sirtuin

I'm curious to hear more thoughts on the DHEA aspect of this study. From what I've read, DHEA seems to increase estrogen in men. Is this not the case with lower dosages and different forms (7-Keto?) I've also read that it can lower HDL and might be associated with prostate cancer risk. In other studies, I read "we found that DHEA increases this critical process of cholesterol accumulation in macrophages -- an event which may produce coronary disease." Anecdotal reports include increases in irritability and decreased libido. Digging around on LifeExtension, I found this article: https://www.lifeextension.com/magazine/2007/6/cover_dhea/page-01 I'm not quite sure what to make of this particular hormone available for OTC supplementation.

Here's a recent study comparing an olive oil rich diet vs a low-fat diet, specifically looking at flow mediated dilation with a dose-dependent improvement: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586551/figure/nutrients-07-05356-f005/ Here's another looking at a low-fat diet vs the oil-inclusive diet: https://www.ncbi.nlm.nih.gov/pubmed/19632695 To contrast, here's the % change in FMD in 3 types of carbohydrates with a dose-dependent worsening: http://www.onlinejacc.org/content/53/24/2283/F3 I'm not here to make the argument that olive oil inclusive diets may improve FMD over whole food based low-fat diets, but the data can swing either way you want to swing it. I think it's worth mentioning that olive oil is largely used as a way to sustain life on a higher consumption of lower-calorie (higher polyphenol / micronutrient) vegetable matter than might otherwise be possible in place of sugars and starches. It's not like it's just being consumed in isolation. While examining the mechanics of a cold press manufacturing process, it feels to me like it's less extreme than say, making tofu or any sort of soy-based milk product. If you're having an arugula salad with beetroot and olive oil with 100% cacao and green tea after a dip in the sauna, how bad is endothelial function going to look compared to say, consuming a high-glycemic bowl of rice? How tofu is made: How olive oil is made: It's debatable to me whether an unbiased look at olive oil would see the plant's traditionally-consumed polyphenol-rich oil fraction as standing closer to the health food spectrum's bottom end of deleterious processed foods, or something more akin to a superfood extract on top. Arguing for supreme whole olive fruit superiority over earlier harvested olive oil isn't too unlike arguing against brewed stone-ground matcha green tea as some hypothetically harmful man-made toxin while placing the green leaf itself from which it's extracted in a different light - it's bordering on an unnecessary level of theoretical dietary optimization in the context of modern peer-reviewed scientific journal research. In many of these studies, the olive oil inclusive foods like basil-rich neon-green pesto look at least as heart-healthy as say, a baked potato. It's further debatable to me whether or not it would be more nutritious to trade some of that raw basil leaf infused-oil with fresh-squeezed lemon juice and raw garlic for a more oxidized, more mature chunk of just... well, olive, or a handful of say, oat. It is my suspicion that the foods the oil becomes incorporated within do often produce healthier, better tasting meal options than might be achieved through the lone individual components.

It is interesting when you look on pubmed for olive oil studies. In most of the literature, something like wild salmon with watercress and high-polyphenol olive oil looks every bit as much of a health-promoting food as say, a big bowl of brown rice with tofu and oat milk like Esselstyn might recommend. It certainly does not come off as any sort of cardio-hazard. The amount of new medical data being published is astounding -- these guys went to school so long ago, I wonder if they may have reached entirely different opinions in this current environment. Imagine trying to explain to a 1950's Esselstyn how to perform a basic CatBoost decision tree analysis or run a deep learning model on a heart disease dataset to collaborate with thousands of experts across the planet on the regression problem... when these guys were learning their craft, our technical prowess as a society was at about GameBoy-level (or, I suppose 20 prior to the advance to Pong-level data research skills in Esselstyn's case.) Here's one new article just from 3 weeks ago that will conduct a double-blind randomized cross-over trial with healthy adults. https://www.ncbi.nlm.nih.gov/pubmed/30997730 In an article published this month, grains were seen to be a negative cardio risk factor of the Mediterranean diet, while the oil was seen as protective. https://www.ncbi.nlm.nih.gov/pubmed/30946700 Or, in this preliminary data from the AUSMED Heart Trial, the olive oil-rich diet seemed to outperform the Low-Fat Diet Intervention. https://www.sciencedirect.com/science/article/pii/S0899900718306853

