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  1. In this post to a thread about nuts and mortality, I pointed out that the fatty acid profile in 'bakers chocolate' contains a significant amount of the (probably) harmful 16:0 (palmitic acid) saturated fatty acid than any of usual nuts/seeds that we normally consume, and in fact more than cheese. That got me started on an investigation on the composition, and potential health implications of various chocolate products. As everyone probably knows, the family of different chocolate products is extensive, and the processing that creates them is quite involved. Here is a handy flowchart showing the various steps and products in the chocolate processing pipeline: As you can see, the first step is the pods from the cacao plant are split open to separate the cacao beans, which are allowed to dry and ferment for a few days. These beans are the first edible form of chocolate, and are in fact how I get a significant amount of the chocolate I eat, purchased as 'raw' cacao beans from Nuts.com. Continuing with processing, these beans are split open to remove the 'nibs' and discard the shells, which are edible but mostly fiber (although see below!?) and so don't add much to what we consider the 'chocolaty goodness' - although I rather enjoy the crunchiness of the whole beans sometimes, in moderation of course . The nibs are then ground into what is called chocolate liquor, which is further separated into the fat-free cocoa powder (where most of the healthy polyphenols etc reside) and the cocoa fats called cocoa butter. This cocoa powder and cocoa butter are then mixed back together, along with various other ingredients, and tempered to form the wide variety of chocolate products that we know and love.We can make a list of the various, commonly consumed chocolate-containing products and their ingredients as follows: Cacao Beans = (unprocessed) cocoa powder + (unprocessed) cocoa butter + fiber Cacao Nibs = (roasted) cocoa powder + (roasted) cocoa butter Cocoa Powder = (unsurprisingly) cocoa powder Unsweetened bakers chocolate = (nearly) 100% cocoa powder + cocoa butter Dark Chocolate (70-85% cacao) = 70-85% from cocoa (powder and butter) + 15-30% from other stuff, mostly added sugar. Dark Chocolate (60-69% cacao) = 60-69% from cocoa (powder and butter) + 30-40% from other stuff, mostly added sugar. Milk Chocolate = Dark Chocolate Ingredients + milk or other dairy products With these seven forms of chocolate in mind, I became curious above the relative nutrient profiles of each. So I decided to try to build a scaled-down table like Zeta's table of nut nutrition, discussed in several threads, but the latest version of which (as of 11/7/2015) is available in this post. In fact, rather than reinventing the wheel, I figured I try to add these six additional items to Zeta's latest nut nutrition table (he already has included baker's chocolate). I realized I can't attach XLS files to posts, so I've emailed Zeta the updated table in case he wants to keep the chocolate items in it. But for the purpose of this post (comparing chocolate products) here is a stripped down, rearranged, slightly augmented version with only the chocolates, and only for the fields I was able to dig up and willing to enter (click to enlarge): First, the easy observation. If you are going to eat chocolate in bar form, the four bar options at the bottom show you're getting more chocolate (likely a mixed blessing since it includes the saturated fats) and less added sugar the darker the chocolate you eat. Not surprisingly, as you can see from the two green arrows, fat content drops, and sugar content increases, as you go down in cacao content. The manufacturers are basically substituting sugar (and other ingredients) for real chocolate components as you move away from the darkest form (unsweetened baking chocolate). So, ignoring the (controversial) saturated fat, from a health perspective its probably "the darker the chocolate the better". This web page has good information about the details of dark chocolate, for those interested in learning more about what "cocoa %" really means. Next, another easy observation. If you want to avoid the saturated fats in chocolate, but still get the healthy polyphenols etc, your best choice is to eat your chocolate in cocoa powder form. Without the fat, it is a lot less calorie dense, and has a lot more fiber than the various chocolates in bar form. Obviously palatability is an issue, but I find mixing it into coffee, perhaps with a little sweetener (I prefer erythritol or pure stevia), makes it quite pleasant. See the bottom of this post for other suggestions in this regard. Now the complicated bit. I was disappointed with the nutrition information I could find on the two least processed forms of chocolate - raw cacao beans and cacao nibs. If fact, I'm skeptical about the nutrition information for these two listed in the table above, especially for the beans. But let me first address the nibs. I expected the nibs to be pretty nearly equivalent to unsweetened baking chocolate in composition, and therefore nutrient content, believing baking chocolate to be (more or less) the melted down nibs formed into bars/squares. But at least if the available nutrition information is to be believed, this isn't the case. Somewhere between nibs and unsweetened baking chocolate, quite a bit of fiber is removed, and (perhaps) replaced by cocoa butter. As you can see from the kcal/g comparison of the two, the baking chocolate is significantly more calorie-dense than the nibs. So, if you're looking to get the good stuff from chocolate, while retaining the "mouth feel" of the fat chocolate normally contains, I'd say its better to go with the nibs rather than baking chocolate. With the nibs, you get more chocolatey-bang for your calorie-buck, and they are less refined than baking chocolate, which is probably a good thing. Finally, my personal favorite, the least refined of all, the raw cacao beans. As I said, I was disappointed with the dearth of nutrition information, and the conflicting information that is available. There is definitely something fishy, which you can see if you compare the beans with the nibs in the table above. The biggest red flag can be seen in the kcal/g comparison. According to the available nutrition information, the beans are more calorie-dense than the nibs. I'm virtually certain this isn't the case. First off, as you can see the nibs are where all the fat is - with the beans containing about half the total fat per 250kcal as the nibs. How can the beans be more calorie dense when they contain half the amount of the densest macronutrient? Something strange is going on. The second red flag with the bean data is that the fiber content per 250kcal is virtually identical between the beans and the nibs (17.9g vs. 17.3g). This seems crazy, since the difference between the dried beans and the nibs is that the beans contains both the nibs and the shells, and the shells have got to be relatively high in fiber. Finally, and most mysteriously, the nutrition data for the beans seems to be missing a whole lot of calories. If we use the (admittedly somewhat naive and inaccurate) Atwater equations for converting from grams of fat, net carbohydrates (i.e. total carbs - fiber) and protein to calories (i.e. calories = 9 * fat + 4 * net_carbs + 4 * protein) we get (9 * 12.5) + (4 * (25 - 17.9)) + (4 * 7.1) = 169.3 kcal. But according to the nutrition database, we're supposed to be looking at a 250kcal portion! So that's 1/3rd of the calories missing. Even if we give a calorie or two per gram for the fiber, there is still quite a few calories missing from the available nutrition data. In contrast, if we apply the basic Atwater equation to the nibs, we get 246.3 kcal for what is supposed to be a 250kcal portion size - i.e. almost perfect, even without adding any extra calories from fiber. So what I started out this investigation most interested in discovering, namely how the nutrition of raw cacao beans compares to other forms of chocolate, ends up being left pretty much unanswered. I'm going to continue to consume a mixture of (ground) cacao beans and cocoa powder (with more cocoa powder than beans) in my coffee, to get both the pleasure and the health benefits of chocolate. Speaking of health benefits, for anyone who's gotten this far, Dr. Greger just sent a good write-up on the cardiovascular benefits of dark chocolate, with links his own recipes / strategies for getting the health benefits of chocolate without the saturated fat. --Dean
  2. Dean Pomerleau

    So Why Don't We Brew Our Chocolate?

