It's been a while since this transpired here, but I've been pre-occupied with family issues and have preferred to devote the internet time and energy I have to "projects" of greater interest to me. At this point this will probably make more of a mountain out of a molehill of this discussion, but I have spent enough time on this here and there to post it up and make good on my promise to repost deleted comments and publish those in moderation limbo.
One issue I had in this discussion was that Kurt seemed to repeatedly imply that I was somehow anti-fat in the diet, which I'm not - hence the highlighting in this post. My overarching perspective on this topic is that diabetes is characterized by both hyperglycemia and elevated NEFA and these have both separate and combined deleterious effects on tissues, metabolism, etc., thus overall health. My position/concern is that in adopting a VLC diet to gain glycemic control, there is a trade-off in exacerbating the circulating NEFA levels. I'm not in any way claiming to have all the answers, but I'll continue to post on my research into this topic and share it with my readers. And yes, it is research, not just "reading" ... primary scientific research is only one type of activity that meets this definition.
There are exactly zero cultures to look to for epidemiological evidence of the safety of long term very low carbohydrate consumption. The Inuit? Check out their climate and what they eat. It doesn't equate for most avid VLCHF folks. Neither does the Masai. If I'm forgetting something let me know. We certainly have no long term studies on the outcomes for consistent VLC dieters. Claims that this is the healthiest way to eat for life are simply opinions. My purpose with this blog was to organize and share what I've found looking to the scientific literature for evidence that my WOE was indeed healthful.
FWIW, I eat at the high end of low carb these days as a result of my findings. I may go VLC for a stint at some point to see if I can shed these last pounds, but I will again transition to the way I'm eating now once I do. Why? Because there are multiple long-living healthy cultures who have demonstrated the healthfulness of the right sorts of carbohydrates. That, my friends, is just where I come out on this. YMMV
There are exactly zero cultures to look to for epidemiological evidence of the safety of long term very low carbohydrate consumption. The Inuit? Check out their climate and what they eat. It doesn't equate for most avid VLCHF folks. Neither does the Masai. If I'm forgetting something let me know. We certainly have no long term studies on the outcomes for consistent VLC dieters. Claims that this is the healthiest way to eat for life are simply opinions. My purpose with this blog was to organize and share what I've found looking to the scientific literature for evidence that my WOE was indeed healthful.
FWIW, I eat at the high end of low carb these days as a result of my findings. I may go VLC for a stint at some point to see if I can shed these last pounds, but I will again transition to the way I'm eating now once I do. Why? Because there are multiple long-living healthy cultures who have demonstrated the healthfulness of the right sorts of carbohydrates. That, my friends, is just where I come out on this. YMMV
- Kurt G. Harris MD said...
- I think you are partly on the right track in your vindication of insulin. I think you are barking up the wrong tree by worrying about NEFA. I think if NEFA is elevated in diabetics it is an effect an not a cause. Kind of the way you think the elevated insulin is an effect of the pathology producing liver IR, and is not the cause, right? Most papers I read that talk about "liptoxicity" in regard to NEFA or FFA are just veiled extensions of the lipid hypothesis. If something bad is happening, it must be a fat causing it! Show me an epidemiologic marker of NEFA levels that tracks coronary risk at one tenth the magnitude HBA1C does, and I'll start to worry. 'Til then, I know which poison I prefer.
- CarbSane said...
