Ketogenic Diet – Diabetes Cure?

 

[HD: This is the second part of my duo about Diabetes and the Ketogenic Diet.  In Part 1, Why This Endocrinologist Hates Diabetes, I discuss…uh…why I hate diabetes.  You don’t have to read Part 1 to appreciate Part 2, but I recommend it just for context.]

The available strategies for weight management in type 2 diabetics don’t work very well.  It’s not that the advice to eat less and move more is bad, but people just aren’t very good at following it in a way that is sustainable, producing lasting results.  On top of that, I give them diabetes medications (e.g. insulin) that may impede their progress.  So, I ask: what can we do to control blood sugar and reduce weight, which will ultimately lead to better long-term control of glucose levels by reducing insulin resistance?

Enter the Ketogenic Diet!

Those of you who are familiar with not only my writing style, but also what gets my quack-o-meter dialed up to 11, are probably thinking, “Ooh…I can’t wait to see HD rip KD a new one.  Let’s get it on!”  As much as I enjoy debunking extreme diets based on lousy/no science (hcg diet, anyone?), I also enjoy presenting ideas that are extreme, but also may have merit.  This is one of those times.

So what is a ketogenic diet (KD)?  There are plenty of sites where you can dig into the details, so I’ll present just a quick overview.  In general, it’s a very low-carbohydrate diet that tends to be high in fat.  There are various iterations, but a common macronutrient percentage-of-daily-calories breakdown would be 70/20/10 fat/protein/carb.

70% fat?!  That sounds revolting!  I’m clicking back over to my Twitter feed now.  See ya!

Listen, I’m with you.  I don’t have any desire to eat ketogenically.  I trim every last bit of fat off my steak before a bite enters my mouth.  However, if I was overweight with diabetes and I had already tried “everything,” I think I would be receptive to hearing more.  And in fairness to KD, it’s quite possible to do it without chomping on a stick of butter like it’s a Clif Bar.  So, for those of you with some residual interest, read on.  The rest of you, I hope the Kardashians did something really interesting today.

When should we think about eating a Ketogenic Diet?

First, it has actually been around as a treatment for refractory epilepsy since the 1920s.  And it has been used as a treatment for obesity since the 1960s, so it has some longevity.  Over the last decade or so, it has been investigated as a tool for helping treat: diabetes, PCOS, neurological/respiratory/cardiovascular diseases, cancer, and acne.

Um, the claims for KD kind of sound like the claims that have been made for low-dose naltrexone – it seems to treat everything.  That’s raising red flags on my quack-o-meter.

Ah, young Jedi, I have taught you well.  You should be skeptical about anything that purports to treat everything, and that includes KD.  I am not saying that KD is the magical answer to all of our medical problems, but there is some compelling science that suggests it may be able to back up some of its seemingly fantastical claims.

What happens to our physiology when we eat a Ketogenic Diet?

After a few days of fasting or eating a very low-carb diet (<50 grams/day), glucose reserves become insufficient for normal fat oxidation via the Krebs cycle.  Remember the Krebs cycle from Intro to Biochemistry?  Neither do I.  Glucose reserves are also insufficient for the central nervous system (CNS) to use as fuel.  Since the CNS doesn’t have access to sugar, and it can’t use fat for energy, it is forced to find alternatives.

At this point, the body is overproducing acetyl coenzyme A, which I’m only mentioning because this leads to increased production of ketone bodies (KB).  This is called ketogenesis and occurs in the mitochondrial matrix of the liver.

Under normal conditions, the concentration of KB in the blood is < 0.3 mmol/L, while glucose is present at 4 mmol/L.  When KB increase to around 4 mmol/L, the brain will start to use them as fuel.

Glucose levels in the blood will be in the low-normal range, maintained by glucogenic amino acids and from glycerol liberated by lysis from triglycerides.  Don’t worry if that sentence sounded like gibberish; I just want to get the point across that the ketogenic diet does not result in hypoglycemia (low blood sugar), as long as you’re not taking medications that lower blood sugar.  If you are taking such medications, they will almost certainly need to be adjusted down or stopped on KD.

Does the Ketogenic Diet produce weight loss?

Before I answer that, let me say that I dislike the question, “What is the best diet for weight loss?”  First, I hate the word “diet,” as it implies a temporary change in eating habits – usually through draconian calorie restriction – which is not a solution to the chronic problem of obesity.  Anyone who has ever dieted knows that cutting calories drastically will result in weight loss.  They are also painfully aware that the return to a more sustainable intake is associated with regain of all the lost poundage (kilogramage for our European and other metrically-inclined friends) and then some.

To reframe the question, I would ask, “Is the ketogenic style of eating typically associated with weight loss?”  The answer is, it depends (like almost everything in medicine).  Remember, you’re now getting somewhere around 70% of your daily calories from fat.  Since fat is the most calorically dense nutrient (9 calories/gram, compared to 4 calories/gram for protein and carbs), you have to be careful when loading up the diet with fat.  It would be easy to gain weight on KD by eating so much fat that your daily calorie intake increases above baseline.

However, because you will take in a fair amount of protein with the fat, and protein turns the brain’s hunger center off, appetite can be suppressed without having to think about counting calories.  There is also a suggestion that levels of the appetite-regulating hormones ghrelin and leptin change on KD, leading to greater satiety.  It is also possible that there is a direct effect of ketone bodies on appetite suppression, but this is conjecture.

Studies show that these very low-carbohydrate diets have the potential to produce more weight loss than a similar calorie standard diet.  Is it all due to decreasing appetite and increasing satiety?  Probably not.  There are some other key differences between KD and a standard diet:

  • Reduced lipogenesis (fat formation) and increased lipolysis (fat breakdown)
  • Increased metabolic efficiency in consuming fats
  • Increased metabolic costs of gluconeogenesis (glucose synthesis) and the thermic effect of proteins

Does the Ketogenic Diet cure or reverse diabetes?

