The main finding is that the oxidation of glucose can blocked, even in the presence of large amounts of injected insulin, by a modest quantity of a particular small molecule. This form of insulin resistance, if you want to call it that, does not seem to occur at the cell surface, so it's probably not mediated through the failure of insulin to mobilise GLUT4s. And, as glucose seems to enter the cells and disappear, the presumption has to be that it is "non oxidatively disposed" as the modern parlance has it. Probably to glycogen, there's not really anywhere else for it to go.
So what is this evil chemical which blocks glucose oxidation even in the face of hyperinsulinaemia?
Beta hydroxy butyrate. That's it. Ketone bodies (acetoacetate seems to work as well) are triggers for insulin resistance. Hence the appalling problems of type two diabetics on the Atkins induction diet. What problems? Oh, normoglycaemia and weight loss! Well, maybe there are problems long term or or or...
Again ketone bodies, one of the hall marks of carbohydrate or total calorie restriction, channel glucose away from muscles, toward brain and add a modest supplementary energy supply to brain tissue too.
It's exactly what you expect on an adaptive basis, exactly the same function as palmitic acid performs and clearly the two metabolic pathways are closely linked, though ketones seem to work downstream of the action of palmitic acid.
The fact that ketones do still allow insulin to move plasma glucose in to cells, and probably store it as glycogen, might be of interest to those who's blood glucose seems to do strange things after they eat medium chain triglycerides. MCTs (in rats anyway) undoubtedly spike both insulin and ketones, but usually result in normoglycaemia (insulin resistance?). But this is in a carbohydrate fed, glycogen replete rat. If you are initially glycogen depleted the shift to replete glycogen under ketones from MCTs might just leave you hypoing. No one has looked at this as far as I'm aware but ItsTheWoos' experience is interesting on this front...
Actually, looking carefully at the graph from Yeh and Zee, glucose does dip through an amount which might be clinically noticeable...
Anyway, there you have it. Metabolic poison number three, beta hydroxy butyrate. Evolution sure made a lot of b@lls-ups on the way to where we are today. I'm doomed, as always.
Peter
Why is the rat glucose so high in both feeding groups?
ReplyDeleteMy understanding is that normal rodent blood sugar is the same as normal human blood sugar and in this case the three and four hour values (and the pre-feed fasting) are in the diabetic range for fasting glucose.
So, are ketones a good thing or a bad thing? I noticed you mentioned that you eat just enough carbohydrates to keep you OUT of ketosis. Is this part of the reason why?
ReplyDeleteI have been browsing you site for awhile, and find it fascinating and very informative. Keep up the great work!
I'm sorry, but I'm unclear. Why is it a good idea to channel glucose away from muscle tissue? I thought we wanted it to go to muscle tissue to be burned for energy...
ReplyDeleteI'm obviously missing something.
Hai Peter,
ReplyDeleteThank you so much for taking the time to figure out why coconut is so paradoxical for me. That makes a lot of sense. The graph plainly shows MCTs have a hyperinsulinemic, hypoglycemic compared to corn oil. Knowing this, everything makes so much sense. I suspect I have some kind of intrinsic, possibly genetic problem with insulin function (it does not appear typical insulin resistance). In general, anything that raises insulin tends to be a risk factor to cause hypoglycemia in me, even things that logically should not cause hypoglycemia (such as a large bolus of protein). It is almost as if my counter regulation is FUBARed, or perhaps my ability to deactivate insulin... who knows. It's almost as if insulin works "too well" for me.
I'll file this under "stuff that works for people with garden variety obesity, but won't work for someone with my issues". It seems I make too much insulin, but use glucose pretty normally. Yes, chronic vulnerability to hypoglycemia, with rebound ravenous over eating that can lead to fat storage and even higher insulin... this is the outcome. Must avoid any pure hypoglycemics.
Jenny... Peter did say the rats were tortured more or less. Perhaps the stress of being abused and attacked caused hypercortisolemia and mild diabetes?
ReplyDeleteJenny, my guess is that the rats didn't enjoy the restraint for tail venepuncture and back in 1976 the needles may have been quite large compared to the needles we might use today. They also measured quite a lot of parameters, which may have needed a large (by rat standards) sample which would have been hard to get. I'd think stress.