- Welcome to my blog Kurt! Regarding the NEFA and the lipid hypothesis, I'm amazed at the HUGE body of research on NEFA out there, much of it in the diabetes realm. While you'll often see statements like "obesity caused by high fat diet", etc., the research on mechanisms, progression, etc. is quite solid by the much-maligned scientists. For starters, dietary fat is not even mentioned in most studies as these researchers are well aware that the source of NEFA is release from fat cells. I've blogged on a number of articles on the development of IR (the root of all metabolic evil), and the NEFA seems to come first and precipitate the other things. Two such posts: http://carbsanity.blogspot.com/2010/07/progression-of-insulin-resistance.html http://carbsanity.blogspot.com/2010/10/insulin-resistance-taubes-v-frayn.html I think you may find this review article a bit of a paradigm shifter: http://www.springerlink.com/content/8G1GPV7741K2B34T/fulltext.pdf Lastly, my personal interest in this is due to the fact that I get the occasional racing heart so when I discovered the connection between elevated NEFA and sudden cardiac death, there's no way I think I can ever dismiss this from my mind! http://carbsanity.blogspot.com/2010/05/sudden-cardiac-death-and-free-fatty.html Contrary to the whole "LDL clogs arteries" arguments, where there is little to no evidence that the cholesterol itself does anything, a large fraction of the NEFA research relates to how the NEFA directly impact cell function even leading to cell death. Scary stuff! In all honesty, I really hope I'm barking up the wrong tree. That so long as carbs are uber low elevated NEFA should not be worried about. But I haven't found that "get out of jail free card" yet. I'll keep looking ;)
- Kurt G. Harris MD said...
- Thanks for the response. My own reading so far does not make me fear NEFA in the least. Even if it is pathologically elevated as part of METSYN, I believe it is only an effect, not a cause. The applicability to HFLC diets or fasting is not appropriate. NEFA has to cause muscle (not liver) IR or one will not be able to feed the brain - Yes I am with Peter on that. The reversibility of this phenomenon has been documented for over 50 years. NEFA levels rise when you fast- do you think fasting is dangerous? You will be in quite a quandary if you decide that NEFA and elevated blood glucose are both threats, kind of like Dr. Davis who is afraid of both glucose and saturated fat! I will read those references.
- CarbSane said...
- Kurt, I look forward to your replies once you've read those references. If they don't give you reason to pause, I look forward as to why.
- CarbSane said...
- Re: NEFA levels rise when you fast- do you think fasting is dangerous? They rise, but are not excessive, and rise because they are subsequently taken up by our cells and burnt for energy. NEFA levels rising excessively in the fed state is my concern. You will be in quite a quandary if you decide that NEFA and elevated blood glucose are both threats, kind of like Dr. Davis who is afraid of both glucose and saturated fat! If it were just *me* deciding it I would agree, but there's a ton of research indicating that NEFA alone have direct deleterious effects.
- Kurt G. Harris MD said...
- @Carbsane You said: "I've heard Stephan Guyenet say something like that he's uncomfortable with carbs <20% but not really elaborated as to why. I've certainly not seen any evidence that just because sat fats aren't "dangerous" that we should be swigging shots of fat between meals and cooking beef in butter. " I can't speak for Stephan, but I'd be pretty shocked if the reason Stephan thought eating, say 20% carbs was healthier than eating 10% had anything at all to do with not wanting to eat too much fat. The benefits of increasing carb intake by 100% are a more likely explanation than the benefit of decreasing fat by a mere 15%. Stephan elsewhere has alluded to it being "counterproductive" to eat VLC if you don't have to due to diabetes. I can think of two reasons on my own that this is the case, whatever Stephan thinks. 1) As you approach ketosis and get in the VLC range, peripheral (not pathologic, just muscle) insulin resistance HAS to increase to avoid hypoglycemia and keep BG stable. This means you become more "carb sensitive" the less CHO you eat. If you do binge or do cyclic carb loading, this peripheral IR does not change quick enough to prevent significant BG spikes - higher than would be the case if one were used to getting more total calories from CHO. So you may eat less but actually experience more time with dangerous (>140) BG levels, even if you are normal. If you do not binge or cycle CHO, fasting BG on VLC can rise to the point that AUC for BG is the same or even higher than if you ate more CHO. And due to peripheral IR, you have the same AUC for insulin and fasting insulin as you had at higher CHO intake. You you have gained nothing in terms of what your tissues see of BG or insulin 2) Eating VLC makes it hard to get micronutrients and solubel fiber -which Stephan believes in for sure 3) Performance for the physically active is substantially better at 20% than at 10% - you are at 2x the ketosis threshhold - which I think is no accident. Stephan has also said he eats a lot of carbs because they are cheap!
