130 replies to this topic

[Nate-2004]

Before I began keto just over two weeks ago my A1C for last year tested at 5.5% which was a little alarming to me. I became more interested in insulin and glycation especially after watching this video.

 

The last two times I tested my fasted blood glucose in the morning it's been 109 and 106. This worried me a bit so I looked up more on this phenomenon and I saw lots of people had similar issues. 

 

Explanations were made but what stood out in one of the post replies (none of these were articles) was that keto can increase insulin resistance, which is the opposite of what I'm basically trying to accomplish.

 

I should probably get more blood work done and test my A1C but I was wondering if others knew more about this issue here.

[tunt01]

I'd be curious to hear other views on A1C in a ketogenic diet. 

 

One thing I'd be careful of doing on a ketogenic diet is focusing too much on the fasting glucose number.  I would think the AM Cortisol Awakening Response would stimulate glucose, and given that you are not running on glucose it's probably just hanging around in bloodstream, making it look like you are pre-diabetic.

 

You'd probably want to see your fasting insulin levels, what your glucose looks like through the rest of the day (which will dictate A1C) before getting too concerned.  Otherwise the fasting AM glucose might be misleading as to your overall physiology.

 

 

[Darryl]

In rodent experiments, high fat diets have been used for decades to induce insulin resistance. Ketogenic diets have similar effects.

 

Jornayvaz et al, 2010. A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain. Am J Phys-Endocrin Metab, 299(5), pp.E808-E815.

Garbow et al, 2011. Hepatic steatosis, inflammation, and ER stress in mice maintained long term on a very low-carbohydrate ketogenic diet. Am J Phys-Gastro Liver Physio, 300(6), pp.G956-G967.

Ellenbroek et al, 2014. Long-term ketogenic diet causes glucose intolerance and reduced β-and α-cell mass but no weight loss in mice. Am J Phys-Endocrin Metab, 306(5), pp.E552-E558.

Handa et al, 2014. Long-term low carbohydrate diet leads to deleterious metabolic manifestations in diabetic mice. PloS one, 9(8), p.e104948.

Mei et al, 2014. A small amount of dietary carbohydrate can promote the HFD-induced insulin resistance to a maximal level. PloS one, 9(7), p.e100875.

 

The only very long-term human studies of ketogenic diets are in children with intractable epilepsy, and some similar effects seem to occur:

Arslan et al, 2016. Is ketogenic diet treatment hepatotoxic for children with intractable epilepsy?. Seizure, 43, pp.32-38.

 

Incidentally, try this exercise. Examine the diets used in any animal study on ketogenic diet. You'll likely find the ketogenic diet has 8-9% of calories from protein, while the control chow has 18-20% of calories from protein. I've now found this in the first 8 studies I looked where I could determine diet composition, so I suspect its universal. The health effects (both good and bad) could arise from restriction of carbohydrates and ketogenesis, but they they could also arise from protein restriction.

[tunt01]

 

Incidentally, try this exercise. Examine the diets used in any animal study on ketogenic diet. You'll likely find the ketogenic diet has 8-9% of calories from protein, while the control chow has 18-20% of calories from protein. I've now found this in the first 8 studies I looked where I could determine diet composition, so I suspect its universal. The health effects (both good and bad) could arise from restriction of carbohydrates and ketogenesis, but they they could also arise from protein restriction.

 

I noticed that in the recent Roberts, et al. paper on Ketogenic, LCD diets extending life in mice.  I presume you are referring to that paper, among others.  Here is what Roberts said in their paper about the macronutrient decisions in the diet:

 

 

There has been considerable interest in the impact of dietary macronutrient composition on longevity, with several studies focusing on protein or methionine restriction as an approach to increase lifespan (Miller et al., 2005; Orentreich et al., 1993). In our study, lifespan did not significantly differ between the LCD and KD groups despite higher protein intake in LCD animals compared to the KD animals. Furthermore, no increase in lifespan was observed in rats fed diets in which protein content was decreased to levels, and in a proportion, comparable to those of our study (Nakagawa and Masana, 1971; Ross and Bras, 1973).

 

Another study found that survival was not increased in rats consuming a 12% versus 20% protein diet (Davis et al., 1983).     Thus, available evidence does not support the idea that level of protein is primarily responsible for the increased longevity in our KD mice. It has also been proposed that a low dietary protein to carbohydrate ratio drives longevity (SolonBiet et al., 2014).