ReplyDeleteHi Gobears, not really, I think that ketone bodies are good good good if you are glucose deprived. I think insulin resistance is essential if you are glucose deprived. BHB, like palmitate, should induce insulin resistance. I'm just waiting for BHB to get tarred with the same brush as palmitate...
The nice thing about this normal adaption to physiological insulin resistance is that it allows you to function perfectly well under pathological insulin resistance. It doesn't seem to fix the pathology but it certainly side steps it.
Charles, glucose is fine for energy if you have some glucose available. If you have no glucose you will drop in to ketosis to save your remaining glucose for your brain. Burning your last 10g of glucose in your biceps is a bad idea... The MCT is the interesting one. Humans have been eating coconuts for a long time. They seem to be a perfectly ordinary food. MCTs certainly do odd things, but I'd expect the system to balance itself out. This makes me doubt that the hyperinsulinaemia following MCTs is pathological, but you never know...
Peter
Its,
ReplyDeleteIt was the rabbits which were injured beyond comprehension. The rats just got restrained...
P
Brilliance beyond WORDS!!!!
ReplyDeleteJenny and Peter,
Maybe these are diabetic rats?
-G
I have experienced "sugar crashes" after eating a lot of virgin coconut oil on quite a few occasions, too. I typically cook my eggs in it and often would eat a couple of table spoons while cooking. I was puzzled as why this was as MCTs are ideal fuel, but why did I feel like I just slammed a can of coke shortly afterward?
ReplyDeleteHi Peter,
ReplyDeleteThanks for the answer about ketones. How about your own diet, if I may ask. Do you keep in ketosis or just out of ketosis, and why? I noticed on another one of your posts you mentioned staying "just out of ketosis". I found that interesting and hard to understand, as many low carb diets promote staying in ketosis.
ItsTheWooo wrote:
ReplyDelete"It seems I make too much insulin, but use glucose pretty normally. Yes, chronic vulnerability to hypoglycemia, with rebound ravenous over eating that can lead to fat storage and even higher insulin."
What if insulin isn't the main cause for hypoing? There's been quite a lot writings on adrenal fatigue related to too low-carbing; especially if you are "adrenal type person" and not losing weight while doing it.
Elaine Gottschall (thank you, Peter, telling me about her) used special carbohydrate diet (SCD) also as a causal treatment for adrenal fatigue related symptoms which (as I've understood) include: chronic fatigue syndrome, fibromyalgia, IBS, anxiety and depression.
If you connect two diets with excellent results (SCD and J.Kwasniewski diet) you would get somekind:
high fat, low carb, moderate high-quality-protein, probiotic, banana-diet,
which might be quite close to optimal diet for all of us. :)
Hi Peter,
ReplyDeleteSo do you use MCTs in any significant amounts in your diet? It's started to seem like almost every vegetable oil, including the so-called "safe" ones like olive and palm, are showing themselves to be damaging to those whose systems are already "broken".
I have noticed this MCT "crash" as well when I've been very steady on OD and then eat coconut oil. Perhaps my body was more damaged than I thought when I started all this.
I've not really done a lot of looking on the idea of a sugar crash in normal people after MCTs very much. I'd remembered the MCT rats as being normoglycaemic, which technicaly the numbers are, apart from what I'm considering stress hyperglycaemia. I also have vague memories that coconut contains either a salicylate or similar which might augment insulin secretion, though purified MCT wouldn't do that as per the rat experiment...
ReplyDeleteI eat a little coconut as a block of macerated coconut and as occasional sauces on Ken Hom recipes, but it's not a big feature. I don't much worry about ketosis as I rarely test strongly positive (I rarely check anyway) and it's mostly exercise that ups my ketones. I seem to hill walk on ketones. But yes, stress response is one reason I try to avoid extreme ketosis.
Gunther, maybe low glycogen levels and high insulin secretion are likely to encourage lower blood glucose levels after MCTs. It doesn't have to be pathological insulin resistance... As I recall Stephan discussed the coconut based diets on Tokelau and there was a significant amount of carbohydrate as well as the coconuts.........
Peter
Hm. Then that leaves me to believe that perhaps there's a REGIONAL integrity that must be maintained on any of these paleo-inspired diets.