    All, So (dark) chocolate and other cacao-derived products (i.e. cacao beans, nibs, cocoa powder) have a lot of beneficial phytochemicals (polyphenols, flavonols, etc). These have been shown to be beneficial for both the cardiovascular system and the brain - this is pretty well established, so I'm not including references (I know you are disappointed...). Alright - maybe one reference [2] - a review of CVD benefits of chocolate. Later... - here is another [4], on brain benefits of chocolate. But as we've discussed recently, these chocolate products have some things we'd rather avoid ingesting, including saturated fat (except for cocoa powder), and potential heavy metal contaminants, especially cadmium. What other food items have this same "take the good with the bad" quality? Two spring to mind - coffee and tea. But in these two cases, we don't take the good with the bad. We process them in such a way as to get the good without the bad. I was reminded of this today when responding to this post on the potential heavy metal contamination associated with consuming matcha green tea - where the tradition is to eat the tea leaves. By brewing green tea, and discarding the leaves, we retain the beneficial tea polyphenols but eliminate the heavy metals. Similarly, in this discussion we talked about getting the benefits of coffee beans by brewing and then filtering them, with paper (or possibly? metal) filters to eliminates the cholesterol-raising diterpenes cafestol and kahweol that the beans naturally contain, while retaining the health-promoting phytochemicals in coffee. So why don't we do the same thing for chocolate? Namely, why don't we grind, brew and filter the coffee beans to extract that beneficial polyphenols into the water, while leaving (most?) of the heavy metals and saturated fat in the solid "chocolate grounds"? Well, I can think of one possible reason we don't do this - we like the taste and mouth feel of actually eating the chocolate. But putting that (admittedly big deterrent for some) aside, is there reason to believe this strategy wouldn't work to get most of the health benefits of chocolate without the potential downsides of heavy metals and saturated fat, not to mention the extra calories? First, regarding eliminating the 'bad stuff' by brewing and filtering chocolate. For heavy metals, it would seem no different from tea or coffee. Since the heavy metals appear to remain locked in the plant matrix of the discarded solids (coffee grounds or tea leaves), I see no good reason to think it would be different with the heavy metal contaminants in cacao beans. Anyone think otherwise? Regarding the other 'bad stuff' in cacao / chocolate - the saturated fat. Its hard to find nutrition information on coffee beans (as eaten) - without any chocolate coating... CRON-O-Meter comes up empty. But I did find two references to the calories in coffee beans themselves. The first lists 100g of coffee beans as having 406kcal, 10.2g of fat, with 4.8g of it saturated. Not too far from raw cacao beans in fact. The second also listed 10g of fat per 100g of beans, with somewhat fewer calories (300kcal). Either way, these illustrate that coffee beans themselves contain a lot of fat, but as we all know, brewed coffee has virtually none. So clearly fat doesn't get extracted to the liquid as a result of brewing and filtering coffee beans, so I would expect the same for cacao beans - right? What about the other side of the equation - should we expect the 'good stuff' in chocolate to get extracted to the water when brewed and filtered, like it does for tea and coffee? Again - I don't see why not. As I understand it, based on information from [2] (a very good source of info about polyphenols in cacao, BTW) and [3] (also a good source), the taxonomy of beneficial phytochemicals (with special emphasis on those in cacao) goes something like this: All Phytochemicals All Polyphenols All Flavonoids All proanthocyanidin? All Flavanols catechins - in either monomeric or multimeric (procyanidin) forms epicatechins - in either monomeric or multimeric (procyanidin) forms ... ... See here for list ... .. Note: I'm not exactly sure about this taxonomy, especially where proanthocyanidin fits in - the literature is very confusing. But the important thing is that the main phytochemicals in cacao are catechins and epicatechins, which should be familiar to people. They are (among) the healthy phytochemicals found in green tea. So clearly if they are water-soluble in green tea, they should be water soluble in ground cacao beans as well, it would seem. So, as a result of all this, it seems logical to me that grinding, brewing and filtering cacao beans should get rid of the bad stuff (heavy metals, saturated fat, and calories) and extract the good stuff (the polyphenols) into the resulting watery brew. Note - I should have said this earlier, we aren't talking about brewing hot chocolate here - where the cocoa powder is mixed in with the liquid and consumed. We're brewing ground cacao beans, filtering (with a paper filter) to separate the liquid from the grounds, then discarding the grounds and drinking the coffee-like chocolate brew. But what to do with the beans before grinding them? In particular, should they be