tag:blogger.com,1999:blog-36840063.post3884658267148659298..comments2024-03-27T22:57:00.742+00:00Comments on Hyperlipid: Uncoupling control in defence of FFAsPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger34125tag:blogger.com,1999:blog-36840063.post-3839463560707829822019-03-13T12:27:04.262+00:002019-03-13T12:27:04.262+00:00Hi Peter,
Thank you for approving my two previous...Hi Peter,<br /><br />Thank you for approving my two previous comments which are highly critical of your views on carbohydrates. I appreciate that.<br /><br />Although we'll probably never agree about diet & nutrition, I like the way you moderate the comments here. Keep on keeping on!<br /><br />Cheers, Nige<br /><br />P.S. Hi Galina L. See, I'm not dead! :-DNigel Kinbrumhttps://www.blogger.com/profile/03368973941328529619noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-82994794260415199922019-03-13T08:42:23.015+00:002019-03-13T08:42:23.015+00:00"You did nothing wrong, I blocked you on twit..."You did nothing wrong, I blocked you on twitter for my own sanity sake, after you wrote that you are not going to read Peter comment that I linked."<br />You've mis-represented what I wrote <b>yet again</b>.<br /><br />From <a href="https://mobile.twitter.com/NigelKinbrum/status/1104783672677449731" rel="nofollow"><b>https://mobile.twitter.com/NigelKinbrum/status/1104783672677449731</b></a>:-<br />"I have no interest in Peter D's utterly biased opinions.<br /><br />FFAs are CONSTANTLY HIGH on LCHF/keto. This increases insulin secretion but inhibits insulin synthesis.<br /><br />Didn't you read <a href="https://mobile.twitter.com/NigelKinbrum/status/1104615197925359616" rel="nofollow"><b>https://mobile.twitter.com/NigelKinbrum/status/1104615197925359616</b></a> ? This confirms that I'm right & Peter D's wrong."<br /><br />I wrote that <b>after</b> I read Peter's reply to what you wrote. Still, a man sees what he wants to see and disregards the rest (apologies to Simon & Garfunkel).<br /><br />"Saturated fatty acids synergize with elevated glucose to cause pancreatic beta-cell death." by El-Assaad W. et al."<br />This is irrelevant to what I wrote. The problem to which I'm referring is increased insulin secretion combined with reduced insulin synthesis, leading to depletion of insulin within beta cells, leading to loss of the 1st phase insulin response.<br /><br />You repeatedly mis-represent what I write due to severe cognitive bias, which is why <b>I've blocked you</b> on Twitter. It's impossible to debate somebody who repeatedly uses the Strawman fallacy. Unfortunately, Peter doesn't use Disqus for the Comments section here, otherwise I would block you on here as well. This is my final reply to you. <b>Any further comments from you to me will be ignored</b>.<br /><br />Goodbye.Nigel Kinbrumhttps://www.blogger.com/profile/03368973941328529619noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-88765774496024347332019-03-12T23:40:36.045+00:002019-03-12T23:40:36.045+00:00Nigel,
You did nothing wrong, I blocked you on tw...Nigel,<br /><br />You did nothing wrong, I blocked you on twitter for my own sanity sake, after you wrote that you are not going to read Peter comment that I linked. The one where he quotes this paper:<br /><br />"Saturated fatty acids synergize with elevated glucose to cause pancreatic beta-cell death." by El-Assaad W. et al.<br /><br />I had a bad experience once with a friend, whom I had to block after 18 years (in real life, not on-line!) who was overwhelmingly rational to the extent that his super-logical mind became his own enemy preventing him to move forward, learning new things. I wasted so much energy debating him, with nothing constructive ever coming out of it, that I developed an allergy towards people like that.