- Kurt G. Harris MD said...
- Sorry, I normally can spell "soluble.."
- 20 PM
- Kurt G. Harris MD said...
- "BTW, re: NEFA we discussed previously, you might be interested in the subject of my recent post: http://carbsanity.blogspot.com/2011/02/non-esteried-fatty-acid-metabolism-and.html" Have seen it and left a comment there....
- 10, 2011 1:03 PM
- Stephan said...
- Hi CarbSane, My perspective is that excess glucose and FFA are both damaging, particularly in combination. But what does "excess" mean? I think the key word in Frayn's sentence is "inappropriate" release of FFA. I think you know about the Randle cycle. Glucose and FFA are in a sort of balance with one another. Postprandially in a lean healthy person, a carb-containing meal increases glucose and insulin, and FFA are suppressed by 80-95% for hours. Without carb, FFA may increase postprandially. But there's no glucose spike in that case. Personally, I think the most dangerous thing is when you have someone who doesn't adequately suppress FFA during a glucose incursion. Then you have high levels of both. That seems to result from insulin resistance preventing the complete suppression of hormone-sensitive lipase. The insulin resistance is probably mostly the result of chronic cellular energy excess in my opinion, and that in turn is mostly due to energy imbalance. Obesity is a marker of energy imbalance but lean people can be out of balance as well (and that may be the most dangerous because adipose tissue isn't taking the pressure off the lean tissues). The point is that in my opinion, elevated FFA without elevated glucose may not necessarily be "inappropriate". It occurs normally during fasting, for example. Yes, elevated FFA inhibits glucose metabolism and insulin's glucose-suppressing action, but it kind of makes sense from a physiological standpoint. I'm not convinced it's pathological. When you have high postprandial glucose but you fail to suppress FFA, like one sees diabetes and upper body obesity, then you're in trouble.
- Kurt G. Harris MD said...
- @Carbsane I totally agree with Stephan here. I've read the Frayn paper and most of your posts on NEFA. I have to say you are threatening to make the same mistake your friend GT is making - confusing internal metabolite behaviour with food behaviour Hyperglycemia bad ergo eating carbs bad vs Inappropriately elevated NEFA bad ergo eating a lot of fat possibly dangerous Both non-sequiters Maybe focus more on the "hyper" and "inappropriate" modifiers. The question is which foods (or non-foods) are causing what. if you have read any of my recent posts, I think "macronutrient ratios" is barking up the wrong tree as the concept of macronutrient itself is bereft. It's about the poisons that cause metabolic syndrome, not mixing "macro" ratios like you are making a cake.... or fearing either of the two evolutionary fuel sources - starch or LCFAs. Re: your personal "heart racing". VLC, to the degree it may create relative hypoglycemia, is likely to have periods of elevated epinephrine where your adrenal glands are trying to liberate glucose from your liver to drive up BG -this is just homeostasis, no matter how uncomfortable, and as long as you were in sinus rythym, would have zero relationship to the type of arrythmia that you seem to be worried about. It has nothing to do with an arrythmia precipitated by altered metabolism in someone with a fresh infarct du to fatty acids. People on VLC or atkins induction report tachycardia all the time. I don't recommend steady ketosis, but more arrythmias are associated with high carb than with low - esp atrial fibrillation, which is serious.
- February 10, 2011 6:22 PM
- Kurt G. Harris MD said...
- Just to be clear, tachycardia due to epinephrine in response to hypglycemia, not a result of high NEFA per se. Could be dangerous - in the same way exercise would be -IF you had a pre-esisting conduction abnormality or valvular aortic stenosis or IHSS - but the solution is higher carb intake to avoid hypoglycemia, not lower fatty acid consumption
- King said...
