I don’t even gain weight on them, even when it’s 2500 calories of MUFAs in one day. After getting a CGM, I’ve replaced fruit with more nuts => it increases my calorie consumption and I wonder if there’s a tradeoff in SOME WAY when MUFAs don’t seem to increase any of the normally “bad” biomarkers in any of the studies…
Thebigger concern might be elevated triglyceride levels? (postmeal even if not fasting)
Free-roaming Fats, Oxidative Stress, Inflammation, and the Effects of AGEs
Several common symptoms of metabolic disorders, which often exacerbate each other, could also accelerate cognitive decline.
Dyslipidemia
Dyslipidemia is an imbalance in the various fats found roaming in the blood. Triglycerides become particularly elevated in metabolic syndrome and have been associated with cognitive impairment. In mice, these fats crossed the blood-brain barrier and triggered leptin and insulin resistance, which increased appetite and reduced cognition. Lowering their blood triglycerides reversed these effects, presenting a potential path to alleviate cognitive impairment and improve weight loss in people with obesity.
You can of course still gain body fat from eating nuts, but it would take a lot of work because they’re good at decreasing appetite and the fats contained in whole nuts aren’t absorbed nearly as well as when the nuts are ground into nut butter.
Other than calories (which I don’t worry about too much for the above reasons), IMO the most important thing is to eat raw nuts whenever possible, since roasted nuts are higher in advanced glycation/lipoxidation end products. Roasted nuts also are high in antioxidants and other goodies, so they’re probably still overwhelmingly health-promoting, but I’d prefer to cut out AGEs whenever possible, so raw nuts have the best of all worlds!
I’ve wondered about this too because of the recent negativity towards seed oils. If seed oils are unhealthy, then perhaps the nuts that contain them are as well?? Perhaps most of the negative effects of seed oils are due to their lower heat point. I actually haven’t seen a convincing study regarding this, even though I’ve recently been avoiding seed oils.
Perhaps MUFAs are indeed the distinguishing factor?
When it comes to omega-3 v.s. omega-6 nuts are still heavily skewed towards omega-6. And many nuts are way up the list in both omega-6 vs. omega-3, as well as percent of omega-6 Fatty acid ratio in food - Wikipedia
I still haven’t been able to make too much sense of this literature apart from that supplementing omega 3 is helpful, and that one may want to take the heat points of the oils into account while cooking.
Nuts still have saturated fat (even if not THAT much). It still adds up if you eat 1500 calories of nuts per day.
And that can elevate LDL cholesterol. Mine are not terribly elevated, but like, on careful examination of the data (after controlling for confounders), more LDL is not necessarily a good thing (though you’d have to go to small lipoprotein sizes like Lp(a) to see the type that really matters). HDL is elevated too but it’s unclear if HDL is even “good”
I’m not expert on the cholesterol literature, but fyi, I have recently heard multiple people say that rather than the pure LDL numbers the following are more informative when it comes to signalling cardiovascular risk:
a) Triglycerides to HDL ratio
b) LDL-C numbers
I also went into a bit of a rabbit hole about purported benefits of stearic acid which is a saturated fat.
My hypothesis is that we are probably dealing with very simplistic categories of saturated fat v.s. MUFA v.s. PUFA , and more research is needed to understand how different specific fatty acids affect our metabolism. With that said I do try to lean towards having more MUFA — I made keto brownies yesterday with avocado oil lol.
as far as cholesterol, the biggest thing that seems to matter for risk is apob (particle count). in other words, how many particles are floating around, as opposed to the volume.
LPa is generally genetic, and does not get effected by what you eat in any meaningful way
raw unsalted nuts, should not effect your particle count
I personally find, that i dont eat nearly as much nuts, if they are raw and unsalted.
if you are eating them salted, is a different situation. too much salted will be converted into fructose, which is not good.
10% of the fat of macademias is saturated (keto ppl LOVE macademias, but really, there’s not much basis in health for this, also ppl under keto even generally have fasting glucose levels that are not too far below those of others)
1/15 of the fat of almonds is saturated
pecans (which keto ppl also like) have higher saturated percent than almonds.
Say all you want about the saturated vs unsaturated debate, but saturated fats do increase hypothalamic microinflammation and ROS (though it’s TYPE of saturated, and whether odd-or-even chained, that also matters [eg palmitic acid is way worse than stearic acid]
We identified seven trials with 15 comparisons of the effect of saturated fat (SFA) replacement on Lp(a). While replacement of SFA with carbohydrate, monounsaturated fat (MUFA), or polyunsaturated fat (PUFA) consistently lowered low-density lipoprotein cholesterol (LDL-C), heterogeneity in the Lp(a) response was observed. In two trials, Lp(a) increased with carbohydrate replacement; one trial showed no effect and another showed Lp(a) lowering. MUFA replacement increased Lp(a) in three trials; three trials showed no effect and one showed lowering. PUFA or PUFA + MUFA inconsistently affected Lp(a) in four trials. Seven trials of diets with differing macronutrient compositions showed similar divergence in the effect on LDL-C and Lp(a). The identified clinical trials show diet modestly affects Lp(a) and often in the opposing direction to LDL-C. Further research is needed to understand how diet affects Lp(a) and its properties, and the lack of concordance between diet-induced LDL-C and Lp(a) changes.
Moreover, mono-unsaturated fatty acids were shown to extend the life span in C. elegans mediated by H3K4me3 modifiers [283]. High glucose levels negatively affect lifespan and induce age-related maladies such as diabetes. Accordingly, glucose restriction can be expected to extend life span as suggested from studies in human fibroblasts that demonstrate glucose restriction-induced DNA methylation changes and histone modifications targeting for instance hTERT and p16 expression [284]. As stated before, a link between glucose metabolism and epigenetic aging was also found in drosophila
An isocaloric moderately high-fat diet extends lifespan in male rats and Drosophila
the enzymatic catalyzing component showed that cellular fatty acid storage (viz. triacylglycerol synthesis), FAO, pyruvate metabolism, branch amino acid metabolism, tricarboxylic acid (TCA) cycle, and oxidative phosphorylation were all elevated in the CENs (Figure 3c). Consistently, in the secretory and demand components, we found that the CENs released more carbon dioxide and fewer TCA intermediate metabolites (Figure 3e).
@InquilineKea It doesnt mean high-fat is good in a ideal situation. Mice are fed refined kibble probably so its not a ideal situation to begin with. In Okinawa (one of the longest lived populations) the ancestral diet had only 6% fat , and 85% carbohydrate. But it was carbs like SQUASH not CRACKERS.
I do think fresh MUFAS in moderate amounts is good , not high amounts though
Well excess free fatty acids also destabilize the lysosomes over time (esp LAMP2A). again, relationship with circulating TG oleic acid is unclear
But the cell seems to be better able to buffer itself against excess lipids than against excess glucose! All because of Seipin/Spartin! (both highly expressed in brain)
Neither DGAT1 nor DGAT2 is singularly essential for TAG synthesis or droplet formation, though mammalian cells lacking both cannot form lipid droplets and have severely stunted TAG synthesis. DGAT1, which seems to prefer exogenous fatty acid substrates, is not essential for life; DGAT2, which seems to prefer endogenously synthesized fatty acids, is.[17]
