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  1. 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.
  2. In general, I tend to avoid dairy and stick closer to a paleo-like diet. While my lipids look fine on a high fat diet, they don't look great on a high saturated fat diet. The simple trick that I found to achieve stellar lab work was to ditch the cheese, butter, and coconut oil. It was a simple trick that brought my LDL down into the 70s while eating a ketogenic diet. So, I've ended up with a mostly vegetable covered plate with a bit of seafood / lean meat / eggs since I find these much easier to digest than beans and grains. I don't eat a ton of meat, but it's enough to patch the hole that would exist if I was just trying to run around on broccoli and almonds. Kefir does look like the micronutrients would fit my goals, although I could do without the 12 grams of sugar (if I'm going to eat sugar, I'd prefer something like blueberries rather than lactose, galactose, etc.) Perhaps I'm being overly picky in my selection and something like calcium-carbonate-fortified almond milk would do the trick. Thinking more about micronutrients -- do you one-meal-a-dayers make any effort to get sodium or potassium in during the fast (say if you're going to go for a run and lift weights?) I would imagine that a low-carb diet would benefit from a higher sodium intake, though it seems like a problem if you eat an entire day's sodium in a single sitting.
  3. It's comical to see "Fruit punch with calcium citrate malate" in a serious academic paper on improving the nutrient density of a vegetarian diet. If that's going to make the list, why not just include "calcium tablets." Chinese spinach looks off the chart -- I wonder if that means there's a ton of oxalate, or if this is my solution. I don't think I've come across the stuff at my local grocery store.
  4. sirtuin

    Olive oil? Healthy or not?!

    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.
  5. Assuming the other 50-60g of protein in my diet contains tryptophan, would its absence be as relevant as the overall boost in glycine? "The average adult human (70 kg; 30-50 years; sedentary) requires nearly 15 grams of glycine per day to synthesize collagen (12 g/d), non-collagen proteins (1 g/d), and other important compounds such as porphyrins (240 mg/d), purines (206 mg/d), creatine (420 mg/d), glutathione (567 mg/d), and bile salts (60 mg/d).[4] However, glycine synthesis is limited to about 2.5 grams per day, suggesting that humans require about 12 grams of dietary glycine to satisfy daily metabolic requirements.[4]"
  6. I hadn't considered mineral water, that could be a great tip. I'm surprised it wouldn't fall under the potentially hazardous umbrella of a calcium supplement, like the calcium carbonate you would find in say soy milk boasting "More calcium than milk!" (yikes) I get a decent amount of Ca from almonds and spinach, but it's debatable how much of that I'm able to absorb. I do supplement magnesium with my meal, which could tip things further to the lower side (although I've also read it paradoxically improves uptake.) I have read that thyroid hormones can be among the largest disruptors for lipid balance wrt cardio health, where CR does tend to push things toward the lower side. With male hormones / thyroid activity in mind, are foods like soy & flax of any concern or are they largely seen as beneficial? As an alternative to plant-based isolated proteins, what's the consensus on gelatin / collagen as a low-methionine source of aminos and glycine? This was an interesting study from a couple months ago, where whey protein (possibly a useful source of calcium and glutathione-boosting cysteine?) had a much different effect on mTOR than I would expect, while the other amino acids ratios are fairly similar to common plant-based protein options: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6466539/
  7. sirtuin

    Olive oil? Healthy or not?!

    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
  8. Right now, I'm experimenting with a one-meal-a-day regimen. I tend to feel better on a low-carb diet than the others that I've tried. While I don't think I have any major metabolic issues, beans, grains, sugars, and starches do tend to leave me on the foggy / bloated side post-consumption, while food like nuts, avocados, and olive oil are much closer to the nootropic anti-inflammatory end of the food spectrum for me. Every time I run the experiment, it's quite apparent how much better I feel and sleep on the lower-carb diet with elevated ketones. While my lipids look good, there is some concern over eating so much fat in a sitting (occasionally north of 200g for a meal on a 2700kcal activity day.) The problem I'm seeing on cronometer is that my calcium intake is often lacking -- some days, it's only around 400 mg (dark leafy greens.) My protein intake is also on the lower side, at around 50-60g (nuts + eggs / meat), and fiber clocks in around 25g. This is about what I can fit into a reasonably huge dinner. If I space this out over an 8hr window or so, I can more or less double the numbers at a similar caloric intake with more food volume. I'm curious if it would make sense to use something like a vegan protein powder to do a sort of low-carb veg-rich shake (with added fiber?) to boost the numbers, or if there are any other hacks / supplements / foods that come to mind to balance out this eating window / macro ratio. Or, if this is of little concern, assuming I'm lean and fit. Thoughts?
  9. sirtuin