- I think you guys who are concerned with CS "making the same mistake" as Taubes is overlooking the fact that Taubes wilfully misrepresents studies to fit in with his lowcarb/insulin ideas whereas CS is presenting and commenting on factual research without trying to make the conclusions fit with a predetermined viewpoint. Have you even read the above quoted research? I realize it's challenging to read and understand (because it's very technical and littered with acronyms), but it really is a bit of an eyeopener. And I highly disagree that the concept of macronutrients is bereft. As calories go, it's all energy to the body, but the source and quality of the foods you eat really does matter for your health.
- CarbSane said...
- @Stephan: Welcome to the Asylum. Thanks for your input. Re: The point is that in my opinion, elevated FFA without elevated glucose may not necessarily be "inappropriate". It occurs normally during fasting, for example. Yes, elevated FFA inhibits glucose metabolism and insulin's glucose-suppressing action, but it kind of makes sense from a physiological standpoint. I'm not convinced it's pathological. When you have high postprandial glucose but you fail to suppress FFA, like one sees diabetes and upper body obesity, then you're in trouble. I look at this from the POV of if low carbing is potentially dangerous. I can't change whatever risk I took with the way I lost my weight, but I can change what I do now. NEFA is almost completely ignored in the low carb community, and actually celebrated (anything that increases lipolysis) even when there's no indication of actual increases in total oxidation rate. You have a lot of IR and T2's "self treating" and lowering BG levels. However, my research demonstrates in most, the "inappropriate" NEFA release from adipose tissue PREcedes the hyperglycemia. The study I linked to () demonstrates an inappropriate NEFA release in both lean and obese subjects. This study (http://www.ajcn.org/content/91/3/578.abstract- BTW if you have access to the full text I would love a copy!) showed increased fasting and 24hr exposure to FFA's. They correlated with increased LDL - something that is very common on low carb diets.
- I've come across a virtual tsunami of literature and studies indicating that chronic IR follows and is instigated by elevated NEFA. If a dietary approach increases NEFA while decreasing a downline symptom (BG) it can potentially cause a progression of IRS and the related risks. That certain other biomarkers, like fasting triglycerides, are generally lower may (note the may) not be reflective of what's really going on and provide false assurances.I've got several related posts in the works. I hope you'll read them and provide feedback.
- CarbSane said...
- Sorry, the study I linked to was: http://www.jlr.org/content/48/10/2236.full
- CarbSane said...
- I do hope you'll read some of the stuff I'll be posting in the coming weeks.
- CarbSane said...
- Oh ... Also re: fasting and NEFA (from your prior comments). The incidence of heart attacks is several fold higher within the first 3 hours of awakening....
- Stephan said...
- Hi CarbSane, I think excess circulating energy in any form, whether from FFA or glucose, is harmful. I certainly don't think FFA should be ignored, as they are potentially just as damaging as glucose in my opinion. My main point is that the concept of "excess" is poorly defined in the case of FFA. We know a fair bit about what excess FFA means in the context of a typical mixed American diet (or at least we have correlations), but not much about what it means in a low-carb context in which the metabolism resembles fasting in some ways. Regarding the increased heart attack risk in morning, I think it's tough to pin that on FFA. You've just been laying still for hours, and you might dislodge a thrombus by getting up. There are many things that are physiologically different about the morning relative to the afternoon. When you say elevated FFA precede hyperglycemia, are you talking about fasting hyperglycemia or postprandial hyperglycemia? That's a critical distinction, as the latter is a much more sensitive marker of glucose homeostasis problems. In any case, would you mind posting that reference? I imagine you read the "gluttony and sloth" paper on lipotoxicity. They speculate that excess circulating FFA leads to ectopic lipid accumulation (muscle, pancreas, liver, etc.), which leads to glucose homeostasis problems. I think it's plausible. But what causes the excess FFA? Their model of choice for supporting their hypothesis is a db/db mouse, which has no leptin signaling and is therefore also profoundly insulin resistant. Insulin resistance in adipose tissue causes a defect in the suppression of lipolysis, the same way the liver doesn't suppress glucose production when it's insulin resistant. And what causes that? Probably chronic energy imbalance, exacerbated by some other factors such as a lack of short-chain fatty acids, minerals, omega-3s, polyphenols, etc.