 

However, the results of the present study are not consistent with this hypothesis. Nonetheless, additional studies are needed to determine if dietary protein contributes to improved physiological function and longevity in KD mice. It is also possible that the optimal dietary macronutrient composition may differ between an animal that is fed ad libitum and one that is not.

 

 

 

 

Darryl - What do you think about the conjecture they are making here?  They are obviously leaving it up to 'further investigation', but why design a study that is :

 

 

Calorie Design of Diets (Roberts, et al)

• Control:  18% protein, 65% carb, 17% fat
• LCD (Low Carb Diet):  20% protein, 10% carb, 70% fat
• KD (Ketogenic Diet):  10% protein, <1% Carb, 89% fat

 

 

But notice the g/kg protein level between Chow and KD is the same at roughly 200 g/kg.  It seems like they designed it to keep the weights of the protein intake the same, while letting the caloric intake 'fall where it may'.  For example, the fat g/kg and carb g/kg are about 630 each (KD, Chow/ad lib).  What do you think about this kind of study design?  I don't understand how they targeted 11.2 kcal/day, other than they made up the difference with the fat (17% of the chow diet).

 

I guess I wonder how are these isocalorically the same?  I guess that this table represents the nutritional values per kg of diet weight and then the mice were held at 11.2 kcal/day based on how it was administered, such that they got a lower protein intake.  Maybe that's it.

 

I've just talked myself around in a circle here, I guess.  If anyone has thoughts on the study design and flaws, I'd be curious.

 

Roberts MN, Wallace MA, Tomilov AA, Zhou Z, Marcotte GR, Tran D, Perez G, Gutierrez-Casado E, Koike S, Knotts TA, Imai DM, Griffey SM, Kim K, Hagopian K, Haj FG, Baar K, Cortopassi GA, Ramsey JJ, Lopez-Dominguez JA. A Ketogenic Diet Extends Longevity and Healthspan in Adult Mice. Cell Metab. 2017 Sep 5;26(3):539-546.e5. PubMed.

[Darryl]

The actual protein intake won't be the same (at least in isocaloric diets) as the total calorie density is much higher with KD.

 

Recommend anyone seeing the title of the Roberts et al. paper look more closely. KD or HF diet reduced lifespan, but cyclic KD (one-week KD/one-week chow) modestly increased survival. Cyclic HF increased median lifespan but markedly decreased maximum lifespan.

 

My impression is that it isn't so much carbohydrate restriction and ketogenesis that was responsible for the effects (most notably not lifespan, but improved memory), but metabolic inefficiencies imposed by having to readapt on a weekly basis, akin to the effect of intermittent feeding/fasting.

 

 

 

Edited by Darryl, 06 October 2017 - 08:24 PM.

[tunt01]

Darryl, I think that's a different paper.  Which paper is that graphic from?  The Roberts paper I put up didn't have cyclic HF, cylic KD.  Unless that is from a supplement that I can't seem to find.

 

EDIT:  NM.  I found it.  It's the Newman, et al. paper in the same issue of Cell Metabolism.

Edited by prophets, 06 October 2017 - 08:47 PM.

[Nate-2004]

By the way I'm testing my blood ketones as well, later in the evenings and I've consistently been getting around 2.9 to 3.1. I don't know if I'm adapted yet but the positive effect on my cognition has been quite noticeable and I'm already looking pretty good around the abs.

 

The studies Darryl posted are disconcerting though. I had heard the exact opposite about insulin resistance and keto. I don't know if I should continue this. I also don't know if this diet is what is responsible for the drastic improvement in my tremor, since I am also simultaneously doing the mitochondrial dynamics protocol Turnbuckle is doing.

 

 

My impression is that it isn't so much carbohydrate restriction and ketogenesis that was responsible for the effects (most notably not lifespan, but improved memory), but metabolic inefficiencies imposed by having to readapt on a weekly basis, akin to the effect of intermittent feeding/fasting.

 

I read this study before starting and my plan was to go a month on keto and then off again onto a regular balanced diet.

Edited by Nate-2004, 06 October 2017 - 08:58 PM.

[tunt01]

2.9 to 3.1 is definitely ketosis.  Anything greater than 0.5 is technically in some form of ketosis.  Before eating, I get 1.0-1.5 eating 1 meal a day (has some carbs/potatoes) with a 24 hr fast.

[Nate-2004]

I don't know why this article seems to be saying the opposite, but maybe it really does have more to do with changing it up frequently.