ReplyDeleteIn other words, where's there's a diet high in coconut (Kitava, Tokalau), there's high carbs. Where there's one high in animal fats (Masai, Inuit), there don't seem to be coconuts and people are running on a lot of ketones.
It's the mixing of these that could create problems for some I think. Coconut and high ketones in a diet don't seem to appear together. Nature really covers all her bases!
Hi Peter:
ReplyDeleteHow much carbohydrate is required per day to "just" stay out of ketosis?
Thanks for the post.
Hi Olga, that's difficult to say as we're all different and, to be honest, I don't really measure/count much nowadays. A ketosix supply will tell you for yourself. For me between 40 and 80g/d is probably about right, unless I get the chance to nip up Ben Lomond, at which point I probably ought to eat more but don't usually get round to it...
ReplyDeletePeter
Hi Peter:
ReplyDeleteThanks for the prompt reply. So if you're staying out of ketosis. Are you still able to burn body fat for fuel? I'm trying to understand exactly how the system works in a broad sense. So if you stay out of ketosis, but reduce you're fat intake so that you are a little hypocaloric, relative to your daily caloric needs you should still loose fat?
Also, I'm in Canada, eh. What does "nip up Ben Lomond" mean :)
Nip up Ben Lomond. It's weird what fat lazy rats do for fun when eating high fat diets!
ReplyDeleteRe ketosis; people burn fat on Weight Watchers so running low carb and yet non ketotic certainly allows fat loss. Lutz and Groves, both long timers, suggest around the 70ish g/d of carbs. They are not aiming for maximum short term weight loss, that was Dr Atkins' forte...
Peter
Ben Lomond is lovely! Thanks. Yes, I think I already knew the answer to my own question, but all the information overload starts to get confusing.
ReplyDeleteOne last question. I'm trying to find ways to increase fat in the diet. For so many years we have all been trying to avoid fat at all costs, that it's amazing, how one really has to go out of the way to actually eat fat! I'm trying to approach the levels suggested by Jan Kwasniewski, but some of his recipe suggestions, I suspect, are more appealing to a Polish palate. Any suggestions on how to greatly increase fat but not carbs. The easiest way I can think of is to drink 35% cream with each meal. Yummy, but I'm sure it will get tiresome eventually. Thanks.
Peter, Ahh thank you for the correction. I need to work on reading more closely
ReplyDeleteWestie – problem with the assumption of adrenal fatigue is the following:
1) my hypoglycemia was worst when I was not restricting food (i.e. eating lots of insulin-generating food)
2) my hypoglycemic tendency improves with every subsequent year of low carbing (if it was “adrenal fatigue related to low carbing” I would see a trend of worsening hypoglycemia). For example, I can now drink coffee while sleep deprived without any hypoglycemia. This was not possible before.
3) I don’t have problems losing weight if I restrict carbs and calories so as to optimize insulin and fat metabolism. I am very often energetic (sometimes too energetic, hehe) and I am thin now (120#/65in)
I’m not so keen on the idea of adrenal fatigue anyway. It is irrational, in my opinion. Your classic low adrenal patient has none of the symptoms of an obese stressed out person. The low adrenal patient is hypotensive, hypoglycemic, thin, weak, fatigued. THIN, did I mention that? Adrenal hormones are crucial for appetite – they antagonize leptin function in CNS and raise insulin.
There is a trend of people calling “being stressed out” as “adrenal fatigue”. Don’t ask me, I don’t get it. Stress causes high cortisol, and high cortisol leads to all the problems people confuse with low adrenals (being obese, over eating. glucose problems, mood impulsivity/lability and depression). Low adrenals involve low cortisol which causes anorexia and frailty.
The fatigue in so-called “adrenal fatigue” is usually secondary to mood disorders and metabolic syndrome (induced by stress/genetics) or completely unrelated conditions like hypothyroid (yes adequate cortisol affects the conversion of t4->t3 but most people are not low in cortisol with fatigue). The fatigue in real low adrenal is related to true hypocortisolemia which means low catecholamines, low SNS, low thyroid, and thus low energy.