<br /><br /> I am also borderline "Aspie", like you (scoring 28 or 29 on Baron-Cohen's scale, with the threshold being 30). I am so glad to see that you decided to post in the "enemy's" camp. I hope you have read Peters's replies which apply directly to our Twitter conversation. <br /><br />I have to add that the theory that FFA or saturated fat would damage pancreas, on its own has to be incorrect for the reasons other than just the paper above. Fatty cuts of meats have been human staple diet for hundred thousands of years so it is extremely unlikely that this stuff would suddenly somehow become harmful to any of our organs. Furthermore, in my own personal observation, when I started on my high animal fat low carb nutrition in 1999, I could only consume up to ~20-30g of carbohydrates. My body was insulin resistant and glucose intolerant though not to the extent of clinical DM.If high FFA would indeed harm beta cells then this condition (IR) would have persisted or worsen. In fact the opposite happened! My IR gradually went away and was healed on eating mostly fat! After about 5-7 years (and even now) I found that I could actually eat a high carb meal (potatoes and rice for example) if I wanted to, way above the initial 20g limit! <br /><br />Stan (Heretic) <br /><br /><br /> Stan Bleszynskihttps://www.blogger.com/profile/03922719716458272303noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48527593955695384662019-03-12T19:38:10.536+00:002019-03-12T19:38:10.536+00:00Hi Peter,
You've raised some interesting poin...Hi Peter,<br /><br />You've raised some interesting points. As achieving optimum health is <b>never</b> a waste of time, I'd like to discuss them, if that's O.K. with you. If it isn't, this post won't pass moderation! :-D<br /><br />1. My approach <b>improves</b> metabolic flexibility.<br />Your approach <b>worsens</b> it.<br />Healthy humans don't get energy from carbs <b>or</b> fats. They get it from carbs <b>and</b> fats, in ratios which vary constantly for optimum operation & glycogen storage levels. Your blog header is a false dichotomy fallacy. :-/<br /><br />2. I agree that chronic hyperinsulinaemia is bad.<br />You keep your insulin low by minimising your exogenous carb intake, maybe insulinogenic proteins too.<br />I keep mine low by maximising my insulin sensitivity.<br /><br />3. You get hyperglycaemia if challenged with a meal of absolute garbage, due to 1.<br />I don't. I can eat <b>whatever I want</b> (in reasonable amounts, of course!) without getting postprandial hyperglycaemia, hyperinsulinaemia & its associated drowsiness followed by rebound ravenous hunger. Two hours after swallowing 75g of glucose, my BG was 3.7mmol/L in September 2008. Fasting BG was 5.0mmol/L.<br /><br />4. I'm now metabolically flexible, so nothing would happen if I ate a fatty leg of lamb and nothing else. I have plenty of storage capacity available in liver, muscles & fat mass to clear glucose &/or TGs from circulation in good time.<br />Unlike you, if you ate five doughnuts.<br /><br />5. "It's just not an approach I'm interested in." That's illogical.<br />Before October 2015, illogical statements would melt my brain figuratively speaking. Since I saw a neurodevelopmental professional who diagnosed me with Asperger's Syndrome, I've learned how to cope with life's illogicalities, so I don't care.<br /><br />Cheers, NigeNigel Kinbrumhttps://www.blogger.com/profile/03368973941328529619noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-57814272671011708232019-03-12T09:38:13.801+00:002019-03-12T09:38:13.801+00:00There , you see, we have opposite approaches. My o...There , you see, we have opposite approaches. My own plan is to eat to stimulate the minimum insulin secretion and to respond as little as possible to that signal. LC, high saturated fat.<br /><br />The bottom line is minimising insulin signalling.<br /><br />You have your own approach where clearly, however you have done it, systemic insulin exposure is low, ie normal BMI. This is clearly very possible. It's just not an approach I'm interested in. Equally obviously I regard decreasing insulin synthesis as a positive development, as is glucokinase down regulation and as is the deconstruction of excess complex I in the ETC. All of which happen with my approach. All of which will allow hyperglycaemia if challenged with a meal of absolute garbage. So I don't do that.<br /><br />To me, the question is, what would happen to yourself given a fatty leg of lamb and nothing else to eat? Like me eating five donuts. There are lots of other "what if"s too but you realise no one convinces anyone of anything on t'internet, so let's not waste too much time on it.<br /><br />Two sides (minimum) to every approach.