roasted, like coffee beans are? Perhaps to reduce bitterness, but if one wants to maximize polyphenols, it seems from [1] that grinding raw beans would be best. You won't be surprised to learn that this isn't a novel idea. In fact, there are several commercially-available products for brewing cacao as you would coffee. The two most popular are Crio Bru and Choffy (cute name!). They are both a bit more expensive than coffee, although pretty close to the price of premium coffee beans. Not surprisingly, they are both roasted, presumably to improve flavor and reduce bitterness. They recommend using a french press to brew, which I have, but I wonder if the Aeropress will work as well (Choffy's website says yes! and gives instructions). Here is a good overview from a "chocolate geek" about brewing chocolate, including a review of Crio Bru and Choffy products. It sounds very promising, and not hard to do. You can also buy ground brewing chocolate from his website as well. In the long-run if I like it and the above reasoning isn't shot down..., I'll probably grind my own raw beans or lightly roast the beans myself before grinding (I've roasted coffee beans before using an air popcorn popper - its a piece of cake). But for now, I've ordered one of the Crio Bru varieties from Amazon (Choffy was more expensive and not available via Amazon Prime). It should arrive in a couple days and I'll let you know what it is like relative to coffee. In the meantime, I'm very curious about what other people think of this idea. I can certainly imagine people balking at the diminished enjoyment of drinking coffee-like chocolate rather than eating the 'real thing' or even drinking cocoa, but I'm most interested about people's thoughts on the health angle. Also if you've ever actually tried brewed chocolate, I'd love to hear what you think! --Dean ------------ [1] Food Chem. 2015 May 1;174:256-62. doi: 10.1016/j.foodchem.2014.11.019. Epub 2014 Nov 8. Flavanols, proanthocyanidins and antioxidant activity changes during cocoa (Theobroma cacao L.) roasting as affected by temperature and time of processing. Ioannone F(1), Di Mattia CD(2), De Gregorio M(2), Sergi M(2), Serafini M(3), Sacchetti G(4). The effect of roasting on the content of flavanols and proanthocyanidins and on the antioxidant activity of cocoa beans was investigated. Cocoa beans were roasted at three temperatures (125, 135 and 145 °C), for different times, to reach moisture contents of about 2 g 100 g(-1). Flavanols and proanthocyanidins were determined, and the antioxidant activity was tested by total phenolic index (TPI), ferric reducing antioxidant power (FRAP) and total radical trapping antioxidant parameter (TRAP) methods. The rates of flavanol and total proanthocyanidin loss increased with roasting temperatures. Moisture content of the roasted beans being equal, high temperature-short time processes minimised proanthocyanidins loss. Moisture content being equal, the average roasting temperature (135 °C) determined the highest TPI and FRAP values and the highest temperature (145 °C) determined the lowest TPI values. Moisture content being equal, low temperature-long time roasting processes maximised the chain-breaking activity, as determined by the TRAP method. Copyright © 2014 Elsevier Ltd. All rights reserved. PMID: 25529678 ---------------- [2] Nutrients. 2014 Feb 21;6(2):844-80. doi: 10.3390/nu6020844. Cocoa polyphenols and inflammatory markers of cardiovascular disease. Khan N(1), Khymenets O(2), Urpí-Sardà M(3), Tulipani S(4), Garcia-Aloy M(5), Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942736/ Monagas M(6), Mora-Cubillos X(7), Llorach R(8), Andres-Lacueva C(9). Epidemiological studies have demonstrated the beneficial effect of plant-derived food intake in reducing the risk of cardiovascular disease (CVD). The potential bioactivity of cocoa and its polyphenolic components in modulating cardiovascular health is now being studied worldwide and continues to grow at a rapid pace. In fact, the high polyphenol content of cocoa is of particular interest from the nutritional and pharmacological viewpoints. Cocoa polyphenols are shown to possess a range of cardiovascular-protective properties, and can play a meaningful role through modulating different inflammatory markers involved in atherosclerosis. Accumulated evidence on related anti-inflammatory effects of cocoa polyphenols is summarized in the present review. PMCID: PMC3942736 PMID: 24566441 [3] http://www.medscape.com/viewarticle/590371 Quoting from it: The main flavanols present in the cocoa powder are catechins and epicatechins in either monomeric or multimeric (procyanidin) forms. --------[4] http://newsroom.cumc.columbia.edu/blog/2014/10/26/flavanols-memory-decline/ "Dietary cocoa flavanols—naturally occurring bioactives found in cocoa—reversed age-related memory decline in healthy older adults, according to a study led by Columbia University Medical Center (CUMC) scientists. The study, published today in the advance online issue of Nature Neuroscience, provides the first direct evidence that one component of age-related memory decline in humans is caused by changes in a specific region of the brain and that this form of memory decline can be improved by a dietary intervention."