High fat, low carb, moderate protein – I definitely feel BEST on this diet. Too much protein or too much carb will give me BAD MOJO. Too much protein = anger, rage, chaotic moods, hunger (atkins attitude and ineffective weight loss). Too much carb = torpor, hypersomnia, apathy, hunger (atypical depression basically).
High fat, low carb, enough protein = happy me as can be :D
I too have noticed a "crash" after a couple ounces of coconut oil. interesting. of course to some extent that is a refined product and I have no business drinking straight coconut oil; coconut milk or coconut out of the shell has not given me that trouble.
ReplyDeleteolga - use lots of butter and coconut milk in cooking, for me heavy cream never gets old. nuts, avocados. high fat salami, pork belly, fish, etc.
Variants in Neuropeptide Y Receptor 1 and 5 Are Associated with Nutrient-Specific Food Intake and Are Under Recent Selection in Europeans
ReplyDelete"Our data suggest that lower carbohydrate intake, consuming meals with a low glycemic index and glycemic load, and/or higher alcohol consumption, gave a survival advantage in Europeans since the agricultural revolution. This advantage could lie in overall health benefits, because lower carbohydrate intake, consuming meals with a low GI and GL, and/or higher alcohol consumption, are known to be associated with a lower risk of chronic diseases".
Bashed your head? You needed a stiff drink .
"a study of 38,000 people with head injuries, which found that those with alcohol in their blood were more likely to survive. For every 100 people who died when stone-cold sober, only 88 died with ethanol in their veins."
Conection with ethanol being ketogenic ?
Peter, I liked when you posted "What I eat" with a UK slant, such as Sainsbury's Value Mince, and was wondering if you could post an updated version? I'm wondering if much has changed in light of recent research?
ReplyDeleteI don't see a "contact" button so I'll leave this comment
ReplyDeletehave there been any studies showing a small to normal amount of fructose plus PUFA causing liver abnormalities?
all the stuff I've seen has been excessive, prolonged amounts of fructose or PUFA doing these things.
Maybe there's been something that combined "normal" fructose ingestion (say 2 or 3 apples a day), and "normal" PUFA (say 2 or 3 capsules of fish oil or flax oil) and found some worrying effects?
Hi everybody and thanks to Peter who writes amazing stuff.
ReplyDeleteImagine that I have just had some fun and played a game of football. The game was long and my muscle and liver glycogen are low now. I want to feed them (and my brain) with some glucose. I choose to eat some potatoes. In this case they will give me about 60 grams of starch. To keep those potatoes palatable (and Kwasniewski happy) I will add 60 grams of fat from butter to my meal. But now there is that palmitic acid and a danger of IR. My guess is that a meal like this would digest pretty slowly and cause a large insulin AUC.
In a case like this should I drop the butter and have a dry meal without the butter. Intense and short insulin spike. But now I will get hungry in a couple of hours... Who likes to eat constantly? How much starch can my body handle with that much palmitic acid causing IR? Pedantics?
That should not be a problem.
ReplyDeleteEating potatoes (300-400g??) with butter (60g only?) should not be a problem, since palmitic acid molecules from butter do not enter directly into the blood stream (because fat cannot swim in water/blood). Rather they are packed (with other ingested fats) into water soluble cabs called chylomicrons and moved to storage very effectively, if there are that much carbohydrates to use first.
The "palmitic acid wave" comes from liver only after the insulin has done its task with sugars. And, depending on what you have eaten before, that palmitic acid may well be originating from carbohydrates, not butter...
Hi Ken,
ReplyDeleteJust skimmed the intro so far. Where does that leave the food pyramid? Oh, where it belongs! And these Cloggies just seem to take it for granted that LC and low GI are associated with less chronic disease. Bring on the Dutch cheesecake and gin, the later with the water frozen out in a deepfreeze before drinking....
Alcohol and ketones: Yes, I suspect this may be where the benefits derive vs the problems from hepatic lipidosis... I have a vague post do-able around that idea.
Dillon, not much change except my cream fermenting fell to pieces on the move to Glasgow and I haven't restarted the production line. Now I'm back to work I'll probably need yogurt in preference to the cream I'm on at the moment as it travels better! My wife has a whole load of gluten free recipes which we've adapted to LC but the essence is unchanged.