 

https://www.ruled.me...lin-resistance/

[tunt01]

I think it has more to do with going through periodic fasts that trigger ketosis (through fasting, not nutrition).  The point is to metabolically stress the body and reset insulin sensitivity to carbs to going to a very low calorie/fasted state for an extended period of time.

 

It's like Darryl said, intermittent fasting/feeding.  How you get there is up for interpretation.  Some people eat one meal a day and engage in daily ketogenesis through intermittent fasting.

[Chupo]

 

 

 

Calorie Design of Diets (Roberts, et al)

• Control:  18% protein, 65% carb, 17% fat
• LCD (Low Carb Diet):  20% protein, 10% carb, 70% fat
• KD (Ketogenic Diet):  10% protein, <1% Carb, 89% fat

 

 

 

 

 

 

The interesting thing is that even the LCD group lived longer despite having slightly higher protein intake than the control group.

Edited by Chupo, 07 October 2017 - 01:45 AM.

[Chupo]

I don't know why this article seems to be saying the opposite, but maybe it really does have more to do with changing it up frequently.

 

https://www.ruled.me...lin-resistance/

 

Keto improves HOMA, which is a way of calculating insulin resistance. They plug your insulin and glucose levels into an equation.  Keto (and CR sometimes) does give you physiological insulin resistance to reserve glucose for the brain. If that didn't happen, you'd probably go into a coma and then die in short order.

 Have a HOMA test done, or even just insulin.  That should tell you what you want to know.

Edited by Chupo, 07 October 2017 - 01:53 AM.

[normalizing]

im still confused about insulin and ketogenic diet. i read so many articles that ketogenic diet prevents diabetis, and then you have this guy posting so many articles against it and going through back and fourth with current research, i cant seem to find one answer and its just all over the place. is it that difficult to find out if it works or doesnt, i mean whats so complicated about that??

[Nate-2004]

Same here hazy, I'm baffled. My main goals were:

 

1. To see if it had an effect on tremor.

2. To improve overall insulin and A1C situation.

3. To reduce glycation.

4. To see if it would make fasting easier.

5. To see what cognitive effects it had.

6. Extend youthspan.

7. Lose some fat around my belly.

 

Most of those have been quite successful really so far, except who knows about 6 or 3 or 2 or 4 yet... though I can seem to go longer without food.

Edited by Nate-2004, 07 October 2017 - 04:15 AM.

[Chupo]

Rapamycin increases longevity and also induces insulin resistance. So much so that if you're eating carbs while on it, you can become diabetic. Acarbose has a similar effect regarding blood glucose.

 

Here's a study showing that Acarbose (a carb blocker) increased longevity and even though blood glucose increased, insulin and IGF-1 decreased. The effect was mainly in males, perhaps because the control females already had low insulin to begin with:

 

 

https://www.ncbi.nlm...les/PMC3954939/

 

 

Edited by Chupo, 07 October 2017 - 03:57 AM.

[Darryl]

Darryl, I think that's a different paper.

 

Oops, you're right. I was thinking "Keto/lifespan paper from Cell Metab from last month", and was totally unaware of the other Roberts et al paper. In penance, I worked out the %kcal ratios using the 4/4/9 Atwater factors for Roberts et al.

 

        Control  Low-Carb  Ketogenic

Protein   20.5     22.4      11.7

Carbs     63.6      8.2       0

Fat       15.9     69.4      88.2

 

median    886       943      1003

90%       1064     1123      1175

 

I think Roberts et al are a bit premature to dismiss protein restriction as a potential contributor to their lifespan extension. Compared to CR, there are fewer protein or amino acid restriction lifespan studies in mice, but most tell a consistent story: Ross, 1961, Miller & Payne, 1968, Barrows & Kokkonen, 1975, Fernandez et al 1976, Leto et al 1976, Segall et al, 1976, Stoltzer 1977, Goodrick 1978, Horáková et al 1988, Ooka et al, 1988, Orentreich et al, 1993, Richie et al, 1994, Zimmerman et al 2003, Miller et al, 2005, Sun et al, 2009, Solon-Biet et al, 2014. The last, particularly, suggests a gradient of longevity outcomes from protein intake, even in the range of keto diet studies. WRT Roberts et al's counterexamples of studies where no lifespan benefit from protein restriction was seen, they seem to have delved deep. I can't find freebie access to Nakagawa and Masana 1971 or Ross and Bras 1973, and Davis et al 1983 strikes me as anomalous in the background of other studies, all the more so because no significant harm was seen even pushing protein up to 28% in the ad lib group. One protein restriction study has also found functional memory/behavioral benefits: Parrella et al, 2013. Roberts et al. seem to misapprehend Solon-Biet et al as attributing lifespan benefits to protein:carbohydrate ratio, when its results, and the lab heads' prior hypothesis, is that the ratio of protein to non‐protein energy is key. 