<br /><br />All the best<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-8220357312521379812019-03-12T05:43:44.782+00:002019-03-12T05:43:44.782+00:00Hi Peter. I'm only posting here 'cos of my...Hi Peter. I'm only posting here 'cos of my "debate" with Stan on Twitter. He blocked me after I dismissed your objections. Debate with Stan is futile, as he's learned nothing about how the body works.<br /><br />Having fixed my IR, I can eat anything without getting adverse effects. A recent randomised crossover trial of produce-based LCHF vs HCLF I ran on myself showed that my brain works best on HCLF, so that's what I eat now. I've been maintaining a BMI of 23.9 since last September on my produce-based HCLF diet + treats. I concentrate my fat intake into 1 meal (from sardines or mackerel) to stimulate gall bladder emptying.<br /><br />People who have working beta cells should try to reverse their IR, as long-term LCHF/keto impairs beta cell function. This is *not* an improvement! <br /><br />If IR is irreversible &/or beta cells are damaged irreversibly, LCHF/keto is fine.<br /><br />Cheers, NigeNigel Kinbrumhttps://www.blogger.com/profile/03368973941328529619noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-31727589552626529862019-03-11T05:46:23.625+00:002019-03-11T05:46:23.625+00:00Hi Nigel, nice to see you're still around!
Pe...Hi Nigel, nice to see you're still around!<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-83364265614895008932019-03-10T23:09:22.368+00:002019-03-10T23:09:22.368+00:00What's with you LCHF'ers & strawman fa...What's with you LCHF'ers & strawman fallacies?<br /><br />It's not an issue of toxicity. Chronic high FFA causes an imbalance between insulin secretion & insulin synthesis, resulting in reversible loss of 1st phase insulin response. This causes very high postprandial BG when carbs are eaten. <br /><br />https://t.co/t9HS3yzp1k?amp=1Nigel Kinbrumhttps://www.blogger.com/profile/03368973941328529619noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-65735313621438531822019-03-10T19:29:21.236+00:002019-03-10T19:29:21.236+00:00Yes, I’ve got the cell death rate for beta cells w...Yes, I’ve got the cell death rate for beta cells with palmitic acid up to 400micromolar in either glucose 5mmol/l vs glucose 20mmol/l. Glucose 5mmol/l allows palmitate 400micromolar to be completely non toxic.<br /><br />The paper is here<br /><br />https://www.ncbi.nlm.nih.gov/pubmed/12933690<br /><br />but the extracted graph is in this post<br /><br />https://high-fat-nutrition.blogspot.com/2012/08/protons-fadh2nadh-ratios-and-mufa.html<br /><br />People will be so embarrassed when they realise how badly they have been had by the LF brigade! But for now they still believe!<br /><br />All the best<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-56583035601439148222019-03-10T16:09:51.794+00:002019-03-10T16:09:51.794+00:00Thanks, that's what I thought too. I am surpr...Thanks, that's what I thought too. I am surprised how few studies are available on the effects of the high serum FFA concentration alone, that's why I asked. I couldn't find any. My suspicion is that the pancreatic beta cellular damage (as reported. for example in the following study, see below) was due to glucose+FFA combination, in-vitro. <br /><br />"Chronic Exposure to Free Fatty Acid Reduces Pancreatic b Cell Insulin Content by<br />Increasing Basal Insulin Secretion That Is Not Compensated For by a<br />Corresponding Increase in Proinsulin Biosynthesis", by L. Cornelius Bollheimer et al., <br />Pubmed article PMC508661<br /><br />Best regards,<br />Stan<br /><br /> Stan Bleszynskihttps://www.blogger.com/profile/03922719716458272303noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-36772327851244356122019-03-10T06:33:51.349+00:002019-03-10T06:33:51.349+00:00Hi Stan, the biggest problem with the paper is tha...Hi Stan, the biggest problem with the paper is that the authors appear to consider that LDLc is the cause of CVD. As such there is no common ground for any sort of discussion, If, as I do, you consider that one of the core drivers of CVD is chronic hyperinsulinaemia, there is no way of dropping to the level of stupidity that describes eu-insulinaemia in these terms: “As expected, patterns of 24-h insulin concentrations in the High Fat group lacked a physiologic pattern, remaining low and blunted (Figure 1A), which assumedly contributed to the lack of FFA suppression”. Words fail me. They have no concept of normal physiology.