To answer that question, we have to look at what happens to diabetics’ physiology if they change from a standard diet to KD.  People with type 2 diabetes are insulin resistant, diverting a fair amount of dietary carbohydrate to the liver, where it is converted to fat, as opposed to being oxidized for energy in skeletal muscle.  By switching to KD, dietary carbohydrate is restricted to a level so low that it does not get converted to fat.  Remember that more visceral body fat = more insulin resistance = higher blood sugars.  So, if we can decrease visceral fat by restricting dietary carbohydrate, we can decrease insulin resistance, thereby lowering blood sugars.

In addition, studies show that higher levels of ketone bodies (3 mmol/L) are associated with lower glucose output from the liver, another win for the blood sugar level.

Interestingly, these changes in glycemic control and the necessary reduction of diabetes medications happen before significant weight loss has occurred, like what we see immediately after gastric bypass surgery.  This would suggest that there are other factors at play (as mentioned above) in the improvement in diabetic control, making the point that sugar intake does correlate with diabetes risk, independent of weight or sedentary lifestyle.

Stop teasing me with all this mental masturbation and give me the bottom line!  Does eating a Ketogenic Diet cure or reverse diabetes?!

Gosh, you’re impatient.  I promise I will answer this, but let’s first look at some data.  A 2008 study compared the effects of a low-carb, ketogenic diet vs. a low-glycemic index diet on glycemic control in type 2 diabetes (Westman EC et al. Nutr Metab [Lond]).  The LCKD showed better A1c (3-month average blood sugar) reduction, weight loss, and increased HDL over the 6 month study period.  Diabetes medications were reduced or eliminated in 95% of the LCKD group vs. 62% of the LGID group.  Sounds promising so far, no?

A 2017 study compared a LCKD vs. a standard, ADA “plate method diet” in overweight people with type 2 diabetes (Saslow LR et al. JMIR).  The results were better in the LCKD group with respect to weight, A1c, and triglycerides.  However, the intervention group got way more attention than the control group, with mindful eating coaching; plus, the control group diet wasn’t novel, probably explaining why the dropout rate was 50% compared to 8% of the LCKD group.  With small numbers to start with, that study did not impress me.

To muddy the waters a bit more, I’m going to throw in a 2014 22-week study in mice (mice data ≠ human data, but bear with me), which showed that LCKD caused glucose intolerance, reduced pancreatic beta- and alpha-cell mass, higher cholesterol and triglycerides, and did not result in weight loss (Ellenbroek JH et al. Am J Physiol Endocrinol Metab).  It’s possible that the type of fats (high saturated, low polyunsaturated) served to the mice may have made things look way worse in this study.  Perhaps results would have been different had they served more polyunsaturated fats with omega-3’s.

I’m obviously not performing a meta-analysis here, but what I’ve presented was fairly representative of the body of literature out there on this subject, until now…

Enter Virta Health

Virta Health is, according to their own website, “an online specialty medical clinic that reverses type 2 diabetes without medications or surgery.”  [HD: I have no financial relationship with Virta Health, though I would welcome them as an advertiser on this site if they were so inclined.  Relax, I’m not going to smooch their behinds just to make a few bucks; I’ll give you my honest impression of their operation.]

So how are these guys any different from your local weight-loss shop that offers the ketogenic diet?  You know – the one in the strip mall with the “Lose Weight Here!” banner hastily tacked up and listing to port, pasted over the old sign for Deb’s Dry Cleaner.  Well, first off, they’re approaching this problem with some degree of scientific rigor, and they score major points for that.

Virta partnered with Indiana University and published a paper in 2017, detailing their 10-week results from a trial consisting of 262 patients.  As you can imagine, the results were favorable with respect to A1c reductions, weight loss, and medication reduction/elimination.  I’ve already tipped my hand and made it clear that I think what they’re doing has merit, so let’s take a moment to cover the flip side of the coin – weaknesses.

First, the paper was published in JMIR (Journal of Medical Internet Research).  Despite the fact that it has a very respectable impact factor of 5.175 (just below my beloved Journal of Clinical Endocrinology and Metabolism at 5.455), I don’t have as good a handle on how rigorous the peer-review process is for submissions to the journal.  At least there is a peer-review process, and revisions must be completed prior to publication.  But, given JMIR’s mission to fast-track publications and get information into our hands faster than traditional print journals, one has to wonder if the quality of the studies accepted is on par with JCEM, Thyroid, and other top journals in Endocrinology.

Second, though the study had a robust number of participants, it was very short, there was no similar-calorie diet control arm, and the patients in the study were not representative of my patient population (average A1c at entry was 7.6, compared to my patients in the 9-12 range).  The question is whether patients who have had diabetes for longer durations – or have much worse control at baseline – can achieve results similar to the study population.  Remember that such patients may have significantly decreased pancreatic reserve, such that they will need diabetes medications regardless of what they eat and how much weight they lose.

Virta has recently released but not published their 6-month data, and I will commend them if they continue to release data every 6-12 months for the entire, planned, 2-year study duration.  Their 6-month data shows 89% retention of study participants, which is a testament to the program, as most people don’t last that long in other commercially available weight management programs.  Inexplicably, they allowed subjects to decide whether or not to test their A1c’s at the 6 month mark, so the average A1c of 6.1 among those 108 people should have a huge asterisk next to it – did the people who knew they were not doing as well refuse the A1c test?

They have robust data for weight, though; their subjects lost an average of 12% of body weight, with 81% of people losing at least 5%.  Given that we usually don’t get more than 5-10% weight loss with appetite suppressant drugs like phentermine, this is impressive, especially if it can be maintained.

What makes Virta Health special?

Well, they’ve set up a comprehensive program to tackle an intractable problem that nobody else has managed to figure out a solution to and scale that solution.  Sure, you probably have some local, academic institution with an incredible diabetes and obesity program, but that doesn’t do the rest of the country any good.  Plus, patients want remote care nowadays.  I typically counsel at least one or two people daily to go to some sort of formal weight management program.  You know how many follow through with that?  Less than 5%.  Why?  Most common answer: “I don’t have the time.”