[tunt01]

stuff 

 

 

 

That Solon-Biet paper looks really interesting.  I missed it the first few times you posted about it.  I'm going to give that a read.  Thx.

 

Darryl, how do you deal with meal frequency (time restricted feeding) and intermittent fasting/ketosis?  Do you just monitor your blood glucose fasting/postprandial or do you care if your body goes into mild ketosis intermittently?  Restricting protein intake to ~8-13% of kcal is pretty straight forward, but maintaining insulin sensitivity and an 'approriate' AMPK axis is the risk of excess carbs.

 

One issue I noticed from watching some videos w/ Rhonda Patrick/Sachin Panda re: intermittent fasting is that they state any non-water product (coffee, tea) technically breaks a fast because it causes enzymatic liver processing of xenobiotic substances.  That seems like a real stretch to me, but do you take that into consideration when trying to fast?  I guess it all comes down to glucose levels and maintaining insulin sensitivity on a case by case basis.

 

I think I am going to end up on a one meal a day (OMAD) or some kind of 2-3 day fasting/feeding cycle (alternate day fast) of a heavier carb day (with tuber starches) day followed by a low calorie (with no starches, ~700 calories of veggies/salad) trying to drive ketosis on a rhythmic ~48-72 hr cycle.

[Nate-2004]

I find it easier to intermittent fast 24 hrs once a week than to do the time restricted eating 16/8.  They say those two things are different though similar. I do tend to restrict any carbs to later in the day when I eat. That's because apparently insulin resistance is higher during the morning when you have those cortisol spikes. Worst time to be eating bagels and donuts if you ever eat those.

 

Until they do more study on intermittent fasting, supposedly 48 hrs is when ketosis reaches a more optimal point without being on keto. I have yet to test this because I find fasting so freaking difficult to do. My hope was and still is that becoming more keto adapted would help make fasting easier. Who knows till I try. Gonna go as long as I can today and see how it feels.

 

I am coming off keto today, slowly rolling out the carbs after I fast into my fission day. I won't be eating till after the workout. I'll be adding in an extra 30g of carbs per day to ease back in (like an apple or adding banana to my kale/spinach/tomato/blueberry/flaxseed smoothie). 

 

 

Edited by Nate-2004, 08 October 2017 - 04:07 PM.

[sthira]

I think I am going to end up on a one meal a day (OMAD) or some kind of 2-3 day fasting/feeding cycle (alternate day fast) of a heavier carb day (with tuber starches) day followed by a low calorie (with no starches, ~700 calories of veggies/salad) trying to drive ketosis on a rhythmic ~48-72 hr cycle.

I've been documenting one meal per day for more than two years. I'll share my experience that IF, fasting and CR(ON) are beneficial habits (for me) even if no one yet understands mechanistically how. With time, patience and care, you can feel it for yourself -- lighter on your feet, less body wide inflammation, stronger, looser limbs, more endurance, clearer thinking, brighter eyes, better sleep, better skin, and other intangible attributes.

My issue is sustainability -- can I keep doing it even through temptation, peer pressure, on days I don't want to, or just can't or just get damned tired of it?

So I set little flexible goals for myself, and use gimmicky tricks to stay motivated. Cronometer helps. I document what I eat and when, how many hours have elapsed between my last meal and now?

Today, Sunday 10/8/17 -- I'm eating between 1-4pm. That daily feeding window has fallen into a natural rhythm of between 1-4pm, sometimes longer, sometimes shorter. I avoid night eating. Every day I'm aiming at IFing for more than 20 hours. How many days in a row can I keep my record going of 20+ hours? I reward myself for doing it. It might sound silly or obsessive, but it's a pattern. Training my body is something like training a dog's: use positive reinforcement.

I combine the daily intermittent fasting with more extended fasts of less than ten days. Monthly fasts sometimes, other times they're seasonal. Is it too much? Too little? Shrug... Science drops away. More than ten days of water-only, though, might require supervision. I get too weak, too dizzy to perform.

My diet remains strict, too: almost exclusively whole plants -- fruits, vegetables, legumes, nuts, seeds, rarely grains but sometimes sardines.

If fish, then fish low on the food chain, and sardines are indicated by the Monterrey Aquarium as presumably more environmentally sustainable. Big maybe.