<br /><br />As regards FFA toxicity, yes, hyperglycaemia, especially post prandial, causes beta cell death in the presence of physiological fasting FFA levels. Obviously palmitic acid is the best facilitator of glucotoxicity. Also (obviously) Figure 1 lacks glucose levels, unsurprisingly for a garbage study like this. But we know from Table 2 that the HC diet increased 24h glucose (a little, despite weight loss) while LC dropped 24h glucose (a lot). And what is physiological for FFAs in the presence of low glucose? We know from<br /><br />Prolonged Fasting Identifies Skeletal Muscle Mitochondrial Dysfunction as Consequence Rather Than Cause of Human Insulin Resistance<br /><br />that when slim people don’t eat for 60 hours the mean physiological total FFA level is over over 2000micromol/l and palmitate is quite possibly over 1000micromol/l, this is normal (unless people think not eating for 60 hours is going to kill your pancreas!). So 800micromol in the presence of unreported but low glucose? Probably normal.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-24824445909174962662019-03-09T22:37:49.822+00:002019-03-09T22:37:49.822+00:00Regarding supposedly detrimental effects of FFA cl...Regarding supposedly detrimental effects of FFA claimed by some researchers, this paper was mentioned in the course of a debate with some high-carbers on Twitter (I am not posting the link because of the spam cop rule, but you can google the title):<br /><br />"Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet", by Teri L Hernandez et al., Am J Clin Nutr. 2010 Mar; 91(3): 578–585.<br /><br />Appart form being short (6 weeks) the study shows some unusually high peaks of serum FFA, for patients on Atkins eating 20g of carbohydrates. Not sure if (1) this is problematic (though there are some other papers indicating that the high level of FFA seems to be damaging for pancreatic beta cells (is it really?).(2) not sure if that study is representative for normal people on a low carb diet. What do you think?<br />Regards,<br />Stan (Heretic)<br /><br /><br />Stan Bleszynskihttps://www.blogger.com/profile/03922719716458272303noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-37832249503043292672014-10-11T20:13:35.651+00:002014-10-11T20:13:35.651+00:00Hi Guillermo, going back to Veech’s paper on keton...Hi Guillermo, going back to Veech’s paper on ketones and metabolism in cardiac muscle, the gain with ketones was an increase in energy yield from ATP hydrolysis rather than increased ATP production. Table 1 has the basic data. http://www.fasebj.org/content/9/8/651.full.pdf<br /><br />Qori, not much help from me, I don’t really exercise deliberately nowadays. I walk miles and will surf when I can (not much at the moment but this will eventually change as the children grow up).<br /><br />Raphi, I’d guess HIT activates AMKP and almost certainly generates superoxide, although it’s not an area I’ve read in to very much.<br /><br />Passthecream, they are looking for a drug which mimics palmitic acid in its free acid form. Simply skipping carbs will be asking for far less in the way of unintended consequences…<br /><br />Jack, under Crabtree there is extensive mtDNA damage. All you need is for a subgroup of badly damaged mitochondria which happen to reproduce more rapidly than healthy mitochondria and you might well be looking at a single cell converting all of its mitochondria to rapidly replicating duds. I’m guessing autophagy should be “aware” of this but it speaks of why some people may have long term issues with adaptation to a fat based diet.And the issues could be quite loclaised.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-53871589623865630832014-10-11T17:49:09.448+00:002014-10-11T17:49:09.448+00:00It's a Catch-22 situation. The body (start wit...It's a Catch-22 situation. The body (start with mitochondria) can't remodel unless given a need to do so and with appropriate environmental conditions.<br /><br />It probably starts this way:<br />Need to remodel (getting rid of damaged complex1 from years of glucose burning) --> (restrict glucose-ketogenic-high intensity exercise - endurance exercise - induce uncoupling) --> Apoptosis --> autophagy --> fusion --> fission --> mitobiogenesis.