Virta has physicians and health coaches continuously guiding their clients, remotely.  Unlike in-person doctor visits that may take place once every few months, the Virta team has touch points as frequently as the needs of the client dictate.  Having a hard time figuring out what to eat for breakfast because you’re bored with what you’ve been doing?  Talk to the health coach.  Feeling the “keto flu” in the early stages of the program?  Chat with the physician and health coach.  Down because you feel like you’ve stalled with your progress?  Get a pep talk and some pointers for breaking through that plateau from the health coach.  If it sounds like I’m enthusiastic about this type of program, it’s because I am.  I could never, in a million years, offer this level of service to my patients.  But I believe it is what many of them need to be successful and to sustain that success.

Would most diabetic patients do significantly better with a personal health coach and frequent check-ins with their physician?  Probably.  Do they need to follow an extreme diet, or is it the intensive followup that drives the results?  Long-term, I suspect that the intensive followup will prove to be the most important part.  But in the short-term, it’s clear that KD causes blood sugars to drop dramatically, even before much weight loss has occurred.  As I said earlier, I would have liked a similar calorie, standard-diet control group so we could really gauge over time the relative importance of the dietary interventions vs. the intensive followup.

Um…HD?

Yes?

You’ve managed to get almost 2500 words into this thing without answering the question you promised you’d answer…

Yes, I’m aware of that; it’s called building suspense.  Or maybe I’m just too verbose and I get off topic; I’ll shift gears now.  If you want to hear more about Virta Health, listen to one of their doctors, Jeff Stanley, on Dr. Scher’s Boundless Health podcast (Episode BH011).

Does the Ketogenic Diet cure or reverse diabetes?

In my opinion, I think it is overly optimistic and slightly misleading to say that KD cures or reverses diabetes.  I would prefer that Virta Health and other proponents of KD use terms like “diabetes in remission” or “diet-controlled diabetes.”  Here’s why:

In order to label someone “cured” of type 2 diabetes, I think that person should meet two criteria: she should have normal glucose tolerance/no insulin resistance, and she should have pancreatic reserve capable of disposing of any glucose load to the system.  Let me explain.  By the time someone is diagnosed with type 2 diabetes, she has been insulin resistant and has had impaired glucose tolerance for years.  She has already lost up to 50% of her beta cell (insulin-producing cells of the pancreas) function by the time the blood sugars are high enough to make the diagnosis of type 2 diabetes.  As time goes on, beta cell function continues to decline, until eventually the patient makes so little insulin that non-insulin drugs are no longer sufficient to control the disease, and insulin replacement therapy is needed.

In order to be “cured” of diabetes, beta cell function should be sufficient to handle any glucose load that comes in to the body.  If beta cell function is still fairly low while on KD, then the diabetes is really just in remission or diet-controlled for as long as that person is eating a ketogenic diet.  If that person falls off the ketogenic wagon, we can assume that she will either immediately have poor glucose tolerance, or she will soon develop high blood sugars as her physiology goes back to her prior abnormal state and her weight increases.

In my estimation, this does not represent a reversal or cure of the disease.  It certainly represents an impressive remission, just as gastric bypass surgery can induce remission in type 2 diabetics.  But what do we tend to see over the next decade or two after bypass surgery?  You guessed it.  Patients begin to regain their weight, and the diabetes returns with the weight.  Cured?  Not so much.

The Ketogenic Diet might reverse diabetes.

Whaaaattttt???

This is what I love about medicine.  Just when you think you’ve made a cogent argument and you’re ready to smugly take your seat, somebody comes out with a study that challenges that argument.  In the February 2017 issue of the journal Cell, a study was carried out by researchers from USC, MIT, and some place in Italy of which I’ve never heard.  But if they partnered with USC and MIT, we should probably be impressed.

In the first part of this study, they looked at mice with type 1 diabetes, mice with type 2, and normal mice.  They put the mice on what they call a fasting regimen, which was basically a ketogenic diet.   At the end of each 4-day cycle of KD, the mice were fed regularly for up to 10 days to ensure they regained their body weight, before beginning the next fasting cycle.  They went through 3 cycles of fasting/regular feeding.

In the type 2 diabetic mice, after the fasting cycles, insulin secretion was restored and insulin resistance was reduced.  The researchers think that beta cells were regenerated.  In the type 1 diabetic mice, the fasting cycles resulted in an increase in the number of beta cells generating insulin (remember that type 1 diabetics should make little to no insulin).

In the second part of this study, they recruited healthy, non-diabetic, human volunteers, who underwent three cycles of a similar fasting (KD) regimen.  They then took blood from these healthy people and applied it to cultured pancreatic cells from humans with type 1 diabetes.  The results seemed to suggest that it is possible to reprogram cell lineages and generate insulin in these diseased pancreatic islet cells.

Is this overwhelming evidence that the Ketogenic Diet reverses diabetes?  No, of course not.  Over the years, we’ve seen several promising diabetes “cures” come and go.  The Cell study is interesting, for sure, but mouse data is notoriously difficult to extrapolate to humans, for one.  Secondly, the human data from that study was basically in vitro data, so we really don’t know if that effect would translate into clinically meaningful remission from diabetes in a real human.

Wrap-up

Type 2 diabetes and obesity are two extraordinarily vexing problems that we have mainly failed at controlling with lifestyle modifications alone.  The Ketogenic Diet is an extreme eating strategy that may hold great promise for those who can stick to it long-term.  In my opinion, for the majority of people out there, KD is not a do-it-yourself proposition.  In my office, the most common phrase I hear with respect to KD is, “I did the Ketogenic Diet…for 2 weeks.”  There are just too many ways to fail on this diet, and I believe expert guidance is needed.

I think companies like Virta Health have the right approach, offering a remote, comprehensive program with physician oversight and frequent feedback/coaching.  I think their early data is promising, and I’m excited to see if they can show sustained remission from diabetes over the course of years.  If they can, it will be a game-changer in the Kingdom of Endocrinology.

 

Are you a doctor who treats diabetes or a person living with diabetes?  Have you found success with the Ketogenic Diet?  Do you think it’s extreme and difficult, or did you/your patients acclimate pretty quickly?  Would you refer your patients to a company like Virta?  Why or why not?  If you have diabetes, do you think a program like Virta’s would be something you could stick with, assuming it’s affordable?  Comment below!