But don't think any disciplined lifestyle behavior is actively repairing damages caused by intrinsic and extrinsic aging. Maybe IF, fasting, CR and a plant based Mediterranean diet are healthier than alternatives.

Meanwhile, we're in limbo that might last years or decades; we're waiting for the first leg of legitimate anti aging technology to emerge, like Waiting For Godot, which may be senescent cell removal. But until then, what else can we do? Stay disciplined, stay focused and informed, keep our collective eyes on the first bridge.

Edited by sthira, 08 October 2017 - 04:47 PM.

[Chupo]

I find it easier to intermittent fast 24 hrs once a week than to do the time restricted eating 16/8.  They say those two things are different though similar. I do tend to restrict any carbs to later in the day when I eat. That's because apparently insulin resistance is higher during the morning when you have those cortisol spikes. Worst time to be eating bagels and donuts if you ever eat those.

 

 

It's just the opposite. Dr. Fung recently made a post about it.

 

"The same food will also elicit different insulin responses at different times of the day. Eating the same food at dinner (compared to breakfast) gives you almost 30% more insulin effect. In other words, food is more fattening when you eat it later at night. But the bad news for late eaters does not stop there. If you look at the circadian rhythm for hunger, you’ll find that hunger is lowest in the morning and greatest in the evening 8:00 pm or so."

 

[sthira]

Fung: "...But the bad news for late eaters does not stop there. If you look at the circadian rhythm for hunger, you’ll find that hunger is lowest in the morning and greatest in the evening 8:00 pm or so."

But the good news is retraining the body for earlier feeding is not only possible, but natural.

[tunt01]

If one is eating on a time restricted basis (one meal a day), this amount of insulin release may not matter and I'm not sure it's accurate in the context of a time restricted feeding.

 

Humans did not evolve to eat first thing in the morning.  Food wasn't available.  They had to go forage for it and eat it later in the day.

[Darryl]

stuff

 

Prophets: I've been a one large meal a day kind of person for many years. The results on time-restricted feeding just offered a justification/rationale. For reference, my daily meal is centered around lower-GI starches, and my dietary approach to longevity is focused on methionine moderation/restriction, improving gut microbiota/barrier, hormetic phytochemicals, lowering LDL. I've tried a couple 2-day non-caloric fasts, and would like to push that towards bimonthly 5-day fasts. Coffee and tea seem fine, as I'm unaware of how they might prevent FGF-21, IGF-1, or AMPK mediated responses, and if I recall correctly Nrf2 induction has some synergies here.

 

I don't buy a number of suggestions from Dr. Patrick. I think its fine to just powder broccoli seed rather than waste time sprouting. She puts more stock into benefits of low carb/ketogenic diet than I do. I don't doubt that interesting things are going on, but we don't get to experience cellular longevity if we keel over from a heart attack or fatty liver. The daily and more frequent monitoring of blood glucose by some keto advocates seems, uh pathological. Those without impaired insulin sensitivity don't have to worry. Those who are so invested in the idea that low-carb will finally work for them if only they take it to greater extremes, while willfully ignoring harmful consequences to insulin sensitivity, systemic inflammation, blood lipids etc. seem to have a perverse set of priorities. Who knows how many untimely Byron Richards, Seth Roberts, Bob Harper type events it will take before the cherry picking stops.

Edited by Darryl, 08 October 2017 - 11:44 PM.

[tunt01]

more stuff

 

 

Everything you say makes perfect sense.  So the final question becomes, how do you get all your vitamin/nutrient intake in a single sitting?  Can you and do you check/verify that you are getting your recommended dietary intake in a single meal?  

 

I prefer one meal a day, but I can't seem to ever eat enough given the volume of veggies it seems to take vs. the amount of food I can physically eat.

[sthira]

On one meal per day I'm hitting 92-96% daily RDA. What I lack -- biotin, D, B12, sodium -- is mostly because I don't eat processed food, meat and dairy. If I didn't weigh and measure and document my food, I don't see how I'd know if I was hitting RDA or not.

[Nate-2004]

 

I find it easier to intermittent fast 24 hrs once a week than to do the time restricted eating 16/8.  They say those two things are different though similar. I do tend to restrict any carbs to later in the day when I eat. That's because apparently insulin resistance is higher during the morning when you have those cortisol spikes. Worst time to be eating bagels and donuts if you ever eat those.

 

 

It's just the opposite. Dr. Fung recently made a post about it.

