@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