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41 Replies to “Ketogenic Diet – Diabetes Cure?”

  1. First of all, thanks for this amazing post. There’s so much fluff out there about KD and I’m elated to see a serious treatment.

    Some questions about this part though:
    Reduced lipogenesis (fat formation) and increased lipolysis (fat breakdown)

    Intuitively it seems that if you are getting ~70% of your calories from fat and are in caloric balance, both lipgenesis and lipolysis would increase and equalize.

    Increased metabolic costs of gluconeogenesis (glucose synthesis) and the thermic effect of proteins
    I thought it was well-established that fat is easier to metabolize than protein, and that carbohydrates are unpredictable because of the wide variations. Fiber for example, is very difficult to digest (by definition) and the gluconeogensis cost of actual glucose is exactly zero. The ketogenic diet is not particularly high in protein. The CDC cites average protein intake at 16% and fitness enthusiasts frequently far exceed 20%. (Full disclosure–I eat 40% protein and my weight dropped dramatically when I started doing that.)

    1. Thanks for the kind words and the insightful questions, Christine.

      Insulin levels will drop during a ketogenic diet, because one is not eating carbs, so one doesn’t need as much insulin to drive sugar out of the blood and into the cells. Insulin promotes the storage of fat (among other things), so decreased insulin levels should lead to decreased lipogenesis (fat formation).

      Because the body isn’t seeing as much dietary carbohydrate, it is adapting to using fat as an energy source, hence the increased lipolysis. At least, that’s my understanding of how it all works. There is probably a biochemist out there who could school us both.

      Regarding your second point, there is a hypothesis that the body’s use of protein is an “expensive” process, leading the body (in the initial phase of a very low-carb KD) to spend more calories using dietary and tissue protein to create glucose via gluconeogenesis, as compared to “less expensive” diets that are not low-carb diets. Basically, the body is thought to burn more calories using protein for its needs than when burning other nutrients. I don’t actually know if this is one of the main mechanisms behind why low-carb diets seem to work so well, but it seems like it could be at least part of the explanation. Because there is a fair amount of protein in a KD that sneaks in with all the fat, it is thought to be a metabolically expensive process for the body. But in order to buy that, you have to believe that a calorie is not a calorie is not a calorie, and the macronutrient composition of our diets does matter when it comes to losing weight.

      If that doesn’t answer your question, please let me know. Also, if you want to read a bit more about these issues, check out this paper and the papers it cites: Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets

      1. Nice post! I’m not a biochemist but I’ve been interested in ketogenic diets and intermittent fasting for a few years.

        I’ve read that de novo lipogenesis is not a significant pathway in humans except under very unusual circumstances (see the studies by Marc Hellerstein). Obese and diabetic people seem to have a slightly increased but still very minor rate of de novo lipogenesis and I’ve seen some scientists question whether it might be greater in some cases that have yet to be observed. But the research that’s out there suggests that humans don’t convert a practically significant amount of carbohydrate into fat. Even then, though I believe that insulin does play a role in the lipogenesis pathway, the substrates for lipogenesis need to be present. This only happens when someone is in positive energy balance.

        I would suggest that fat oxidation is important to consider along with increased lipolysis. If caloric expenditure and intake were fixed, then overall fat oxidation would increase on the KD. More fat storage might occur after a meal followed by more lipolysis during fasting due to the lack of glycogen. But this couldn’t lead to more weight loss unless expenditure or intake changed.

        Kevin Hall did some studies, meta-analyses, and review papers on the subject. He found that very low carb diets and very low fat diets both led to some very minor, practically meaningless increases in energy expenditure. In one small study, he did find temporary slight increase in energy expenditure in a KD like you mention. I don’t think it’s saying that a calorie is not a calorie, but that expenditure may change at the extremes of the macronutrient composition of the diet.

        Here’s where I might get schooled by an endocrinologist, but my understanding is that insulin doesn’t drive sugar out of the blood so much as accelerates the process since there are a variety of GLUT transporters that don’t require insulin with some simply being activated by high blood glucose. It’s also my understanding that it is really a failure of insulin to shut down liver glucose production at the liver that results in both type 1 and type 2 diabetes. Thus, high blood sugar gets worse after a carbohydrate meal but it is not a failure to clear the glucose from the meal. It’s that the liver keeps dumping extra glucose into the blood on top of the amount from the meal.

        1. “But this couldn’t lead to more weight loss unless expenditure or intake changed. ”

          Correction: except for some water weight from the glycogen

        2. Thanks for raising these questions/issues. I think that the following chapter on the pathophysiology of diabetes is helpful to clarify things better than I ever could in a brief comment: http://www.endotext.org/chapter/pathogenesis-of-diabetes/pathogenesis-of-type-2-diabetes-mellitus-6/.

          You have to register to read Endotext, but it’s free.

          By the way, type 1 diabetes is quite different from type 2, in that the primary problem is an autoimmune attack on the pancreas, resulting in complete or near-complete insulin deficiency.

  2. Totally off topic, but since I was just researching it and your blog post popped up in my email,
    do you have any opinions on use of spironolactone for acne in women?

    1. I’ve seen it be helpful in PCOS-related acne but I seem to recall limited data the last time I looked, which was admittedly yeas ago.

  3. I’m not impressed with Virta Health or Dr Scher.

    I lost 45 lbs ten years ago and have kept off 40 lbs of it even moving through my sixties. I got all the support and encouragement I needed from a Registered Dietician and my PCP, who took the time each Tuesday at my weigh-in to excuse herself from her patient, pop out, give me a big smile and thumbs up, and then get back to her patient. I eat a balanced diet, low in fat and high in plants. I’m a vegetarian (I use yogurt and eggs). I do not exceed 1200 calories/day and aim for 1000. Still see the dietician from time to time.

    It just ain’t rocket science, and YES, it takes discipline. I quit whining when my numbers fell quickly into the normal range–as did my BP and cholesterol as well.

