear now that you can loose weight/ increase metabolism on a non-ketogenic high fat-low protein diet, which I wasn't convinced of before.

"...to prevent weight loss, it was necessary to increase energy intake consecutively in the following weeks of the LPHC intervention, and at the end of week 5, energy provision was increased by 19% (2.4 ± 0.8 MJ) in the LPHC diet (Fig. 2g). This increase in energy intake was accompanied by a 270% elevation in fasting plasma FGF21 levels at week 5 compared with pre-intervention (Fig. 2h). The increased energy intake was not attributed to alterations in physical activity level,..."

https://pmc.ncbi.nlm.nih.gov/articles/PMC11946896/#Sec2

@Mauritio thanks for the update. Looking forward to when you have the opportunity to do more!