This was an interesting recent article published in the journal Atherosclerosis this year: http://www.atherosclerosis-journal.com/article/S0021-9150(15)30192-1/abstract TMAO slows aortic lesion formation in this mouse model and may have a protective effect against atherosclerosis development in humans. Surprisingly, and independently from treatment group, TMAO levels inversely correlated with aortic lesion size in both aortic root and thoracic aorta. Looking at egg consumption in ApoE4 carriers, which have a higher pre-disposition toward heart disease and alzheimer's via poor lipid metabolism: http://ajcn.nutrition.org/content/early/2016/02/10/ajcn.115.122317.abstract Egg or cholesterol intakes were not associated with the risk of CAD. Each 1 additional egg (55 g)/d was associated with a multivariable-adjusted HR of 0.93 (95% CI: 0.50, 1.72) in the ApoE4 carriers. Each 100-mg/d higher cholesterol intake was associated with an HR of 0.95 (95% CI: 0.73, 1.25) in the ApoE4 carrier. The study found that a high intake of dietary cholesterol was not associated with the risk of incident coronary heart disease -- not in the entire study population nor in those with the APOE4 phenotype. Moreover, the consumption of eggs, which are a significant source of dietary cholesterol, was not associated with the risk of incident coronary heart disease. The study did not establish a link between dietary cholesterol or eating eggs with thickening of the common carotid artery walls, either. Looking at the lack of an association of egg consumption and calcified atherosclerotic plaque in the coronary arteries: http://www.ncbi.nlm.nih.gov/pubmed/25642410 There was no association between frequency of egg consumption and prevalent CAC. Odds ratios (95% CI) for CAC were 1.0 (reference), 0.95 (0.66-1.38), 0.94 (0.63-1.40), and 0.90 (0.57-1.42) for egg consumption of almost never, 1-3 times per month, once per week, and 2+ times per week, respectively. In that study, the more eggs were eaten, the lower the risk was for calcified plaque in the arteries. http://www.ncbi.nlm.nih.gov/pubmed/23880191 The consumption of more than one egg per week was associated with a lower coronary atherosclerotic burden. You can basically drown a rat in dietary carnitine and you don't see any increase in vascular disease... or, fed to rabbits, it can reverse atherosclerosis. There also doesn't seem to be an association of choline intake and cardiovascular disease in humans -- in fact, the best way to elevate TMAO is to feed seafood to a person, which lowers heart disease to a greater extent than a vegan diet. Choline consumption is associated with improvements in cognitive function, hepatic lipid metabolism, and DNA methylation. I'm not completely sold on the low choline / low carnitine / low egg diet, for fear of TMAO. I've read that resveratrol + PQQ + garlic can help with gut remodeling to limit TMAO production, all 3 of which I currently supplement. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782876/ There is an immediate need to increase awareness among health professionals and consumers of choline as an essential, but currently suboptimal, nutrient, and further, to highlight the critical role it plays throughout life, especially for pregnant and lactating women. New analysis of NHANES data indicates that for the majority of the population choline consumption is far below current dietary recommendations. Increasing awareness of the pervasiveness of suboptimal choline intakes must become the focus of public health efforts in order to promote optimal health. Education regarding the richest food sources of choline can assist in reaching this goal. Paul Jaminet has an interesting write-up on the TMAO scare: http://perfecthealthdiet.com/2013/04/lessons-from-the-latest-red-meat-scare/ How Does TMAO Produce Atherosclerosis? The explanation offered by the Hazen group is that TMAO suppresses “reverse cholesterol transport” conceived broadly as the process of migrating excess cholesterol out of macrophages for transport to the liver and excretion in feces via the bile. Basically, the idea here is: Atherosclerosis begins with metabolic syndrome, a state characterized by high LDL levels and caused by endotoxemia (high levels of endotoxins entering the body from the gut). As we’ve discussed (“Blood Lipids and Infectious Disease, Part II,” July 12, 2011), LDL particles have an immune function. They are oxidized by microbial cell wall components. The resulting oxLDL particles are taken up by macrophages, which then present the microbial cell wall components to other immune cells for antibody formation. Endotoxemia initiates the process of atherosclerosis by (a) poisoning the liver to cause metabolic syndrome which raises LDL levels, and (b) oxidizing LDL – since endotoxins are bacterial cell wall components that can oxidize LDL – and driving the oxLDL into macrophages. After macrophages have separated the microbial cell wall components from their accompanying LDL particle, the cholesterol and fat have to be exported to keep them from building up in the cell. If cholesterol and fat cannot be exported quickly enough, the macrophage is injured and becomes a “foam cell.” Disabled foam cells accumulate in specific locations and form atherosclerotic plaques. TMAO suppresses bile acid creation, reducing the excretion of cholesterol from the body and leading to higher LDL levels and a greater likelihood that macrophages will become foam cells. If this is true, then TMAO is not intrinsically atherosclerotic. TMAO in blood only becomes atherosclerotic in the context of metabolic syndrome brought on by endotoxemia. What causes endotoxemia? A dysbiotic flora generated by a diet high in sugar, flour, and omega-6 fats Looking at oxLDL and metabolic syndrome: http://www.ncbi.nlm.nih.gov/pubmed/23021013 Egg consumption was associated with lower oxLDL and improvements in inflammatory markers, lipid profiles, and insulin sensitivity. Higher dietary cholesterol seems to increase bile acid creation.