    Methylation Supplementation

    I'm curious if any of you have supplement regimens for "Methylation" support. I've been prophylactically taking 1mg of methyl-b12 and 800mcg of methyl-folate for a few years after learning of my +/+ C677T polymorphism (among others.) More recently, I've tacked on B1, B2, and B6 (P5P.) I've been thinking about readdressing this stack and pulling back on everything but the b12 & b9, then maybe experimenting with trimethylglycine. I did come across this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4262445/ Would TMG be more likely to ferment to TMAO or promote cardiovascular disease, or might this be a health-promoting cardio-protective supplement? Have you experimented with dialing in an ideal b-vitamin complex to address things like C677T?
  10. This reminds me of when I wanted to get a masticating juicer specifically for the fresh fruit pulp (minus a lot of the sugar) rather than the juice. With beets, I would be curious about the oxalates adding up -- for a while, I was eating 1-2 large beets a day with lots of beet greens throughout the week, but I've since cut back for slight concerns about the oxalate content. For a while, I was maximizing my fiber intake (on a per day basis), while lately I've been playing with decreasing fiber on a per meal basis. Wolfing down 1 feast-like meal a day with 80g of fiber (~6-9 cups of vegetables) had me looking like I just ate a bowling ball by the mid afternoon, where I'm finding a lower fiber diet is a bit more comfortable. Ymmv.
  11. I haven't had anything coconut flavored in a while, and lately I'm craving it. In the past, I used to cook with a lot of coconut oil but I had high LDL / LDL-P. While pulling back on SFA, my LDL-P stabilized under 1,000 and my total cholesterol dropped under 150 with HDL and LDL on near equal terms far above triglycerides -- I do believe this was a better situation for my lipids. I'm looking at: Young Coconuts -- Pulling the meat out (PITA?) and blending with some of the coconut water to make a fresh coconut milk. Mature Coconut Meat Dried Shredded Coconut / Coconut Flakes / Coconut Chips Coconut Flour (defatted) Coconut Manna / Coconut Butter Coconut Milk / Coconut Cream -- full fat in the can, or something like the Silk product (less fat, but lots of additives) Cultured Coconut Milk "Yogurt" -- This seems to come with sugar and additives. Coconut Milk Kefir -- I like the idea of this one, but it seems like a PITA to make and I don't see it offered commercially. Something with "Coconut Flavor" (eg. Coconut Flavored vegan protein or "Coconut Flavor" extract.) What's an ideal coconut product and safe amount to consume? I can probably water these down quite a bit. I'm looking to throw it over some berries or add to fresh-ground nut butter, or maybe in a drink of some sort.
  12. sirtuin


    Those food options sound delicious! Regarding basmati rice, I've had good experience with this one in particular (organic california-grown germinated brown rice): http://www.lundberg.com/product/organic-sprouted-brown-basmati-rice/ I usually rinse it a few times, then cook it al dente pasta style with fenugreek seed, cumin seed, coriander seed, turmeric root, ground black pepper, salt, with a bit of onion, garlic, and parsley. Then, I refrigerate it. Then, consume it with a meal (often tossed with a bit of 300-400 polyphenol EVOO.) Consumed this way, I don't see any major effect on my post-prandial glucose numbers -- much less of an effect than I might get eating a big serving of cauliflower with asparagus and onions. I can practically file this food under vegetables. With safflower oil, I'm not against it so long as I see the key phrase "High-Oleic" next to it (some of those reach upwards of 85%+ MUFA, much more than your average EVOO.) Coconut / dairy / sesame oil / peanuts / soy, I do avoid for now. Coconut sugar doesn't bug me, but I might prefer to see "High antioxidant buckwheat honey", nutrient-rich molasses, organic dates, etc. I tend view coconut sugar as basically sugar, while honey / molasses / dates seem a bit more food-like to me. I don't avoid grilled vegetables at most restaurants, but I don't consume them at home. If I have the option to have these steamed / boiled, I'll almost always request that, unless I'm feeling dangerous. Kombu / kelp doesn't bug me. I don't go out of my way to eat these foods, but I don't avoid them. When I'm not eating much seafood / seaweed (heavy metal avoidance, dioxins, etc.) I often supplement iodine. Roasted root vegetables, I usually avoid. These tend to push my blood sugar up higher than anything else I can eat. I prefer these steamed / boiled, or lightly pressure cooked and cooled. Regarding the legumes, I've had good experience with this one: http://www.bobsredmill.com/chana-dal-beans.html These contain more fiber than they contain net carbohydrates -- that's a better ratio than you would get eating most other foods / vegetables (more fiber : net carbs than eating lettuce, asparagus, arugula, broccoli, etc.) They're hulled, so you're skipping many of the anti-nutrients in the outer layer. I soak overnight with warm water to remove some of the anti-nutrients in the bean. Then, I pressure cook them to further destroy lectins / anti-nutrients and increase their polyphenol density with herbs + spices. Mendosa has a good write up on these beans, where the GI might be as low as 5 or 11.
  13. sirtuin

    What's Wrong with Eggs Now?!

    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.
  14. Who are you? Why hemoglobin A1c is not a reliable marker I was more active on here in the past... apologies for barging back in. I'm looking at A1C as a surrogate for fasting and post-prandial glucose -- I often measure these both and my A1C tends to match up fairly closely if not spot on (I've worn CGM where my A1C measured 2% higher than predicted.) Surely, Lustgarten with all his obsessive biometric tracking has some rough target and approach for reaching it?
  15. <6% seems like a fairly large target -- With some rough math, I could spike my glucose to an average of 180 mg/dL 3 times a day for 2hrs each, then run an average of 100 mg/dL for the remainder of the day and stay within "normal" range. Outside of a diabetic disease state, I can't think of anything I could eat to rise beyond that range. Perhaps 4.2 - 4.6% is the optimal target? For minimizing glycation and reduced its age-promoting effects at 4.6%, you would have to maintain a fairly tight ~80mg/dL fasting range with ~4hrs post-prandially averaging around 100 mg/dL -- I'm not too far off from this range, actually. At one meal a day or very tight control, ~4.4% doesn't seem like an impossible target.