Sanjeev,
I've not seen this, few studies look at what seem like reasonable intakes over some time in humans. But I would just point out that three apples is > 30g of fructose. That's not trivial in the eyes of a LC eater. Also there will be a normal distribution for the incidence of NAFL against fructose intake and someone has to be on either extreme of the curve!
Siberian and LeenaS (hi!). I put up a similar reply on the palmitic acid post. If your liver is reasonably functional there will be no problems dealing with the amount of carbs eaten by a LC eater in the presence of palmitic acid. As insulin rises the supply of FFAs will drop and the liver and muscles will accept glucose, especially if they are well glycogen depleted. I don't see an issue with the amounts we might eat. Maybe problems with half a kilo of carbs with the OD level of fat, but that's the next post.
Hi Chainey, welcome back, feel free.
Peter
I also have a question about carbs: if I'm going to eat them, should I eat just them, eat them with fat, with protein, or with vinegar (for as I have read somewhere vinegar reduces blood glucose spike)? What is your opinion?
ReplyDeleteand thank you for a great blog...
Why is insulin resistance a good thing with low glucose?
ReplyDelete@Kirk "Why is insulin resistance a good thing with low glucose?"
ReplyDeletePeter answered this above (I asked the same question):
...glucose is fine for energy if you have some glucose available. If you have no glucose you will drop in to ketosis to save your remaining glucose for your brain. Burning your last 10g of glucose in your biceps is a bad idea.
Sorry but that doesn't help me understand. What would happen if say, you ate only coconut oil and chicken breast for a year? You would produce a ton of insulin and get more and more insulin resistant? Isn't that the path to obesity and diabetes?
ReplyDeleteSiberian,
ReplyDeleteWhat makes you think your glycogen and glucose would be depleted significantly? Skeletal muscle runs on fat almost exclusively unless in an extremely anaerobic state, like very fast sprinting. If in fact your glucose levels were lower than the acceptable range, meaning your hepatic system could not keep up with demand, you would feel light headed, dizzy, and probably nauseated. If you feel fine then just eat normally as you feel like it and your glycogen stores, if depleted at all, will eventually come back to normal. It's really only there to feed your brain, not your muscles.
I mean just look at me. I run long distance and play Ultimate Frisbee on a zero carb diet. I have no hypoglycemic problems. I have no endurance problems. That is because, as is shown on this blog in many places, there are mechanisms to conserve glucose and those mostly involve increasing fatty acid concentrations in the blood. Also, keep in mind that muscles love to burn fat -- it makes a lot more ATP than glucose with a lot less waste product. So even if going anaerobic there is still lots of ATP to work through (produced from fat) before glucose is needed. And one can only go anaerobic for so long before very serious fatigue sets in. Then you take a break, oxygen levels return, and ATP is produced from fat again. Glucose is still conserved (to keep the brain alive!)
I also read that in the fasted state, the brain will use up to 70% in ketones. So, still, glucose is not as highly demanded as one might think and it is conserved.
Kirk, there is nothing progressive about physiological insulin resistance. You have very little glucose, you divert it to your brain. If you allowed yourself more glucose you would make more insulin, reduce fatty acid release from adipocytes and increase your insulin sensitivity to an appropriate level. Might take a few days.
ReplyDeleteThe problem with pathological insulin resistance appears to come from your adipocytes becoming insulin resistant, probably through over distention with triglycerides, and then releasing palmitic acid even in the presence of as much insulin as your pancreas can produce. They probably got that over distended due to hyperinsulinaemia being used to mop up glucose released by your insulin resistant liver. Your liver gets insulin resistant through fructose. Which means sucrose and HFCS.
The messenger is the same. One is normal physiology, the other is fructose poisoning. That's ignoring issues like bisphenyl A in your fat cells, which probably matters. There is probably an issue with mitochondrial dysfunction in adipocytes which is a trigger for insulin resistance and inappropriate free fatty acid release too.
So on chicken and coconut you would use free fatty acids to keep glucose out of muscles and available for brain, you really would die without this phenomenon. You would not usually become hyperglycaemic, though I know of one person who has achieved this in extreme ketosis for difficult weight loss. A few carbs sorted this out.