It seems like I've read that the DRI for protein is around 56g for men and 46g per day for women. At close to 100 grams of protein per day with 3,000+ calories and 500+ grams of carbohydrates, this seems a bit like a High Protein / High Calorie / Very High Carbohydrate diet, which you're eating via High Glycemic Load / High Volume / High caloric meals containing several hundred of grams of sugar and Stupid High amounts of polyunsaturated fats between hours of daily chronic cardio (burning carbohydrates?), while sitting at a low BMI (Low muscle mass / Low lean mass?) This seems like a bit of an unusual approach to calorie restriction. I suppose the goal here is to create a high level of hormesis and reactive oxygen species and create a caloric deficit by ramping up oxidation?

I picked up some Natto today, after thinking about this post. Crazy looking stuff. It looks like this stuff is usually served as a live culture (acidic?) on top of styrofoam -- I wonder if there are any health issues there? https://en.wikipedia.org/wiki/Polystyrene#Health

Just to clarify, you're saying eating once or twice a day might be actively harmful (priming the liver for hypertriglyceridemia) and that eating several times (3-5x + snacks?) might be a healthier approach No, I'm saying the reverse. The comment about spacing was in response to your suggestion (which I snipped in my reply but have now restored" that "it might actually be healthier to eat several times and snack throughout the day, from soon after waking to just before bed, rather than to spend most of the time fasted and try to eat this as part of large meals." To the contrary: it takes 3-5 hours for your body to work its way thru' the postprandial state, during which the various organs are still being stimulated with insulin and the liver is still producing TG in response; it's more prudent to consume meals late or following the completion of that cycle than to be continuously re-priming the liver. That could be done as one daily meal or several, with meal size varying accordingly, but continuous snacking is imo imprudent. Got it, thanks for the great information and resources to further digest!