  3. All: Since the turn of the millenium, I've been advancing what I've called the DHA-Accelerated Aging Hypothesis (AKA Michael Rae's Fish oil-Accelerated Aging hypothesis (MiRFAA), an acronym coined by the sorely-missed Michael Sherman to refer to an hypothesis built up from an inference he himself had made from a passing reference in Dr. Aubrey' de Grey's The Mitochondrial Free Radical Theory of Aging). It posits that people on CR should avoid intake of long-chain polyunsaturated fatty acids (LCPUFA), AKA highly-unsaturated fatty acids (HUFA), and especially omega-3 HUFA (DHA and EPA, most often found in fatty fish and fish oil), and especially-especially DHA. This is based on a range of empirical observations which are reviewed at the bottom of this post, and also in the introduction to material recently posted by Al Pater (see also (2) below, although it is from 2007 and comes at the subject from a different theoretical POV than I favor). Instead, one should maximize one's intake of fat from healthy, plant-based monounsaturated fats (and, in particular, high-phenolic, high-oleic extra-virgin olive oil), minimize or eliminate omega-3 HUFA, and get one's essential fatty acids (omega-6 and omega-3) from short-chain sources such as flax oil. However, all the data has been either correlative, or to the extent that it has been experimental, it has been studies of the effects of different interventions on mitochondrial (and, less importantly, tissue) membrane composition. There have been no direct tests of the question: will minimizing the intake of omega-3 HUFA further optimize lifespan in CR experimental animals — and thus, potentially, humans? Now, finally, such a study has been performed and published.(1) Extracts below from extended material posted by Al Pater: Now, before everyone goes out and stocks up on lard (or even coconut oil), let me give three reasons to focus on monounsaturated fats (and, in particular, high-phenolic, high-oleic extra-virgin olive oil) and avoid saturated, despite my advocacy of the "DHA-Accelerated Aging Hypothesis" and the particular use of lard in (1). First, there is a widespread misunderstanding (completely reasonable on its face) that has been cycled around amongst advocates of Paleo, Atkins, and "Ancestral" diets that because there is one more double bod in MUFA than in SaFA, that SaFA must be more resistant to peroxidation. In fact, however, they are not: fatty acids' oxidative sensitivity increases exponentially to (roughly) the number of double bonds minus one, so that MUFA and SaFA alike are virtually unoxidisable (1/40 as much as those with two double bonds, such as linolenic acid). This is illustrated here: (This figure is from (2) below, which is also a good review of the underlying correlational data underlying MiRFAA, although it has a different theoretical explanation for the phenomenon than I or Gustav Barja). But then those with two double bonds are twice as oxidizable as either MUFA or SaFA, those with three doube bonds are twice as oxidisable as those with two, those with four are four times as oxidisable as those with two, and so on. α-linolenic acid (ALA = 18:3 n-3) has THREE double bonds; DHA (22:6 n-3) has SIX. Second, there is the structure of biological membrane phospholipids. The phospholipid structure of the membrane of a cell of a given type is dictated by the functions needed by that cell, so that one cell will have more "phosphatidylcholine" and anther more "phosphatidylethanolamine" and a third more "phosphatidylserine" etc (tho' in fact even these names are rough & ready, and each includes several subspecies). In turn, the internal fatty acid structure of those PL are themselves to an extent determined by their nature. Nearly all PL have to have a saturated fatty acid in their sn-1 position, and nearly all have to have an unsaturated FA in sn-2. In some cases, the particular PL needs a very specific UFA indeed, which is why neither CR nor altering the diet has very much influence on the membrane FA composition of the brain or the retina; but others are much less specific, and any ol' UFA (or a range of UFA) will do. What you are doing by altering your diet, then, is shifting the specific UFA that occupies the sn-2 position of your membrane PL. Even if you WANTED more SaFA in your cell membranes (which, for reasons given above, actually would be of no benefit), eating more SaFA will not get you there. (It may, however, be worth noting that high SaFA intake may have an indirect effect that is beneficial on this narrow question of tissue membrane PL unsaturatioin index if you're also consuming a lot of PUFA, because high SaFA intake increases the activity of delta-9 desaturase, which converts some of the SaFA to MUFA (especially, stearic (18:0) [thanks Brian!] to oleic (18:1)). So a high-SaFA diet can (inefficiently) increase the availability of oleic to compete with PUFA at the sn-2 position, even tho' it has no effect on the am't of SaFA in the tissue membranes. You can see this for animals fed lard in several previous studies linked in my appendix below. But consuming more MUFA directly while limiting PUFA is a more efficient way of doing this). And, finally: remember, while I advocate for this "DHA-accelerated aging hypothesis," it remains an untested one in an experimental sense -- and even I think that its effects will be felt on the margin of things, and only in people on CR. By contrast, the epidemiology and clinical trials are pretty clear that SaFA will kill you dead of a heart attack or occlusive stroke, irrespective of whether you're aging a little slower because of an altered cell membrane composition. Personally, I get all the n3 (5 g ALA) & n6 (12 g LA) I think necessary, and it's all from a small am't (2 tsp) of flax oil and very high-oleic, low-n6 fats (high-oleic, high-polyphenol, premium VF EVOO, plus hazelnuts and a bit of avocado); I certainly wouldn't be using conventional safflower oil, and already choose for other reasons not to consume soybeans. APPENDIX: BACKGROUND ON THE "DHA-ACCELERATED AGING HYPOTHESIS/MiRFAA Further down in this post I give a brief and outdated summary, with an assembly of relevant links to previously-posted data. Here, I present what is the The by now well-established facts which constitute essence of the argument: ------------------------------------------------------------------ 1.Across species, double bond content in the mt inner membrane (MIM) -- and esp DHA content -- is inversely correlated with max LS. http://www.ncbi.nlm.nih.gov/pubmed/?term=9788245+11432462 http://groups.yahoo.com/group/crsociety/message/2980 This effect is particularly impressive in comparing outliers, such as