- CarbSane said...
- @Stephan: I think the two blog posts (containing associated links) most pertinent are: http://carbsanity.blogspot.com/2010/07/progression-of-insulin-resistance.html http://carbsanity.blogspot.com/2010/10/insulin-resistance-taubes-v-frayn.html I just received the full text of Hernandez and will do a brief blog post on one aspect of it showing the NEFA levels throughout the day. They are elevated big time and consistently. Re: NEFA and morning heart events, I don't think they are the instigators, but they might well be compounders. I suppose there's enough content here and in my archives to start compiling more summary articles. I've got one on IR in the works. Certainly NEFA will deserve it's own treatment!
- Kurt G. Harris MD said...
- @King "Have you even read the above quoted research? I realize it's challenging to read and understand (because it's very technical and littered with acronyms), but it really is a bit of an eyeopener. " Umm.. yeah, and whole lot more than that besides. I don't consider it challenging and this site (no offense CS) is hardly the discoverer of any of this info on free fatty acids. It's not really an eye-opener at all if you understand it. Only if you think eating food has to be dangerous!
- February 11, 2011 3:50 PM
- CarbSane said...
- It's not really an eye-opener at all if you understand it. Only if you think eating food has to be dangerous! What does THAT mean?
- Kurt G. Harris MD said...
- @Carbsane "the studies linked seem to indicate that a very low carb diet induces a pathological response" That's your interpretation, it would not be mine. It is not pathologic. " I've read (and enjoyed & agree with BTW) your macro-myth post and it's a good one. But in the end all dietary LCFA's must be "cleared" relatively rapidly, and failure to do so indicates metabolic dysregulation." Thanks. Yes, but there is no evidence the LCFA is causing the metabolic dysregualtion. Even granting some of the bad effects of metsyn could be mediated via inappropriate elevation of NEFA, who would trade guaranteed hyperglycemia for the speculative effects of elevated NEFA. We've just agreed you have to eat something. The randle cycle guarantees that there will be an inverse relationship between glucose and ffa availability. The only way to avoid this is to be dead. You can't , a a la Dr. Davis, eat in a way that absolutely minimizes both. This reminds me of telling diabetics how important it is to "manage their cholesterol" while advising them to eat a low fat diet full of glucose.. We know that advice is a massive fail. "Where BG's are concerned in the IR/T2, spikes do still come down in a matter of hours. But look at the pp NEFA's in the above-linked study. They persist 4 hours out and look to be on the uptick. Thus while pp hyperglycemia does not seem to lead to chronic hyperglycemia, pp hyper-NEFA can, apparently lead to a chronic state." It's not leading to anything. If you eat to minimize the NEFA, you will maximize the heck out of your serum BG, because you cannot eat isocaloric without massively increasing carbs if you minimize LCFAs. Or you can do like Davis and substitute PUFA WHICH IS LIKELY CAUSING THE WHOLE METABOLIC DYSREGULATION IN THE FISRT PLACE. OK, sorry to shout, but that is the point of my no such thing as a macronutrinet posts - the way to address the met dysreg is avoid hyperlgycemia (we know that is bad) and eliminate the things causing met dyreg - I suggest wheat fructose and linoliec acid. There is simply no evidence whatsoever that eating LCFAs causes met dysreg. Zero. But there is good evidence for avoiding the NAD (neolithic agents of disease) "So you are not concerned when people report tachy on VLC??" I am not concerned about sudden death in normal people- simus tachycardia would be an antidote to many deadly arrythmias, in fact. The NEFA related one you've written about is in damaged heart muscle.