Just to clarify, you're saying eating once or twice a day might be actively harmful (priming the liver for hypertriglyceridemia) and that eating several times (3-5x + snacks?) might be a healthier approach for better longterm cardiovascular / metabolic health and insulin / leptin signaling? In trying to reduce triglycerides, my thoughts have been that spending more time fasted would reduce serum levels, and I feel like eating less often makes me less hungry (as my meals are more satiating and ketones are elevated in the fasting window.) My thoughts are that timing micronutrients / caloric intake around exercise might promote higher stores of lean muscle mass.

Here are the values for today, the first completely logged day: Sucrose 11g Fructose 34g Glucose 18g Sugar 78g I hope it's the ratio you were interested in rather than the absolute amounts, since today my calories were subnormal as I was too busy to eat much. My first thoughts here are "wow, I'm often eating more sugar / fructose than a fruitarian?" I think weekly averages are probably more useful for analysis. There's a weird effect when calories drop down -- low carb diets can start to look like low fat diets, or high-sugar diets might look low in fructose. Apparently the average American eats around 82 grams of added sugar per day.

I was referring to those articles Dean reviewed, where the fruit servings (sugar by calories, usually eaten raw and low in fat) had mortality lowering benefits as low as any legume / vegetable serving, if not often lower than carbohydrate calories from starches / non-starchy vegetables (cooked, often with fat.) I love eating non-starchy vegetables, but there's not much energy there until drizzled with an oil or eaten with another food that provides calories.

I haven't had an NMR or VAP test. I don't feel much of a need based on my latest bloodwork. More specifically, my A1C is normal (5.2, RR 4.8-5.6), my triglycerides are low (46 mg/dL) and well below my HDL (62 mg/dL). Without NMR or VAP, I don't have info on LDL particle count or size. But at 61 mg/dL, my LDL is lower than my HDL, and my total cholesterol was 132 mg/dL. I'd say I'm at pretty low risk of CVD, despite (or perhaps more accurately, because of!) the preponderance of fruit in my diet. --Dean Very nice! With LDL down under HDL and low trigs, you should be most excellent there. So, at 30% fruit in your diet does this work out to something like 100+ grams of sugar per day (50+g of fructose?) Which fruits are the largest contributors to your fruit calories? It looks like fruit supplied around 39% of my calories yesterday, providing around 20.3 grams of fructose, 20 grams of glucose, 5.1 grams of sucrose, 29.3 grams of fiber, and 43.4 grams of fat.

Excellent information, as usual. Thank you for the detailed response. So, it sounds like it ultimately boils down to calories in vs calories out averaged over some timeframe. The optimal eating window / meal frequency / macronutrient cycling is the one that allows an individual to most comfortably lower their body mass and decrease thyroid activity / metabolic rate / overall caloric intake. If I'm interpreting this correctly, then assuming health biomarkers aren't out of range, a calorie-restricted diet rich in saturated fat, fructose, and sugar from nutritious whole foods and grass-fed animals at a low BMI producing low thyroid / hormonal activity might lead to better longevity than one which promotes a higher-BMI with greater amounts of lean muscle mass and hormonal activity. And, it might actually be healthier to eat several times and snack throughout the day, from soon after waking to just before bed, rather than to spend most of the time fasted and try to eat this as part of large meals, or after exercise, or with a large variance in carbohydrate or protein intake. (Or, another interpretation might show that it's just as healthy to eat once a day with an 1800 calorie high-fat, high-carb, high-protein feast of a meal as it is to eat sensibly throughout the day at an equal caloric intake.)

Have either of you guys had advanced lipids checked while on this sort of diet (NMR Lipoprofile / VAP) ? (or others on a high fruit diet?) I would be very curious to see where triglycerides / HDL / apoB or LDL particles sit on such a diet. If A1C is in an optimal range while TGs are low and under HDL, and LDL particles are few and large while eating 30-70% calories as fruit, this would make me feel much more comfortable about a higher fruit diet. It seems like the 'type' of fruit might be important. Avocados, olives, olive oil, red palm oil, cucumbers, tomatoes, zucchini, bell peppers, etc could all contribute toward a very high fruit diet by calories, while this would be a fairly low fructose diet as compared with one that uses apple sauce / ripe bananas / raisins / date sugar / etc. for a bulk of the calories.