birds, which -- because of their size & high metabolic rate -- would otherwise be predicted to have short LSs (rodents, of similar size & slower metabolic rates, live ~3 yrs; canaries can live > 10 times this long): http://www.ncbi.nlm.nih.gov/pubmed/?term=10337442+10100156+8866736 ------------------------------------------------------------- 2. Within a species, double bond content in MIM increases with aging. https://groups.google.com/forum/?hl=en#!msg/sci.life-extension/0X-nd-3YUIU/za9RsFymjX4J (And de Grey's confirming reply, which nixes my self-imposed caveat): https://groups.google.com/d/msg/sci.life-extension/0X-nd-3YUIU/Fz9Vy3VpT1EJ -------------------------------------------------------------- 3. CR, the most robust and well-studied anti-aging therapy per se (therapies that extend max LS in healthy mammals), retards (2). (Some examples are present in the first post under point (2), above: refs. (1) and (3)). ------------------------------------------------------------------ 4. Feeding all animals yet tested longer-chain PUFA, such as DHA, increases DHA content in MIM. https://groups.google.com/forum/?hl=en#!msg/sci.life-extension/EmmwMfQwgGo/qS-RCQJOx_8J ------------------------------------------------------------------- 5. Specifically, in rodents, feeding fish oil both increases MIM DHA content, AND increases the actual peroxidation of the MIM. https://groups.yahoo.com/neo/groups/crsociety/conversations/messages/2905 Dean's posting of the results is neater: https://groups.yahoo.com/neo/groups/crscience/conversations/topics/7 ---------------------------------------------------- 6. CR opposes the incorporation of dietary EPA/DHA into MIM. https://groups.google.com/forum/?hl=en#!msg/sci.life-extension/d2J6z5WHCsg/rVEzzuduZ7AJ (To understand how these abstracts show this, NB that CL=cardiolipin (diphosphatidylglycerol), a phospholipid only found exclusively (or, some would claim, just OVERWHELMINGLY) in MIM), & MIM contain PL exclusively (no TGs). ----------------------------------------- 7. Although the link is weaker, even solid-organ plasma membrane HUFA levels are inversely related to species max LS in many studies: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10687923&dopt=Abstract ... and CR opposes even organ plasma HUFA, endogenously or from the diet: http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10954013&dopt=Abstract http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11485162&dopt=Abstract Important updates on the effects of feeding different fatty acids on tissue membrane fatty acids are here. ------------------------------------------------------------------ 8. The Ames dwarf mouse, a well-studied and very robust life-extended mutant, also has far lower DHA in its solid organ plasma membranes than wild-type mice: http://www.longecity.org/forum/topic/41110-dha-accelerated-aging-hypothesis/?view=findpost&p=602820 [Edit: added 2014-11-03] ------------------------------------------------------------------ 8. DC, Ma, and Id mouse lines (wild-derived mice with significantly greater lifespans than laboratory strains) also exhibit low membrane peroxidation index. Hulbert AJ, Faulks SC, Harper JM, Miller RA, Buffenstein R. Extended longevity of wild-derived mice is associated with peroxidation-resistant membranes. Mech Ageing Dev. 2006 Aug;127(8):653-7. Epub 2006 Apr 18. PubMed PMID: 16620917; PubMed Central PMCID: PMC2929641. [Edit: Added 2014-11-12] ----------------------------------------------------------------------- Inductive conclusion, from the above & a few other tidbits: eating DHA will lead to more DHA in MIM and tissue membranes; more DHA in MIM and tissue plasma membranes correlates with aging within and across species, and is actively opposed by normal organisms -- an effect upregulated in CR. Eating DHA causes effects which parallel the 'normal' aging process and which oppose known effects of CR, the only proven anti-aging intervention in mammals. So don't eat DHA. References 1. The Influence of Dietary Fat Source on Life Span in Calorie Restricted Mice. López-Domínguez JA, Ramsey JJ, Tran D, Imai DM, Koehne A, Laing ST, Griffey SM, Kim K, Taylor SL, Hagopian K, Villalba JM, López-Lluch G, Navas P, McDonald RB. J Gerontol A Biol Sci Med Sci. 2014 Oct 13. pii: glu177. [Epub ahead of print] PMID:25313149 2. Life and death: metabolic rate, membrane composition, and life span of animals. Hulbert AJ, Pamplona R, Buffenstein R, Buttemer WA. Physiol Rev. 2007 Oct;87(4):1175-213. Review. PMID: 17928583 [PubMed - indexed for MEDLINE]
  4. 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.
  5. By now everyone has heard of the controversial soda tax being considered by cities and states around the US, and being bandied about by our Presidential candidates (the sane ones anyway...). Now comes not just news, but actual results from an even more ambitious tax to discourage poor food choices. Here is the background, from the full text of [1] (pop press article): In October 2011, Denmark introduced a tax on saturated fat... The tax on saturated fat amounted to 16 DKK/kg saturated fat (~$1/lb - DP) in the following foods meant for human consumption if the level of saturated fat exceeded 2.3 g/100 g: meat, dairy products, animal fats that were rendered or extracted in other ways, edible oils and fats, margarine and spreads. The resultant price changes were non-trivial, for example the price of a standard package of butter at 500 g where the content of saturated fat was 52 g/100 g increased by [~$0.33 - DP] (20%). The researchers in [1] took it as an opportunity to see just what impact such a "sin tax" on food would have on it's consumption and on public health. Here is what they found: The tax resulted in a 4.0% reduction in saturated fat intake. Vegetable consumption increased, and salt consumption increased for most individuals, except younger females. We find a modelled reduction in mortality with 123 lives saved annually, 76 of them below 75 years equal to 0.4% of all deaths from ​[non-communicable diseases]. Here is the table representing the authors' model of the mortality differences that would result from the dietary changes induced by the tax: As you can see, increasing fruit, vegetable and fiber intake, and reducing saturated fat as a result of the tax would appear to save ~175 lives per year, but the extra salt people ate, presumably to compensae for reduced palatability of foods with lower SFA, cost ~41 lives, resulting in a net reduction in 123 lives lost, according to their model, mostly from heart disease avoidance (with some extra strokes due to the salt). This savings represents a relatively small fraction (0.4%) of the total non-communicable