<br /><br />End result: rejuvenation of whatever body parts the demands are placed on.<br /><br />Processing glucose occasionally may be the equivalent of fire-drill to teach mitochondria to handle ROS better, I think.JohnNhttps://www.blogger.com/profile/07639308289155393659noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-41051127912652814852014-10-11T17:44:08.261+00:002014-10-11T17:44:08.261+00:00It's a Catch-22 situation. The body (start wit...It's a Catch-22 situation. The body (start with mitochondria) can't remodel unless given a need to do so and with appropriate environmental conditions.<br /><br />It probably starts this way:<br />Need to remodel (getting rid of damaged complex1 from years of glucose burning) --> (restrict glucose-ketogenic-high intensity exercise - endurance exercise - induce uncoupling) --> Apoptosis --> autophagy --> fusion --> fission --> mitobiogenesis.<br /><br />End result: rejuvenation of whatever body parts the demands are placed on.<br /><br />Processing glucose occasionally may be the equivalent of fire-drill to teach mitochondria to handle ROS better, I think.JohnNhttps://www.blogger.com/profile/07639308289155393659noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-65582601587648464912014-10-10T17:06:44.986+00:002014-10-10T17:06:44.986+00:00Guillermo would benefit from reading Ling and my c...Guillermo would benefit from reading Ling and my current blog on protons (Tensegrity #6). It might open your eyes to something biology has missed but Ling has been saying for 60 years now. Anonymoushttps://www.blogger.com/profile/06619419812590914435noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-80767130044226570342014-10-10T07:08:21.733+00:002014-10-10T07:08:21.733+00:00I think I just happened to decrease carb intake sl...I think I just happened to decrease carb intake slowly over the course of a couple years, and now I've been pretty low for another 2-3 years. I used to have a sweet potato binge per week because of cravings, but I haven't done that in about a year either. Perhaps people need longer to adapt or are eating the wrong foods. It's also possible I could have been performing suboptimally all along, but my strength has increased, and my dance endurance is better than most. Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-23519592937405605052014-10-07T17:30:53.135+00:002014-10-07T17:30:53.135+00:00You can once you institute auptophagy to recycle a...You can once you institute auptophagy to recycle all the bad mitochondria.........considering how many mitochondria the brain and heart alone have that is why 18-36 months is the window most people find for adaptation. Anonymoushttps://www.blogger.com/profile/06619419812590914435noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-63143341776921298092014-10-07T13:12:41.010+00:002014-10-07T13:12:41.010+00:00Some people don't have issues with glucose def...Some people don't have issues with glucose deficiency while doing intense exercises because they adapted to working out in a fasted state or ketosis. You just can't jump into keto-adaptation after years of carbo-loading.Galina L.https://www.blogger.com/profile/09156132815504279615noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-42035021270951053252014-10-07T08:21:31.007+00:002014-10-07T08:21:31.007+00:00An extract of the article linked to by "Passt...An extract of the article linked to by "Passthecream":<br /><br /><< What we're doing inside cells is like putting the car's transmission into neutral by uncoupling it from the transmission. Then you step on the gas so the engine runs full throttle but the car doesn't move. If too much of the fuel in the cell is fat, you keep burning it until the fuel gauge reaches empty. Without the interference of fat, you hope that sugar will then enter the cell normally .>><br /><br /><< "We wanted a safe and practical compound to deplete fat inside cells," says Jin. "We went to the literature and found an approved drug that does in parasitic worms what we wanted to do in liver cells." >>raphihttps://www.blogger.com/profile/08992252569979714724noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-53707442130307234912014-10-07T08:11:26.192+00:002014-10-07T08:11:26.192+00:00An interesting post as usual.