- Kurt G. Harris MD said...
- continued.... "From what I've been reading, NEFA doesn't *cause* arrhythmia or ischemia, but it can interfere with recovering from it. So this can be a double whammy with hypo -> arrhythmia and NEFA -> failure to recover. Why take that chance?" Life is full of chances and conditional probabilties. If by avoiding sat fat you increase your risk of atherosclerosis - ischemia, what consolation is it that you're having a heart attack but theoretically less likely to have an arrytthmia from it? "As you say, the solution is to eat more carbs. YES!! But don't tell this to most low carbers who insist that VLC diets are the healthiest option for everyone. " That is the solution to avoiding elevated epinephrine and tachy, but not becaase I think you will die from it and it is not NEFA that is causing it. "I believe that the episodes from LC stint 2 that have been almost absent this go-round are due to my "cheats" (essentially carb-ups) and to my consumption of leaner proteins." may well be the case, and I'm glad to hear that. I have less orthostasis on 20% carbs than 10%. "Just because certain fats aren't harmful in large amounts doesn't mean that eating large amounts is "healthy"." I agree in principle, but I have been trying to look for evidence that any dietary saturated fat (not pufa) can per se cause anything pathologic and I have found nothing. The cardiologists look desperately to prove it and cannot, but try to interpret their own findings that way anyway. "Make sense? I do worry for those eating VLC who are either constantly regaining and losing " Again, I worry that as Stephan has said, that it is counterproductive for several reasons to be VLC. But I think it is that you are losing the benefits of starch in the diet and that you are unnecesarily limiting yourself on VLC - not that the high level of fat itself is of any harm at all. It makes no sense to me that 25% of calories from sat fat is OK, but 30% is dangerous. It makes sense to me that 20% from starch is better than 10% though.
- Kurt G. Harris MD said...
- "It's not really an eye-opener at all if you understand it. Only if you think eating food has to be dangerous! What does THAT mean?" I mean it is not an eye- opener. It is not surprising. I am not shocked. This is not the first time I've heard of this. If you are convinced, like most of the population, that FATS somewhere, somehow, must be deadly, then you can read these papers and be alarmed. I am not alarmed, this is not new information. If a person is searching for evidence of what dangers lurk in their diet, like, "hey did you know that there are FATs in your blood that go up on low carb? OH no!" then they might be alarmed. That is what I see happening here, as I've tried to make clear. Clear enough? To say something is an eye-opener means the person should be surprised or shocked or worried. I am not shocked. It is not news to me and I don't interpret it the way you do.
- Kurt G. Harris MD said...
- "my research demonstrates in most, the "inappropriate" NEFA release from adipose tissue PREcedes the hyperglycemia. The study I linked to () demonstrates an inappropriate NEFA release in both lean and obese subjects. This study (http://www.ajcn.org/content/91/3/578.abstract- BTW if you have access to the full text I would love a copy!)" When you say "my research" do you mean your reading of published papers, or your own actual research? Do you do research in this area? And one of the things that concerns me here is how can you even quote something if you have only read the abstract? That is no better than a press release really. This is one of the ways it is easy to get confused, by giving any attention at all to a mere abstract.
- CarbSane said...