    Of course I have chocolate flourless cake on my birthday, but other than that, I dont make many exceptions–and alcohol has been mostly dropped as well. I miss craft beer, but I LOVE being thinner and NOT HAVING DIABETES. Who is going to stay on a (true) ketogenic diet? People who have children with epilepsy that hasn’t responded to meds go through hell using KD and need tremendous professional help from docs and RD’s. Any healthy diet is reasonably low in carbs and NOBODY needs the empty calories from processed grains.

    1. Toad, for every one of you, there are 100 who will fail. Is the KD hard? Yes, I think so. Will it resonate for some people? Yes. Will many people abandon it? Probably. The thing about losing weight as you have and keeping it off is that, whatever path one chooses, it has to resonate for that person. That’s why I always ask my patients who want to lose weight, “What has worked for you in the past?” I am trying to get a sense of what they will be successful with and what resonates for them. No resonation, no success.

      You have done amazing things with discipline and a sensible eating strategy. But the person next to you may need a slightly different (or very different) approach. They may have more bumps in the road. Or less.

      What companies like Virta and docs like Bret Scher are trying to do is help people get to where you’re already at. What they’re offering may not resonate for you, but you’ve already figured it out. I suspect there are others who will embrace the messages coming from Virta and Dr. Scher. And if not, then hopefully they’ll find something else that works for them.

  4. I think that’s one of the most important take-home messages. One approach does not work for everybody. That’s how it has been portrayed by the medical community for decades. On the flipside, just because the high-fat low-carb approach works for many still does not mean it works for all. But it’s fantastic that is now part of the conversation to offer an alternative for those who don’t respond to the low-fat calorie counting approach. The more individualized we can make the approach, the more likely we are to have success. I hope we can all keep an open mind and critically evaluate each approach on its own merits

  5. The concern for me is the fact that KD raises LDL in a population where ASVCD is the main cause of death and morbidity. You are suggesting this as not a “diet” but a continuous eating strategy. How can you make this recommendation without a much longer term study using CVD endpoints as is required for drugs? Several observational studies have associated high protein, low carbohydrate diets with increased death rates and higher death from diabetes.

    1. Yes, there is a significant subset of people who will see their LDL rise on the KD. For those people, they may not be the best candidates for KD. However, it also may pay to look at what else is going on with those folks. If they are losing weight, improving insulin resistance, and lowering blood pressure, then we have to take that into account. Also, we may want to look at advanced lipid testing for those folks, i.e. is their LDL large and fluffy (not so bad) or small and dense (more likely to be atherogenic). An assessment of LDL particle number might also be warranted in those situations.

      Let me also be clear, I am not making a blanket recommendation that people eat this way. There are those for whom the KD may be a bad idea. However, I would also say that we are not going to get a large trial of the KD using hard CVD endpoints (MI, stroke). There’s just no way that will get funded, as the numbers would have to be astronomical to have statistical power. So we are left with using clinical judgment based on the best available evidence, as well as ongoing assessment of the patient’s biometric data, like the lipid panel.

      As for the observational studies you mentioned, can you provide references?

      1. I’d be happy to link them.

        It seems you are willing to give the diet the benefit of the doubt and waive any requirement for CVD safety being investigated. I suppose that is one way of looking at it.

        The studies are here:

        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989112/pdf/nihms-247461.pdf
        “The overall low-carbohydrate score was associated with a modest increase in overall mortality in pooled analysis (Hazard Ratio, HR, comparing extreme deciles=1.12 (95% CI=1.01-1.24, p-trend=0.14). The animal low-carbohydrate score was associated with a higher all cause mortality (pooled HR comparing extreme deciles=1.23, 95% CI=1.11-1.37, p-trend=0.05),cardiovascular mortality (corresponding HR=1.14, 95% CI=1.01-1.29, p-trend=0.029), and cancermortality (corresponding HR=1.28, 95% CI 1.02-1.60, p for trend = 0.09).

        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555979/pdf/pone.0055030.pdf

        Conclusion: Low-carbohydrate diets were associated with a significantly higher risk of all-cause mortality and they were not significantly associated with a risk of CVD mortality and incidence. However, this analysis is based on limited observational studies and large-scale trials on the complex interactions between low-carbohydrate diets and long-term outcomes are needed.

        http://www.bmj.com/content/344/bmj.e4026

        Results: A one tenth decrease in carbohydrate intake or increase in protein intake or a 2 unit increase in the low carbohydrate-high protein score were all statistically significantly associated with increasing incidence of cardiovascular disease overall (n=1270)—incidence rate ratio estimates 1.04 (95% confidence interval 1.00 to 1.08), 1.04 (1.02 to 1.06), and 1.05 (1.02 to 1.08). No heterogeneity existed in the association of any of these scores with the five studied cardiovascular outcomes: ischaemic heart disease (n=703), ischaemic stroke (n=294), haemorrhagic stroke (n=70), subarachnoid haemorrhage (n=121), and peripheral arterial disease (n=82).

        And finally,

        http://www.cell.com/cell-metabolism/fulltext/S1550-4131%2814%2900062-X

        … high protein intake was associated with reduced cancer and overall mortality in respondents over 65, but a 5-fold increase in diabetes mortality across all ages. Mouse studies confirmed the effect of high protein intake and GHR-IGF-1 signaling on the incidence and progression of breast and melanoma tumors, but also the detrimental effects of a low protein diet in the very old. These results suggest that low protein intake during middle age followed by moderate to high protein consumption in old adults may optimize healthspan and longevity.

        1. Thanks for the links. There is some interesting stuff in there, particularly the second article/meta-analysis. As you are aware, none of the studies you cited proves causality, but I do agree that the data should be taken into account with all the other low quality data we have on the subject.

          It’s not that I’m willing to “waive any requirement for CVD safety being investigated,” as you say. Rather, I am a proponent of synthesizing data that exists and then using good clinical judgment to make a decision. If we waited for double-blind, randomized, placebo-controlled trials to make all of our decisions, we would make no decisions.