I'm curious if some eating windows, macronutrient cycles, and meal frequency practices might offer health and longevity benefits beyond others. One practice might include a large calorie restriction on some days, and a higher amount of calories on other days (possibly at a surplus for hormonal health), which achieves a net caloric reduction on a weekly average. I've also heard of a "fasting mimicking diet" which reduces calories / protein / carbohydrates greatly for less than one week, achieving a net caloric reduction on a monthly average. I've also read about "carb cycling" around activity and "protein fasting" performed once weekly. Exercise and higher levels of non-exercise activity has been mentioned to create a caloric deficit. Then, there's daily intermittent fasting. At one extreme, there's the 22-24hr daily fast with a single large meal. Or, a 20hr fasting and a 4 hour "eating window." Or, 18/6 -- two meals. 16/8 -- two, three, or more meals. Or, two meals a day, with 12 hours between meals. With a focus on health / longevity biomarkers, is there an optimal way to practice CR through IF?

It looks like nibs might offer the ideal trade-off between SFA / contaminants. (Although, nibs sold in california are usually sold with a health warning label due to the heavy metal content.) http://www.sciencedirect.com/science/article/pii/S0308814612012083 http://www.sciencedirect.com/science/article/pii/S0956713511005640 So, with SFA would the main concerns be cholesterol / inflammation / insulin sensitivity, such that a dieter without those issues might be able to consume these fats freely (as in the case of Peter Attia's log) ? I can find dozens of studies that show sugars are toxic, yet fruits seem to be beneficial into a high sugar diet (from natural low-toxin foods) particularly at energy balance or a caloric deficit, where it almost follows logically that I might be able to find dozens of studies that show saturated fats are toxic, yet perhaps cocoa / nuts / saturated-fat-rich-fruits are beneficial into a high SFA diet (from natural low-toxin foods) at energy balance or a caloric deficit.

So, if PUFA and MUFA are healthier to carbs (but come with SFA), and carbs are healthier than SFA (but don't come with PUFA / MUFA), then (in your opinion) for an isocaloric ~2,000kcal diet, would it be best to keep PUFA in the 7-9g range, with SFA in the 18-20g range while consuming more MUFA and less carbs, or keep PUFA in the 12-14gram range with SFA in the <15g range consuming much more MUFA and less carbs, or keep both PUFA in the 7-9g range + SFA in the <15g range consuming much more carbohydrates? If the charts show that fruits have a lower risk profile than fruits+vegetables or vegetables alone, would the bulk of these carbohydrates be healthiest to consume from sugar?

What would be the main concerns with dietary 16:0 fatty acids? It seems like I've read reports from guys consuming large amounts of SFA (eg. 6 egg yolks + added heavy cream + egg whites cooked in coconut oil with especially fatty bacon and cottage cheese for breakfast, with 2 cups of coffee with added heavy cream, whip cream + cheese with lunch, and high fat ground beef with whole fat yogurt with dinner, followed by a decaf with added heavy cream), which produced a TG:HDL ratio around 0.85, LDL-C lower than HDL-C, a low amount of large LDL particles, with very low fasting insulin, very high insulin sensitivity, and low levels of inflammation. If the concern isn't inflammation / insulin sensitivity / particle count / particle size / TG:HDL ratios / LDL-C:HDL-C ratios, why would it be best to limit this type of fat? If I recall, heavy metals and aflatoxins (among the most carcinogenic substances known to man) are most heavily concentrated in cocoa husks / shells, and cocoa tends to be one of the foods highest in these contaminants. It seems like cocoa butter is relatively free of these toxins. On ConsumerLab, Cocoavia (from Mars, Inc) rated quite high in terms of polyphenols : contaminants (with low SFA), but I'm not sure if I like the fact that their "sugar free, unsweetened chocolate" contains more maltodextrin than lecithin with a glycemic index of 136. It seems like many companies offering nibs / powders / beans have been sent letters for violating proposition 65 laws in California.