- Ahh Kurt, I see the problem here. Yes, I'm suggesting that we should eat in a manner so as to keep NEFA at appropriate levels. Elevated NEFA is indeed as deleterious as hyperglycemia, and the two in tandem are a very bad mix. We see both in all untreated diabetics. So to "treat" this by focusing just on one energy substrate and ignoring the other is possibly (definitely IMO) short sighted. How does one reduce NEFA? I am NOT advocating a low-fat lipid-hypothesis-reasoned approach. NEFA is largely controlled by adipose cell function and release from fat cells in normal people. This paper also discussed how impaired trapping can exacerbate the problem because dietary fat is actually not supposed to add to the free fatty acid pool - it is supposed to be transported as triglycerides and taken out of circulation following lipolysis. So, it is not the dietary fats that are causing anything, saturated, PUFA or otherwise. It's the disregulated fat cell that improperly releases the NEFA and/or fails to properly take in FFA's hydrolyzed from chylomicrons that's the problem. And here, low carb eating does lead to a disruption of this process in obese especially, but also in normal lean subjects. Elevated NEFA directly stimulate basal insulin levels but inhibit acute insulin response. They inhibit insulin's vasodilatory effects. They inhibit NO production in vascular endothelium. Cause increases in intramyocellular lipids that cause peripheral IR if they accumulate in a hypercaloric state such that intermediates in lipid metabolism (e.g. ceramides and diacylglycerols) become ROS. I could go on. None of this is eye opening or worrisome to you? I'll be posting some data from the full text of Hernandez in a bit. We're not talking just a little elevated. We're talking consistent and considerable elevation during weight loss on VLC. No concern? As you'll see, these are not normal physiological substrate levels! I don't do primary research any more, but I had done it for almost a decade and was published in peer review journals. I'm well aware of the limitations of abstracts and try to avoid them. The other study was a full text, however, and now I've got the full text of this one to work with. I think we're in agreement on missing out on the benefits of starch with VLC diets. High fat doesn't cause the high NEFA, severely restricted carbs do. Thus some carb consumption can improve NEFA and this should actually (as Shai demonstrated) improve glycemic control. T2's controlling their diabetes through VLC dieting are likely masking their hyperglycemia by keeping dietary carb low. But they're almost definitely exacerbating the NEFA. In the long term there are definite consequences attributed solely to high fatty acid concentrations that should not, IMO, be ignored. I'm not the only one saying this as I'm sure I've posted up quite a few reviews lamenting the lack of focus on this and perhaps overemphasis on just glycemic control.
- Thanks for the discussion (and the explanation)!
- February 11, 2011 5:30 PM
- Kurt G. Harris MD said...
- My typing fingers are getting sore, so I'll have to keep it short "low carb eating does lead to a disruption of this process in obese especially, but also in normal lean subjects." perhaps exacerbation, don't agree with "leads to" - not convinced it is worse than the alternative of hyperlgycemia if they have metsyn "T2's controlling their diabetes through VLC dieting are likely masking their hyperglycemia by keeping dietary carb low." Not masking. Not having it is not masking. "In the long term there are definite consequences attributed solely to high fatty acid concentrations that should not, IMO, be ignored." I don't agree that they are as definite or as dire as what we know are the consequences of hyperglycemia. If I were as snarky as Peter I would say that that explains why Dr. Bernstein has killed so many type IIs with his diet : ) I had a friend with fasting BG of 185 who went down to 118 and lost 40 lbs on VLC and I am supposed to worry about his NEFAs? There reason drug studies of glycemic control increase mortality is because they are doing it with DRUGs, including our friend insulin. I am aware of zero clinical studies that show increased death or morbidity due to elevated NEFA in diabetics on VLC. I would like to see them if you have them, maybe I just haven't seen them yet. OTOH we know how bad hyperglycemia is. Thanks for the conversation. I need to go work on my "FH and lipid hypothesis post".
He also seemed to take offense to my statement that he was confusing NEFA with dietary fat. I'm not sure what other impression I should have been getting with all those (yellow highlighted) references to fat in the diet.
I'm going to deal with Peter's take on the Raz paper at some future date, and when I do, I'll edit in a link to the post.
Yes, folks, I "back published" this to around the time when I completed the post. It's just not all that important to me any more.
There never was a Part II. I'm editing in a link to the follow up post containing additional posts including the one I deleted.
http://carbsanity.blogspot.com/2011/04/to-my-readers.html