Hi Marnee, The other thing I noticed, back when I used to pushbiked more, was that on extreme hill climbs I HAD to stay aerobic, so I paced myself, and did really well within my oxygen delivery capacity. But at the top of the climb I can just up the gears and go, no recovery period, no lactate pain. I'm no sports physiologist but I guess I work almost fully aerobically and mostly on fatty acids. This makes anaerobic stuff very hard but aerobic stuff easy and non exhausting. Plenty more fat where the last lot came from....
Peter
Hi Peter-thanks for the great blog.You mentioned above a preference of yoghurt now. For high fat/min. lactose/cassein and insulin response what is best? Greek/creme fraiche?
ReplyDeleteI still consume daily 300mls+ of tesco double cream-is this still ok unfermented. Is UK dairy still largely pastured or is it now industrial and high in Omega 6.
What are you general thoughts on cheese on optimal diet as i'm a glutton for brie and cheddar.
Sorry about the litany of mundane questions.
Nathan
Part 1 / 2:
ReplyDeletePerhaps I am late to comment here, but I find the graph of insulin and glucose responses to MCT Oil extremely interesting.
First, maybe I am misunderstanding something, but how do you get insulin resistance out of this graph? Far from it, this graph might show hyperinsulinemia, but glucose responds quite rapidly to that?
Second, from what you describe, normal glycolysis is being impaired, but glycogen metabolism is not being impaired. Wouldn't that in fact be a virtue not a vice? Because glycolysis involves oxidation. Disposal to glycogen should be much more efficient and less damaging potentially. Note these comments are in context of a low carb diet, where the muscle can actually put that glucose to use and store the glycogen. Obviously the person on higher carbs that has completely stuffed his muscles with glycogen isn't going to be able to store most of that glucose as glycogen, so I'm not sure what happens to that person.
Here is a similar study, where the (human) patients are fed either a monounsatured fat (olive oil), or a saturated fat (butter), and they graph insulin and glucose post-meal:
http://ajcn.nutrition.org/content/93/3/494.full
And here is the graph of interest from the results:
http://ajcn.nutrition.org/content/93/3/494/F1.large.jpg
Like in the study you post, the saturated fat meal creates hyperinsulinemia, but unlike your study, the saturated fat meal in the study I post also creates complete insulin resistance. If you look at the insulin for saturated fat, it soars to ~500 whereas glucose never responds rapidly, or largely, to this huge insulin input. The body is pumping out more and more insulin, and glucose fails to respond appropriately. THAT is insulin resistance. Your graph to contrast shows clearly that glucose is being used up (presumably as glycogen stores).
What are the differences between the two studies to explain these dramatically different results? One hypothesis might be that all saturated fats - including dairy fats like butter and MCT Oil - create hyperinsulinemia, but only *some* saturated fats (or specific fatty acids) additionally create insulin resistance for all glucose metabolic pathways, including glycogen storage.
If that hypothesis is correct, it would suggest that the low carb dieter who eats a few starchy carb meals a day might want to use MCT Oil as the fat with those meals instead of butter. Because MCT Oil might allow glucose to moderate and be stored efficiently as glycogen. To contrast, butter might cause insulin resistance for all pathways including glycogen, so butter would cause glucose to rise much higher.
The reason that your post is so interesting to me is that I am prediabetic (my father was prediabetic his whole life and it never became diabetes, so probably I share some inefficient genes). In my case, I have achieved remarkable control of my post-meal glucose through a combination of low/moderate carb diet (after initially trying as low as 40 grams/day of carbs and running out of glycogen, I am now back to about 120 grams/day and doing okay) and careful testing of different fats with my three starch meals each day (corresponding to roughly three cups of rice at breakfast, lunch, and dinner). What I have incompletely documented is that with MCT Oil my glucose stays very low after eating just rice. With other fats, it goes quite high. So for example, my fasting glucose might be 80, and after a cup of rice with MCT Oil one hour later I am at 90. For me that is LOW. If I try that same cup of rice with nearly equivalent grams of fat from butter, my glucose one hour later is 105 to 130. (As an aside, I started this journey with fasting glucose of 115 and now have that down to about 85, and I'm trying to keep my post meal glucose under 120.)