          Do I think there is an argument to be made against the KD? Yes, and though the tone of my piece is more positive than negative, I thought that would be clear. But maybe not. I am simply offering my opinion that, if you take a patient with high blood sugars, hypertension, obesity, and hyperlipidemia, a program like Virta’s that includes intense coaching and the KD might help that patient. Could she do just as well or better with intense coaching and a normal, balanced, calorie-restricted diet? Probably. But where is she going to get that coaching? Not from me. I don’t have the time. Will she have an increased risk of dying if she eats ketogenically? Well, assuming that she is not one of the “hyper-responders” when it comes to the lipids shooting up, I would expect that lower blood sugars, lower blood pressure, lower weight, and less fat in the liver would probably increase her health span. I don’t know for sure that it would, but if we talk about someone who is going to stay hyperglycemic and overweight on their usual diet vs. be euglycemic and less overweight on the KD, my money is on them being healthier on KD. And yes, I could be wrong.

          1. None of Dr. Allen’s links were to studies of a ketogenic diet. Many of the “low-carb” diets in his meta-analyses had as much as 40% carbohydrate.

            As Dr Allen is a well-known vegan/lifestyle MD and vocal opponent of low-carb/keto diets, people need to take his rather cherry-picked epidemiological data with a grain of salt.

            The truth is, a ketogenic diet (or WoE / Way of Eating) is now shown in dozens upon dozens of RCT’s to be superior to any other diet for glycaemic control, lipid profile, appetite suppression, and more. Virtually all known biomarkers of CVD are reduced.

            Regarding LDL .. The fact that many experts are now considering LDL a horrible predictor of CVD, especially with regular testing only estimating LDL and only advanced lipid testing looking at the particle type – should mean that we don’t need to set off alarm bells if the diet slightly elevates LDL. My own LDL increased, but advanced lipid testing showed the profile improved tremendously.

          2. Interesting. Never heard of Dr. Allen, but I suppose it’s good to be transparent about our biases. That said, can you cite some of these RCTs showing KD is superior in the ways you mention? I think the KD has merit, but I’m still a bit wary of how high some people’s LDL may go. I’m happy their triglycerides will be low, but I don’t think we can go so far as to say it’s the best eating strategy for controlling lipids. I would also beg to differ that LDL is a “horrible predictor of CVD.”

      2. Take a look at Dave Feldmans work on “lean mass hyper-responders” to LCHF diets . It shows that some of the fittest people have this trait . It is characterised by low trigs, high HDL high LDL with a good ratio of HDL/LDL overall.

        For me as a diabetic – the first stage is reduction in Trigs and LDL then HDL starts to rise and LDL rises alongside it with the ratio of HDL/LDL continuing to improve.

        I would be very happy to become a Lean Mass Hyper responder with Total cholesterol on the high side, eventually !

        1. I’m not sure I would hope for that outcome, as we still don’t know how dangerous these higher cholesterol numbers will turn out to be over the long run. It does beg the question, though, should we be following patients on the KD who have high cholesterol with other measures of cardiovascular risk assessment, like coronary calcium scores, etc? If the patient has diabetes in remission, normal blood pressure, and high cholesterol, we might want to look at other markers of risk to decide whether they need a statin and, if so, how much.

        1. I’m not aware of any hard numbers about fluffy cholesterol. As far as I can put together, fluffy is bad, dense is worse, and the difference isn’t worth calculating. A lot of questionable sites push fluffy, and it’s a real thing studied by real doctors, but I don’t see way of calculating your risk that distinguishes between fluffy and dense, and high fluffy and high dense go together anyhow. Hence doctors don’t test it separately.

          If there is good data I would be grateful if you can link to it.

          1. Christine, you raise a valid point. Large, fluffy LDL is still going to be pro-atherogenic if you’ve got enough of it, especially in cases with really high cholesterol, like in FH (Familial Hypercholesterolemia). But small, dense LDL is more associated with being pro-atherogenic than is large LDL; that much has been shown in studies. So if we’re looking at someone on the KD whose LDL has gone up 30-50 points, I may be less likely to freak out if the overall number is still within spitting distance of reasonable, and most of it is large/fluffy.

            That being said, sub-fractionating LDL has not made its way into clinical guidelines yet from our major medical societies, because it is probably not going to add much to the decision-making process for most people. Diabetic? Take a statin. Have high cholesterol with FH of early coronary disease? Take a statin. Etc. But if we are looking at a subset of people who don’t fit neatly into prior study populations, then we might need to take a more open-minded approach. Personally, I rarely order advanced lipid testing, because it is not going to change my decision in my patient population. But I don’t have many diabetics with A1c’s of 5.7 on the ketogenic diet, doing Cross-Fit 4 days per week.

            There is a nice review of the subject on Endotext (free registration to read): http://www.endotext.org/chapter/utility-advanced-lipoprotein-testing-clinical-practice/.

  6. Two strengths of Vitra plan are there self monitoring of blood glucose and ketones. I think BG monitoring studies in the past haven’t shown benefit because without a low carb recommendation people were just frustrated with high BG numbers. Ketone monitoring is a great way to judge if you are staying low enough in the carb department. Too many carbs equals no ketones.

  7. 1973 “Diabetic” Cardiomyopathy described, with 1/5-1/4 of DM patients getting non-atherosclerotic/non-valvular heart failure. They accounted for 1/5-1/4 of all non-vasc/valve HF patients – the remainder didn’t have DM.
    1975 Most NIDDM patients shown to be hyperinsulinemic, not hypoinsulinemic as expected (beta cell “failure” was only seen in the latest stages).
    1988 Syndrome X -> Hyperinsulinemic Insulin Resistant Metabolic Syndrome described. High Triglycerides, low HDL, obesity, fatty liver common features. Ever see those in DM?
    1997 Hyperinsulinemia as the common feature of “idiopathic” hypertension described in J of Nephrology. Insulin causes renal retention of sodium, phosphate, urate, and promotes proteinuria. Do you see that often in DM patients? Actually, hints of this prior to 1991. See https://doi.org/10.2337/diacare.14.3.173.
    Circa 2000 the other 3/4-4/5 of non-vasc/valve HF patients found to have hyperinsulinemia, and insulin interferes with cardiac use of glucose. Cardiac muscle uses fat for 80% of its needs, then prefers ketones over glucose, but uses glycolysis during exertion. Skeletal muscle at rest also uses fat primarily, glycogen is for running faster than one’s buddy when chased by a bear.
    2016 studies have shown all the common cancers have many growth promoting short (fetal cell) Type A Insulin Receptors, and others, like HER2 on esophageal CA also respond to insulin.
    T-cells, instrumental in eczema, have insulin receptors. Psoriasis is also seen predominantly in hyperinsulinemia.
    MS & Parkinson’s also more prevalent in hyperinsulinemia. Alzheimer’s too? Yep.