 

"The same food will also elicit different insulin responses at different times of the day. Eating the same food at dinner (compared to breakfast) gives you almost 30% more insulin effect. In other words, food is more fattening when you eat it later at night. But the bad news for late eaters does not stop there. If you look at the circadian rhythm for hunger, you’ll find that hunger is lowest in the morning and greatest in the evening 8:00 pm or so."

 

 

 

Either Fung is wrong or he's not talking about insulin resistance. Jason Fung also does not have a lot of credibility with me, he's not even in the relevant field of expertise and he's made some unsubstantiated claims on occasion. The guy in the video, (the link is set to jump to the point I'm talking about) is a specialist in the field of insulin and endocrinology. 

Edited by Nate-2004, 09 October 2017 - 03:30 AM.

[Nate-2004]

 

stuff

 

Prophets: I've been a one large meal a day kind of person for many years. The results on time-restricted feeding just offered a justification/rationale. For reference, my daily meal is centered around lower-GI starches, and my dietary approach to longevity is focused on methionine moderation/restriction, improving gut microbiota/barrier, hormetic phytochemicals, lowering LDL. I've tried a couple 2-day non-caloric fasts, and would like to push that towards bimonthly 5-day fasts. Coffee and tea seem fine, as I'm unaware of how they might prevent FGF-21, IGF-1, or AMPK mediated responses, and if I recall correctly Nrf2 induction has some synergies here.

 

I don't buy a number of suggestions from Dr. Patrick. I think its fine to just powder broccoli seed rather than waste time sprouting. She puts more stock into benefits of low carb/ketogenic diet than I do. I don't doubt that interesting things are going on, but we don't get to experience cellular longevity if we keel over from a heart attack or fatty liver. The daily and more frequent monitoring of blood glucose by some keto advocates seems, uh pathological. Those without impaired insulin sensitivity don't have to worry. Those who are so invested in the idea that low-carb will finally work for them if only they take it to greater extremes, while willfully ignoring harmful consequences to insulin sensitivity, systemic inflammation, blood lipids etc. seem to have a perverse set of priorities. Who knows how many untimely Byron Richards, Seth Roberts, Bob Harper type events it will take before the cherry picking stops.

 

 

I don't think she suggests powdering broccoli seed in fact I asked her about that and the dangers of some anti-nutrients in the seed that diminish on sprouting, and she agreed and said just eat the sprouts or in my case Broccomax with myrosinase with my kale smoothie.

Edited by Nate-2004, 09 October 2017 - 03:33 AM.

[Chupo]

 

Either Fung is wrong or he's not talking about insulin resistance. Jason Fung also does not have a lot of credibility with me, he's not even in the relevant field of expertise and he's made some unsubstantiated claims on occasion. The guy in the video, (the link is set to jump to the point I'm talking about) is a specialist in the field of insulin and endocrinology. 

 

 

Appeal to authority fallacy. Fung cites sources. Bikman doesn't.

Edited by Chupo, 09 October 2017 - 05:16 AM.

[Nate-2004]

 

 

Either Fung is wrong or he's not talking about insulin resistance. Jason Fung also does not have a lot of credibility with me, he's not even in the relevant field of expertise and he's made some unsubstantiated claims on occasion. The guy in the video, (the link is set to jump to the point I'm talking about) is a specialist in the field of insulin and endocrinology. 

 

 

Appeal to authority fallacy. Fung cites sources. Bikman doesn't.

 

 

https://www.google.c...chrome&ie=UTF-8

[Chupo]

Here's yet another study showing more insulin sensitivity in the morning vs evening for the same meal:

 

 

RESULTS:

Fasting resting metabolic rate (RMR) did not change from morning to evening; after-meal RMR values were significantly higher after the morning meal (1916; 95% confidence interval (CI)=1792, 2041 vs 1756; 1648, 1863 kcal; P<0.001). RMR was significantly increased after the morning meal (90.5; 95% CI=40.4, 140.6 kcal; P<0.001), whereas differences in areas-under-the-curve for glucose (-1800; -2564,-1036 mg dl(-1) × h, P<0.001), log-insulin (-0.19; -0.30,-0.07 μU ml(-1) × h; P=0.001) and fatty free acid concentrations (-16.1;-30.0,-2.09 mmol l(-1) × h; P=0.024) were significantly lower. Delayed and larger increases in glucose and insulin concentrations were found after the evening meals.

https://www.ncbi.nlm...pubmed/26219416

Edited by Chupo, 09 October 2017 - 04:05 PM.