deaths in Denmark each year. Questions remain - namely why such a small effect, both in terms of saturated fat intake (only dropped 4%, despite a pretty hefty tax), and in terms of mortality benefit (0.4%)? And the big question - Has their model born out in the five years since the tax was initiated? Has the mortality rate actually dropped as a result of the saturated fat tax? Unfortunately, the answer to all these questions are related. Apparently and not surprisingly, the Danes hated the tax. Rather than seriously cutting back on SFA, they ended up "trading down" (i.e. buying cheaper alternatives with as much SFA as the original) and/or hopping the border to Germany or Sweden where prices were (not surprisingly) 20% cheaper, according to a Washington Post article. In fact, they didn't like the tax so much that it was repealed after about a year - far too short a time to see if it had any long-term health/longevity benefits. Sad, but not surprising. It just goes to show it is really difficult to legislate healthy behavior. But as US cigarette taxes and settlement have shown, these sorts of "sin taxes" are viable but unfortunately quite regressive ways to raise revenue. Not unlike lotteries... --Dean ------------ [1] Eur J Clin Nutr. 2016 Apr 13. doi: 10.1038/ejcn.2016.6. [Epub ahead of print] The effects of the Danish saturated fat tax on food and nutrient intake and modelled health outcomes: an econometric and comparative risk assessment evaluation. Smed S(1), Scarborough P(2), Rayner M(2), Jensen JD(1). Author information: (1)Institute of Food and Resource Economics, University of Copenhagen, Frederiksberg, Denmark. (2)Nuffield Department of Population Health, University of Oxford, Headington, Oxford, UK. BACKGROUND/OBJECTIVE: The World Health Organisation recommends governments to consider the use of fiscal policies to promote healthy eating. However, there is very limited evidence of the effect of food taxation in a real-life setting, as most evidence is based on simulation studies. The objective of this study is to evaluate the effect of the Danish tax on saturated fat in terms of changes in nutritional quality of the diet, that is, changes in saturated fat consumption, as well as other non-targeted dietary measures, and to model the associated changes in mortality for different age groups and genders. SUBJECTS/METHODS: On the basis of household scanner data, we estimate the impact of the tax on consumption of saturated fat, unsaturated fat, salt, fruit, vegetables and fibre. The resultant changes in dietary quality are then used as inputs into a comparative risk assessment model (PRIME (Preventable Risk Integrated ModEl)) to estimate the effect of these changes on non-communicable diseases (NCDs) and mortality. RESULTS: The tax resulted in a 4.0% reduction in saturated fat intake. Vegetable consumption increased, and salt consumption increased for most individuals, except younger females. We find a modelled reduction in mortality with 123 lives saved annually, 76 of them below 75 years equal to 0.4% of all deaths from NCDs. CONCLUSIONS: Modelling the effect of the changes in diet on health outcomes suggests that the saturated fat tax made a positive, but minor, contribution to public health in Denmark. PMID: 27071513
  6. davidleitner

    How Good is Lard?

    I realize this title look like troll-bait, but please hear me out. Given the revived "DHA-Accelerated Aging Hypothesis Validated" thread, I noticed a surprising omission from the discussion. With all the focus on excess O-3 fats (which are clearly a problem), very little attention has been paid to to the fact that the group of mice fed a high-lard diet lived the longest! MR does touch on it here : A lot of the biochemistry is above my head right now, but I understand this to say that eating SaFA is basically a bad way to get your MUFAs. But here is my question: Is the fatty-acid profile of lard improving lifespan by another mechanism(s), perhaps helped along being consumed with a good dose of SaFA? According to Self Nutrition Data, 100g of lard has around 40g of SaFAs and 45g of MUFAs. Similarly, there are considerable SaFA's in human adipose: "compared with adipose fat composition, 27.1 ± 4.2% saturated, 49.6 ± 5.7% monounsaturated, and 23.4 ± 3.9% diunsaturated" according to http://www.jlr.org/content/49/9/2055.full. It seems counterintuitive that our bodies would store SaFA as fuel if if were simply going to kill us dead. And I say this with much much respect to Michael, who I have followed closely. Not in a creepy way :) Thank you for considering this question!
  7. Dean Pomerleau

    Total Cholesterol and Heart Attacks

    [Another one for the "non-CR diet and health" forum. If such a forum ever gets created, I promise I'll use my moderator super-powers to move all these threads to the new forum!] Dr. Greger's latest video titled Everything in Moderation? Even Heart Disease? has this interesting graph from [1] of cardiovascular disease and heart attacks as a function of total serum cholesterol level (click to enlarge): It shows that 35 percent of heart attacks occur in people with total serum cholesterol between 150 and 200 mg/dL. I had no idea it was that high. And virtually no heart attacks occur in people with cholesterol below 150 mg/dL, which is why many people (including me) have said it makes you virtually "heart attack proof". But then I started thinking, wait a minute. Couldn't this simply be a reflection of population statistics, and not reflect a causal relationship between cholesterol level and heart attacks? To understand this possibility, consider a similar plot of height vs. # of heart attacks. Assuming heart attacks are totally independent of height, you'd still see a similar bell curve of the number of heart attacks plotted against height, for the simple reason that height is distributed along a bell curve. So 50% of heart attacks would occur in men below the median height of 5'10" in the US, and furthermore only a tiny fraction of heart attacks (~3%) would occur in men shorter than 5'2", which is two standard deviations below the median. Does that mean that having a very short stature makes you heart attack proof? Of course not, it just means that there aren't many men shorter than 5'2" to contribute to the heart attack statistics. As an admirer of both Dr. Greger's work, I am sometimes disappointed when he uses potentially misleading statistics like this one to advance his perspective on diet and health (i.e. the value of following a plant-based diet - which I very much agree with). So what is the more accurate picture of the relationship between cholesterol and heart attack risk? Here is a graph, from [2], which BTW has a very good overview of various blood markers, including cholesterol sub-components and their association with CHD: As you can see from the graph on the right, CHD mortality rate (as opposed to total # of heart attacks) appears to be pretty asymptotic below 200 mg/dL. It's only when you get up to a total cholesterol of about 225 mg/dL that you see CHD mortality rate rising significantly, above which it goes through the roof. This is what's called evidence-based medicine, and it is why the American Heart Association and European equivalent (the European Societies for Cardiology, Hypertension and Diabetes) recommend keeping total cholesterol below 190-200, rather than necessarily trying to push it below 150 using diet or statins. With the latter, you might end up like this guy : So despite what Dr. Greger suggests, keeping one's total cholesterol below 150 mg/dL, as opposed to somewhere in the range of 150-200 mg/dL, doesn't appear to provide a dramatic benefit in terms of heart attack risk. To be fair, Dr. Greger has another video on the optimal cholesterol level for heart health that does seem to get the science better. It ignores total cholesterol level, and instead looks at all the randomized control trials of cholesterol lowering drugs, which suggest that an LDL level below 70 mg/dL (about 1/2 the average LDL level in US adults, 130 mg/dL) does make one virtually "heart attack proof". But then again, the relevance of results from people who are taking statins, not to mention the relevance for us of statin-induced LDL reduction or other positive effects of statins, make it far from certain that these results apply to people keeping LDL cholesterol low through diet and lifestyle choices. --Dean --------------- [1] Atherosclerosis. 1996 Jul;124 Suppl:S1-9. Lipids, risk factors and ischaemic heart disease. Castelli WP(1). Author information: (1)Framingham Cardiovascular Institute, MA 01701-9167, USA. Over 200 risk factors for cardiovascular disease (CVD) have now been identified. Among these, the three most important are (1) abnormal lipids, including the fact that there are more than 15 types of cholesterol-containing lipoproteins and four different types of triglyceride-rich particles, some of which are very atherogenic, (2) high blood pressure, and (3) cigarette smoking. In addition, many other factors including diabetes, haemostatic factors such as fibrinogen, factor VII, plasminogen activator inhibitors, and new factors such as apolipoprotein E4 and homocysteine, are known to increase the risk of developing clinical CVD. A low risk for CVD requires that these various factors are present in the circulation in the correct proportions. Two simple tests for determining plasma lipid levels can be used to identify those individuals with an atherogenic lipid profile and who are, therefore, at increased risk for CVD. Firstly, the ratio of total cholesterol to high density cholesterol (HDL cholesterol) should be determined, followed by measurement of plasma triglyceride concentrations. This will allow differentiation of whether the low density lipoproteins (LDL), HDL cholesterol or triglyceride-rich particles such as the small dense beta-very low density lipoproteins (VLDL) are the major cause for concern. Once identified, those individuals with a high lipid risk profile should be treated before, rather than after, experiencing coronary heart disease (CHD). PMID: 8831910 ------------------- [2] The Journal of the International Federation of Clinical Chemistry and Laboratory Medicine Vol 13:2 (2003) THE ROLE OF LIPIDS IN THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY HEART DISEASE: GUIDELINES FOR DIAGNOSIS AND TREATMENT Victor Blaton Department of Clinical Chemistry, Hospital AZ Sint-Jan AV, Brugge, Belgium pdf: http://www.ifcc.org/ifccfiles/docs/140206200306.pdf
  8. [Another one for the "Non-CR Health forum"...] Recently there has been much hype in the popular press, including a Time Magazine story, with this provocative cover: that claim we've been wrong about saturated fat (like butter) all along. These stories have been based on meta-analyses like this one [1], that purport to find no association between saturated fat and chronic diseases, even cardiovascular disease. One of my favorite nutrition bloggers, PlantPositive, did a thorough debunking of the Time story and the people & studies it uses as sources. Among other faults of these previous meta-analyses outlined in PlantPositive's post, some of the biggest problems include: Over correction by factoring out serum cholesterol in the analysis - which is elevated by saturate fat intake and so shouldn't be controlled for. Failing to factor out the low cholesterol of saturated fat eaters who take statins to control their cholesterol. Failing to account for the health effects of what people choose to eat instead when they don't eat saturated fat-rich foods. As I recall (but an unable to verify due to the archives being down... ), we talked about all these studies and their shortcomings on the CR email list before. But now, we have something even better than critical analysis of flawed studies. We have a new prospective cohort study [2] of some of the best data available on diet, lifestyle and health from the Health Professionals and Nurses Health Studies. It appears to do a much better job, particularly with respect to the third confounder - food substitution effects. Here is popular press coverage of the new study. The Harvard researchers have followed these two cohorts of 42K men and 84K women for over 30 years, assessing their diet, lifestyle and health repeatedly during that time. This study looked at their fat consumption habits, and in particular changes in those habits over time and how those changes relate to coronary heart disease (CHD). In a nutshell, they found that: Replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from whole grains was associated with a 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10). Here is a graphical depiction of these results: As you can see, trans fat is toxic relative to any other foods, including saturate fat - no surprise. More interestingly, it is about a wash to substitute saturated fat with refined carbohydrates when it comes to heart disease risk. But substituting any of the following for saturated fat results in significantly reduced CHD risk - MUFA, PUFA and whole grain carbohydrates. PUFAs appear particularly protective. Unfortunately the study did not address other healthy carbohydrate sources besides whole grains, like fruits, vegetables or legumes (which I willing to bet would do at least as well as whole grains at reducing CHD risk relative to saturated