    So could KD be the cure to “everything”? Well, if the majority of common ailments are all manifestations of what “too much insulin” can do when it is being resisted by myocytes, adipocytes, and hepatocytes so it bothers everything else, then taking away that insulin stimulation can reverse those conditions.

    Insulin Toxicosis. Just like “ThyroToxicosis”. I’m sure you’ve heard of that. Perhaps Cushings could be ” Cortisol Toxicosis”? Male adolescence is clearly “Testosterone Toxicosis”.

    Too much of a good thing is a bad thing. Always. (If nothing bad is happening it can’t be too much yet. Wide vs. narrow therapeutic index.). Not convinced? Glass of water in a desert vs tsunami. Oxygen at altitude vs causing retinopathy of prematurity. Electromagnetic radiation to see vs sun burn, skin cancer.

    Insulin – dead without it vs 4 of 5 breast cancers Insulin dependent (let alone the estrogen sensitive ones).

    High carb diet = high fasting insulin. Carbs are to be eaten in the fall when pulses & other grains, berries and tubers are plentiful. Canning & refrigeration & sealed bags of potato chips and sugary drinks are our undoing. I am thankful for trucks of cauliflower & broccoli from California in February though. KD may not be sustainable, but LCHF is, together with some Intermittent Fasting. Buy & prepare real food. Don’t consume Edible Industrial Products (except full fat ice cream, and 70% cocoa chocolate – don’t over do it!). This works for my patients.

    Best patient: 52 yo F, 2016 Jun FBG 12.5, A1c 8.8, Insulin 273 pM, 2016 Oct FBG 5.4, A1c 5.6, Insulin 153, 2017 Mar FBG 5.2, A1c 5.3, Insulin 98, 2017 Aug too much lemon water & sick mother, but insulin 72. Target is ~20 pM (3 microU/ml). Not “cured” yet, but coming. Her daughter has PCOS with insulin of 220 pM. Always more patients to help.

    1. My figures close to this. My insulin wasn’t checked on diagnosis – ( indeed at that point I had no clue it was even important and neither did my doctor)
      6 months into keto it was still 138pM, after 12 months 55 pM

      Too much insulin seems to be a root cause of dozens of diseases. In the circumstances its astonishing that fasting insulin is not tested as part of standard fasting blood tests.

    2. Do you have any views on how long it takes and how low does insulin have to be to bring dawn phenonemon down? That is now my only remaining ” high” – so for example over night – around 4.2 DP 6.1 ( for about 3 hours) before I drop back to low 4’s

  8. Immunofluorescence staining studies have shown beta cells are NOT destroyed in NID-DM (calling it type 2 only helps put hyperinsulinemic patients on medicines which raise insulin more, or on insulin itself) but merely go dormant in a stem-cell-like state. MRI have shown as little as 30 g of fat in the pancreas can reduce beta cell function
    With LCHF / KD weight loss insulin production resumes.

    Intermittent exposure to carbs maintains metabolic flexibility rather than GTT “intolerance” seen with those mice.

    1. As part of my strategy, I do tend to have ” treat days” – usually when it’s some party function with lots of ” treats ” on offer. That inevitably results in what for me would be very high carbs – eg 200g. I find it takes less than 2 days to get back into ketosis after one of these events. I figured that was a good way to maintain flexibility .

  9. I was diagnosed with an HbA1c of 11.3% (or 100 mmol) in June of 2015. I went on a low-carb/ketogenic diet almost immediately and have stayed below 30g of carbs per day since then.

    From a personal point of view, I find staying on a ketogenic diet quite easy. This is because I am never really hungry. I have also found many ways to prepare low-carb substitutes for old favorites. When I was still eating carbs, I remember getting ravenous often only a few hours after eating.

    In terms of results, my HbA1c in September 2015 had dropped to 5.3% (34) and has stayed in the non-diabetic range since then. My latest two HbA1c in September 2016 and and September 2017 were 5.0% (or 31 mmol). Average blood pressure is about 109 over 67 and the lipid panel showed HDL of 61, triglicerides 97 and LDL of 131. Heart event risk in the next 10 years based on the ccc-tracker of the American Heart Association is between 1.2% (non-diabetic) and 2.4% (diabetic). I have been on no medication since June 2016, before this only on metformin.

    So, for me the way of eating has been a life-saver. The most important disadvantage of the diet is the time required for shopping and preparing food and exercising when I get home from work, which can be a challenge if you often work long days and commute between 3 to 4 hours per day. Also, having to pay for all testing supplies myself is a bit of a hassle.

    By the way, a ketogenic diet is not a high-protein diet. The amount of protein I consume is no more than before and is usually less than 1g per kg of body weight, resulting in about 50g to 60g a day.

    1. Great job! Glad you found something that works/resonates for you. And yes, it should be clear to all that KD is not a high-protein diet; it’s high fat, moderate protein, low-carb.

      1. I think one important aspect of the ketogenic diet that people miss is regarding the macronutrient profile … While most-commonly high-fat, moderate-protein, low-carb … it’s TECHNICALLY any macronutrient profile that keeps you in optimal nutritional ketosis.

        As such, *generally-speaking* men will have a slightly higher protein intake requirements than women… Those doing heavy resistance training (especially multiple sets to fatigue multiple x a week) will require more protein than those that don’t, etc.