There is no RDA for saturated fat, and as I said two posts ago, you'll get enough SFA from a mix of nuts/olive oil. Got it. Thanks for the links / studies. In the video, Greger mentions a beneficial amount of PUFA being something like "less than 4 individual nuts per day added to the diet" -- that's pretty restrictive in terms of PUFA content. So, it sounds like the healthiest diet under these guidelines would limit olive oil, limit avocados, limit SFA-rich nuts, limit dietary fat, and replace what small amount of SFA would otherwise end up in a vegetarian diet from foods like olive oil / avocados / SFA-rich nuts with PUFA-rich foods like walnuts, and seeds like chia + flax (though not much more than a small handful), while limiting protein, and going all in with carbohydrates from foods like grains, legumes, and fruits while restricting calories (80/10/10 vegan style?)

I'm curious when it's said that PUFA is a better dietary choice than MUFA or SFA, if that applies to the entire dietary intake of SFA into large servings of PUFA, or if this only speaks for the amount of excess SFA ingested after a certain threshold while PUFA is still otherwise limited? (I apologize if this is getting off the topic of nuts & mortality or has already been discussed in depth elsewhere.) Looking at PMID 26429077, it states higher intakes of PUFA are more optimal than consuming this energy from MUFA or SFA, but it seems like those "higher intakes of polyunsaturated fatty acids" which offer a 25% reduction in heart disease are simply a conversion of 5% of the SFA intake over to PUFA intake. If SFA is at 140 calories, that's only 7 calories of PUFA (< a half of one walnut). If one wishes to include more fat in their diet while adhering to this advice, does the recommendation still apply while driving PUFA into 20, 30, 40+ gram zone? If this recommendation of PUFA > MUFA > SFA applies to the entire intake of SFA, then for health and longevity optimization, the current research would point to a low fat diet (although not minimally low), which is high in carbohydrates and high in PUFA (more so than monounsaturated fats) that avoids dietary sources of saturated fat -- Basically, the opposite of a Paleo diet? In which case, it looks like walnuts would be a better daily addition to the diet than macadamia nuts. It's confusing when some sources recommend total PUFA intakes down under 5g, or <9g at the most, viewing this as a dangerous fat, while others recommend this as the most optimal protective fat source.

I found these findings when looking into replacing SFA with more PUFA: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195930/ http://www.ncbi.nlm.nih.gov/pubmed/24723079 Increased risk of cancer. Increased risk of coronary heart disease, cardiovascular events, death due to heart disease and overall mortality. Increased oxidised LDL-C. Reduction in HDL-C. The benefits of a low-fat diet (particularly a diet replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fatty acids) are severely challenged Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats. I believe SFA is also useful for synthesizing hormones like testosterone? Suppose carbohydrates are best limited to around 400-600 calories (20-30% of 2,000kcal) for promoting longevity: http://perfecthealthdiet.com/category/nutrients/carbohydrates/ And suppose polyunsaturated fats are best limited to around 80 calories (4% of 2,000kcal) for promoting longevity: http://perfecthealthdiet.com/notes/#Ch11 And, suppose saturated fat is best limited to around 140 calories (7% of 2,000kcal) (AHA guidelines). Just playing with some numbers in cronometer, with beans and olive oil, I would be looking at around 100 net carbs, 62g of protein, 15.5g SFA, and 12.7g PUFA for a 1800kcal day (~10% CR.) Or, by including macadamia nuts, saturated fat increases by less than a gram (barely over goal), while PUFA is then able to drop down by close to 4 grams down from well over 12g to under 9g (within goal) and the omega-3:omega-6 ratio improves from 9.3 to 7.76. It seems like this would be an improvement and a worthwhile compromise. A large part of the SFA here (more than the amount over goal) would be replaced with 16:1, which I believe is a beneficial fatty acid that has been shown to increase insulin sensitivity, protect pancreatic beta cells, and supress inflammation, and this would also slightly increase 18:0, which metabolizes to more MUFA. Going with an array of green-highlighted options from Zeta's chart and substituting flax, hemp, chia, & almond in place of olive oil and macadamia nuts, while keeping carbohydrates down around 100 net, PUFA increases to over 40 grams per day while SFA drops down to under 7g (too low?) This also greatly increases omega-3, which is 200% more peroxidizable than the already highly-peroxidizable omega-6 components. I suppose this is splitting hairs and the dose makes the poison, although this is the sort of optimization game that I enjoy thinking about.