Up to now, I have not really understood this result. The graph from the study you published, and your discussion, all seem to reinforce my observations about MCT Oil.
Part 2 / 2:
ReplyDeleteI would very much like to do some controlled tests with different kinds of fats, but here is my problem: I can measure glucose but I have no practical way to measure insulin! And it turns out that insulin is actually the more meaningful thing to measure here. Because as the graph in the study I published suggests, if you only follow glucose things can look pretty normal. But insulin resistance is only confirmed by watching insulin grow extremely high, and then watching how glucose responds to that event. You need to follow glucose and insulin together.
Since we appear to have so many biochemists here, can someone explain to me what is the test process / machine used to measure insulin? Is there any practical insulin test within the reach of a home user that doesn't involve at $20K piece of equipment the size of a refrigerator?
This comment has been removed by the author.
ReplyDeleteThis comment has been removed by the author.
ReplyDeleteHi P1,
ReplyDeleteMCTs are very complex. Essentially, they behave more like sugars than fats. If you have the persistence to slog through the Protons thread you can see that they are largely diverted to the liver where the flood of acetyl-CoA is used for a combination of ketogenesis and de novo lipogenesis, to give a mix of palmitate and monounsaturated fat which eventually get exported in triglycerides.
It is quite possible that the generation of palmitate in the liver simply blocks hepatic glucose extraction, so insulin penetrates to the systemic circulation and allows normal glucose uptake as MCTs are not getting past the liver, so there is no systemic insulin resistance.
Most of the work on MCTs was done many years ago and the papers are not as replete with data as modern papers. But the authors are, thankfully, less bent.
Try these discussions
http://high-fat-nutrition.blogspot.co.uk/2010/03/butter-insulin-and-dr-davis.html
http://high-fat-nutrition.blogspot.co.uk/2012/09/protons-pancreas.html
Bear in mimd that the study you are reading was very, very carefully set up to get the graphs. Obviously, w/o the carefully selected carb/protein load there would be no insulin spike at all, and they know this (but forgot that particular control group).
You are also talking about insulin at 150pmol with PUFA vs 220pmol with butter. The control group at the bottom of the graph was just the carb/protein component, i.e. much lower in total calories. Imagine the insulin response with 800kcal of that mix. The group is bent.
Anyway, MCTs are very complex, handle with care.
Peter
BTW adaptation to VLC takes some time. I was fine for chronic aerobic exercise by 3-6 weeks. Full adaption felt more like 6 months for hard stuff. And even then, for extreme hill climbing on my pushbike, I had to tailor my climb rate to my oxygen delivery rate, otherwise the world tended to pink out. I don’t seem to use glycogen facilitated anaerobic fuelling. But at the top of the hill I’d just keep going as if there had been no hill, no oxygen debt to repay…
What do you see as some of the worst possible case risks with MCT Oil?
ReplyDeleteI understand your point about the study I quoted being somewhat loaded. But there are plenty of studies that show butter/dairy by itself can spike insulin. But what really concerns me more is the fact butter/dairy may also cause insulin resistance. All I know is that when I ate very large amounts of dairy cream, my fasting glucose went off the charts.
I understand your response on Davis' post about butter to be that you are not combining it with starchy carbs, and therefore for you the issue of insulin resistance does not matter as much. In my case, I want to eat about 120 to 160 grams per day of starchy carbs (primarily white rice), so it's an important issue for me which fat(s) can I combine with that to give me best control on glucose one and two hours after the meal.
The question is whether the deleterious effects of systemic hyperinsulinaemia are off set by the beneficial effects of ketones. This is very much an aside from my own interest in long chain saturated fats. Of course, my own approach is to mimic caloric restriction without the caloric restriction. Safe starches do not figure in this.
ReplyDeletePeter
Hi Peter, just saw this post and found your blog. Wonderful work you are doing! I am type 1, previous low carber testing out the newly popular keto diet and after a couple weeks of wonderful blood sugars and a drop of 30% in basal rate of insulin, I am experiencing the phenomeon of physiological insulin resistance, or so I believe. Reading this, am I correct in thinking that a few carbs will alleviate this occurrence and lead me back to the happy place of lower insulin needs? I have kept my carbs at under 20 for the 3 weeks now -
ReplyDelete