Care to comment on ...An interesting post as usual.<br /><br />Care to comment on this?<br /><br />http://medicalxpress.com/news/2014-10-diabetes-results.html#ajTabs<br /><br />It seems a bit worriesome to me!Passthecreamhttps://www.blogger.com/profile/01214860448492630477noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-5258342329222146482014-10-07T05:07:30.970+00:002014-10-07T05:07:30.970+00:00Qori,
I lift 4 days per week and have about 7 dan...Qori,<br /><br />I lift 4 days per week and have about 7 dance classes per week. I've never noticed any "glucose deficiency" symptoms like Jaminet and am usually <100g carbohydrate. There have been periods of time where I was having ~50g/day. I'm not sure why some people have issues and some don't. Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-16469152565925500002014-10-02T08:48:22.528+00:002014-10-02T08:48:22.528+00:00Hi Peter,
This http://goo.gl/agZEH9 is the "...Hi Peter, <br /><br />This http://goo.gl/agZEH9 is the "TestDiet 5TSY AIN-93G Atkins/Rodent" used by Wang et al. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2642968/pdf/nihms83334.pdf).<br /><br />It's terrible. So terrible that the the TestDiet website doesn't seem to make it easy to find, except via an email request.<br /><br />Also, love the "NOT for human consumption" disclaimer. Damn right. Except that pretty much the worst of what's in it makes it into all processed foods.<br /><br />It seems the premise of uncoupling per se being an issue doesn't is based on subjects with poorly built mitochondrial machinery incapable of sustaining sufficient mitochondrial ATP levels.<br /><br />J. Stanton surmised that High Intensity exercises could jump-start the mitochondrial adaptations that are often uncomfortable for people suddenly switching to a HF diet. Could this have to do with better uncoupling dynamics?<br /><br />Cheers!raphihttps://www.blogger.com/profile/08992252569979714724noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-19022176990945897192014-10-01T14:58:04.375+00:002014-10-01T14:58:04.375+00:00Jack, Peter or anyone else that cares to provide i...Jack, Peter or anyone else that cares to provide insight; what are your opinions on eating LC/VLC/HF/Ketogenically and regularly exercising/training in a very anaerobically demanding manner?<br /><br />I do this and have no problem sustaining my performance in these endeavours (although I'm aware that my performance/endurance in some of the more glycolytically demanding activities may be improved hypothetically by increased carb intake -Jack you may not agree with this based on what you've written about this).<br /><br />My training consists of weight training and sprintwork. Both being phosphogenic in nature I imagine but becoming more glycolytic during repeated bouts with minimal rest between sets.<br /><br />Essentially i'm interested in how training and eating this way pertains to the type of long-term health so often addressed here. -Mitochondria, Insulin, Cardiac events, Growth factors, DNA damage etc.<br /><br />I have no interest in aerobic endurance as so many in the keto/LC/HF world seem to have and I've not really read much relating to this way of eating with these types of activities and the impact on health<br /><br />Any input on such a matter?<br /><br />RegardsAnonymoushttps://www.blogger.com/profile/12225209167342701364noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-16318742286255793342014-10-01T07:41:49.436+00:002014-10-01T07:41:49.436+00:00hi Jack
seeing that you are on about IR, I wrote t...hi Jack<br />seeing that you are on about IR, I wrote to Gerald Pollack to introduce Danielle Goodspeed's work on salicylate levels in circadian entrained plant tissues being at a zenith, at about midnight, in preparation for the attack of pathogens at dawn when plant surfaces are at dew point with water condensation and IR coming on stream as the earth rotates into the solar flux ( my interest lies in the fermentation of "entrained" green plant tissue in the hindgut). An example of Goodspeed's work - http://www.ncbi.nlm.nih.gov/pubmed/23299428dr jhttps://www.blogger.com/profile/03137256472582167775noreply@blogger.com