On another thread, I was surprised to find that sugar intake wasn't associated with worsened health, where the foods highest in sugars (fruits) seemed to be more protective in many studies than most other plants with regard to cardiovascular disease and all-cause mortality, showing dose-related improvements with greater consumption. Now, I'm curious about polyunsaturated fats, which I generally avoid for health & longevity reasons. I've read articles / books from nutritionists recommending polyunsaturated fats be limited in the diet to promote longevity / decreased mortality. Nuts seem to be my biggest source of dietary PUFA. Are high intakes of PUFA and linoleic acid from natural sources like nuts / seeds benign in the context of calorie restriction when optimizing health and longevity? What's a safe / optimal lower and upper limit of total PUFA? Macadamia nuts seem like the only exception to the rule, where one could boost MUFA without boosting SFA + PUFA, even more so than olive oil -- I wonder if a large daily serving of macadamia nuts is a wise and beneficial habit, or worth avoiding / cycling for some reason (other than price & variety.) Randomly, I've read they're poisonous for dogs, and the mechanism is unknown.

That is interesting that nuts were associated with lower mortality, yet the study is looking at roasted legumes (peanuts.) Are seeds associated with lower cardiovascular risk / mortality, or coconuts, rich in saturated fat and palmitic acid?

I'm curious if there is an "optimal" (or less unhealthy?) way to distribute meals and macro-nutrients across the day. I'd love to hear any ideas on how these can be manipulated for potential health / longevity / cognitive benefits. Currently, I wake up around 7 or 8am, and breakfast is often around 11am. Lunch falls around 2pm. And dinner is around 6pm. This gives me an 8 hour eating window, with a 16hr fasting period. Often, I do fats primarily for breakfast (nuts / seeds / avocado / extra dark chocolate / salad greens + olive oil), where the bulk of any insulinogenic action falls in a fairly narrow 4 hour window. I've noticed my fasting glucose is usually in the high 70's to low 80's, while a high carb meal elevates this into the high 90's (potentially with a spike just over 120 mg/dL for 30-60 minutes.) The more carbohydrates that I put into this meal, the longer glucose seems to stay elevated in the high 90's. At <100g carbohydrates in a meal, glucose is often back into the low 80's just 1 hour after finishing the meal (especially if this meal follows heavy resistance training.) I have not looked into elevations in triglycerides after meals. I'm wondering if my high fat meals might negatively affect arterial flow, and if I would be better eating more carbohydrates with those meals (combining carbs + fats), which might also lower post-prandial glucose. Or, if I would be better eating several meals throughout the day. Or, perhaps if I would be better working out before carbohydrate-rich meals (daily?) or after carbohydrate-rich meals (daily?) I'm not sure if it's unwise to put heavy exercise soon after a high-fat meal, or if that's a healthy habit to lower post-prandial triglycerides. I've also heard mention of a large gap between breakfast and dinner, which provides 2 smaller fasts per day, or a single meal (feast?) across a 2-4hr eating window. I assume these small details might not matter too much compared with caloric restriction itself, but I am curious to hear opinions on the theoretical effects of such fine-tunings.