fat). They also didn't discriminate between the health effects of different types of saturated fats, some of which might not be as bad as others (i.e. those found in plants vs. animal sources). One concern is that when people clean up their diet by eliminating saturated fat, they might also undertake other health promoting lifestyle changes, making it appear that reducing saturated fat was beneficial when it actually was the other changes that made the difference. The authors addressed this potential problem by controlling for a host of other factors in their analysis, including: The multivariable model was adjusted for total energy intake, the energy contribution from protein, cholesterol intake, alcohol intake, smoking status, body mass index, physical activity, use of vitamins and aspirin, family history of myocardial infarction and diabetes, and presence of baseline hypercholesterolemia and hypertension. These results confirm what I think most people have believed all along - that saturated fat is detrimental to heart health, but probably no more so than what people will normally eat instead, crappy carbs. This explains those previous studies that found lower saturated fat intake was often not associated with lower risk of heart disease - people who ate less saturated fat were eating more refined carbs instead, and so weren't any better off. But when you replace saturated fat-rich foods with healthy fats or healthy carbs, you reduce your risk of heart disease dramatically. --Dean --------------- [1] BMJ. 2015 Aug 11;351:h3978. doi: 10.1136/bmj.h3978. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. de Souza RJ(1), Mente A(2), Maroleanu A(3), Cozma AI(4), Ha V(5), Kishibe T(6), Uleryk E(7), Budylowski P(8), Schünemann H(9), Beyene J(10), Anand SS(11). OBJECTIVE: To systematically review associations between intake of saturated fat and trans unsaturated fat and all cause mortality, cardiovascular disease (CVD) and associated mortality, coronary heart disease (CHD) and associated mortality, ischemic stroke, and type 2 diabetes. DESIGN: Systematic review and meta-analysis. DATA SOURCES: Medline, Embase, Cochrane Central Registry of Controlled Trials, Evidence-Based Medicine Reviews, and CINAHL from inception to 1 May 2015, supplemented by bibliographies of retrieved articles and previous reviews. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Observational studies reporting associations of saturated fat and/or trans unsaturated fat (total, industrially manufactured, or from ruminant animals) with all cause mortality, CHD/CVD mortality, total CHD, ischemic stroke, or type 2 diabetes. DATA EXTRACTION AND SYNTHESIS: Two reviewers independently extracted data and assessed study risks of bias. Multivariable relative risks were pooled. Heterogeneity was assessed and quantified. Potential publication bias was assessed and subgroup analyses were undertaken. The GRADE approach was used to evaluate quality of evidence and certainty of conclusions. RESULTS: For saturated fat, three to 12 prospective cohort studies for each association were pooled (five to 17 comparisons with 90 501-339 090 participants). Saturated fat intake was not associated with all cause mortality (relative risk 0.99, 95% confidence interval 0.91 to 1.09), CVD mortality (0.97, 0.84 to 1.12), total CHD (1.06, 0.95 to 1.17), ischemic stroke (1.02, 0.90 to 1.15), or type 2 diabetes (0.95, 0.88 to 1.03). There was no convincing lack of association between saturated fat and CHD mortality (1.15, 0.97 to 1.36; P=0.10). For trans fats, one to six prospective cohort studies for each association were pooled (two to seven comparisons with 12 942-230 135 participants). Total trans fat intake was associated with all cause mortality (1.34, 1.16 to 1.56), CHD mortality (1.28, 1.09 to 1.50), and total CHD (1.21, 1.10 to 1.33) but not ischemic stroke (1.07, 0.88 to 1.28) or type 2 diabetes (1.10, 0.95 to 1.27). Industrial, but not ruminant, trans fats were associated with CHD mortality (1.18 (1.04 to 1.33) v 1.01 (0.71 to 1.43)) and CHD (1.42 (1.05 to 1.92) v 0.93 (0.73 to 1.18)). Ruminant trans-palmitoleic acid was inversely associated with type 2 diabetes (0.58, 0.46 to 0.74). The certainty of associations between saturated fat and all outcomes was "very low." The certainty of associations of trans fat with CHD outcomes was "moderate" and "very low" to "low" for other associations. CONCLUSIONS: Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations. Trans fats are associated with all cause mortality, total CHD, and CHD mortality, probably because of higher levels of intake of industrial trans fats than ruminant trans fats. Dietary guidelines must carefully consider the health effects of recommendations for alternative macronutrients to replace trans fats and saturated fats. © de Souza et al 2015. PMCID: PMC4532752 PMID: 26268692 ------------ [2] J Am Coll Cardiol. 2015 Oct 6;66(14):1538-48. doi: 10.1016/j.jacc.2015.07.055. Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease: A Prospective Cohort Study. Li Y(1), Hruby A(1), Bernstein AM(2), Ley SH(1), Wang DD(1), Chiuve SE(3), Sampson L(1), Rexrode KM(4), Rimm EB(5), Willett WC(5), Hu FB(6). BACKGROUND: The associations between dietary saturated fats and the risk of coronary heart disease (CHD) remain controversial, but few studies have compared saturated with unsaturated fats and sources of carbohydrates in relation to CHD risk. OBJECTIVES: This study sought to investigate associations of saturated fats compared with unsaturated fats and different sources of carbohydrates in relation to CHD risk. METHODS: We followed 84,628 women (Nurses' Health Study, 1980 to 2010), and 42,908 men (Health Professionals Follow-up Study, 1986 to 2010) who were free of diabetes, cardiovascular disease, and cancer at baseline. Diet was assessed by a semiquantitative food frequency questionnaire every 4 years. RESULTS: During 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates from whole grains were significantly associated with a lower risk of CHD comparing the highest with lowest quintile for PUFAs (hazard ratio : 0.80, 95% confidence interval [CI]: 0.73 to 0.88; p trend <0.0001) and for carbohydrates from whole grains (HR: 0.90, 95% CI: 0.83 to 0.98; p trend = 0.003). In contrast, carbohydrates from refined starches/added sugars were positively associated with a risk of CHD (HR: 1.10, 95% CI: 1.00 to 1.21; p trend = 0.04). Replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from whole grains was associated with a 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10). CONCLUSIONS: Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. PMCID: PMC4593072 [Available on 2016-10-06] PMID: 26429077