        Carbohydrate is normally low, but many keto athletes use a more-strategic carbohydrate intake that maintains ketosis, but gives enough circulating glucose to fuel anaerobic+ efforts when required. For example, on a day that includes a leisurely bike ride through the hills I might have only 50g of total carbohydrate … but on a 5hr century ride through the mountains with competitive riders, I’ll have 200g of additional carbohydrate (roughly 40g/hr) in order to get anaerobic+ over 14% grades without ‘bonking’. Lipolysis can’t fuel that kind of effort, and I need some circulating glucose.

        The key is that ketogenic athletes strategically time their intake, and neither “carb up” nor “replenish”. So yeah, some (very rare) days I might have 250g of carbohydrate … but still stay in nutritional ketosis.

        1. Excellent points. My patient population does not consist of keto athletes, but using carbs strategically for long distance activity seems reasonable.

  10. I was diagnosed with diabetes in August 2017 with hba10.3%. The following day I found this paper https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/1743-7075-6-21 . reading this paragraph
    “One female patient had an increased physical activity level during the study period in spite of our instructions. However, her increase in physical activity was no more than one hour of walking per day, four days a week. She had implemented an 11%-carbohydrate diet without any antidiabetic drug, and her HbA1c level decreased from 14.4% at baseline to 6.1% after 3 months and had been maintained at 5.5% after 6 months.”
    I decided to do what she did – i.e. a ketogenic diet. ”
    I had bloods done every three months. Vast improvement across all metabolic markers. Hba1C after 6 months was 5.9% maintained for 9 months since. Weight down by 30kg .
    No coaching at all. A ketogenic diet is not “hard” per se just ” different”.Getting rid of the sugar addiction in the first two weeks ( keto flu) is the hardest part. The absence of crippling hunger pangs through reducing carbs, makes losing weight possible. That is also why one can stick to it. The dramatic reduction in blood sugar was coupled a major improvement in cholesterol and every other marker : eg- TC 5.6 at dx include Trigs 2.7, HDL 1.04 and LDL 3.36 12 months later TC 4.3 Trigs 82, HDL 0.82 LDL 2.4 . GGT at Dx 35 => 14

    A ketogenic diet gave me my life back. It works quickly and effectively to put T2Diabetes under control. It should be the first choice of anyone diagnosed with T2. You don’t need to pay money to others to do it. Just look up dietdoctor.com and follow the recipes there.

    I do still test but only because I like to see the evidence – in practice I already know the numbers will be fine anyway . Once one is properly fat adapted it no longer takes much time because you can eat just once or twice a day and sometimes not at all. Food no longer dominates my life and the stuff I eat is properly tasty. e.g small steak with a generous butter cream and herb sauce and some above ground veg. eating 60-70% fat, 20% protein 15% carbs and 5% whisky ( sometimes ) is a lovely way of life !

    1. I’m glad you’re doing so awesome with this strategy. For many others, it will be both different and hard, however. While it is possible for those who are highly motivated and highly disciplined to DIY it, I think those folks (like you) will be in the minority. Do you really go some days without eating at all?

    2. I have also been able to maintain a keto diet on my own. I started out at a weight just under 500 lbs, diagnosed with type 2 diabetes, pcos, hashimotos, and ibs. My A1c was way out of control and I was packing on weight at an alarming rate. I went from the lean 110 lbs that I maintained most of my adult life to my heaviest of 498 in just under 5 years time. My pcp at the time refused to listen when I insisted that something was horribly wrong with my body and kept blaming me for my weight loss failures. I followed all of his advice and when it didn’t work I was accused of cheating on the diet or not exercising and he eventually told me to seek treatment elsewhere as he was done trying to help me. My next pcp referred me to an endo who diagnosed me with the multiple endocrine disorders. He then put me on the keto diet, along with a weight loss pill, and metformin. 18 months later, I was down 250 lbs and taken off the weight loss pill. I no longer see that endo since he retired, so I now maintain the diet on my own and have maintained my weight loss for 7 years now. I have slipped up and binged on carbs, especially around the holidays, but it always makes me feel sick and I go right back onto the keto diet afterwards. My A1c now consistently stays at or below 5.7, all of my lipids are within normal ranges, and I feel so much better on the keto. My ratios are 60% fat, 30% protein (lift weights to build and tone muscle), and 10% carbs. I eat 1800 to 2000 calories per day and most of my fats come from olives, coconut and other tree nuts, seeds, and fish. My carbs consist of a large variety veggies and berries, with the occasional fruit for desert. My favorite part is that most of my foods don’t require cooking and allow me to snack through out the day, freeing up a lot of time in my busy schedule.

  11. Thanks, HD. Interesting as always. A quick drive-by brain dump. My husband has T1D; diagnosed at age 4. He’s now 54 and is pretty well-controlled. Eating LC helps.

    Are you familiar with Richard Bernstein MD’s work with diabetics? His website is fascinating, especially the Intro. Not quacky at all, but I don’t know if he’s conducted any clinical trials of his methods. I would love to see him do that (even though quality nutritional research is famously hard to conduct). At the very least, I’m guessing he keeps incredibly detailed patient records. http://www.diabetes-book.com/bernstein-life-with-diabetes/

    Peter Attia MD has written very informative blog posts about NK (nutritional ketosis). For example, http://eatingacademy.com/nutrition/ketosis-advantaged-or-misunderstood-state-part-i

    Finally, SBM.com is looking for a few more regular contributors. Would you consider coming out from behind the anonymity veil so you could blog there? Pretty please?

    1. I have a passing familiarity with Dr. Bernstein’s books, mostly in that I’ve flipped through them while browsing in Barnes and Noble. I have not read enough to formulate an educated opinion about his stuff, but I will say that I’ve had many patients who find his books helpful. It’s on my list of all the other things I need to get to, so one of these days…

      I have read some of Dr. Attia’s stuff and listened to him on a podcast or two, and I find him intelligent, engaging, and passionate.

      As for Science Based Medicine, funny you should mention that. I recently sent them a guest post as HD, which they rejected based on their policy of not accepting anonymous posts. So you’ll see it Monday on this site. Bummer, because I thought it would have been great for SBM, but I understand that they value transparency. Thanks for asking, though.

  12. I don’t think anyone here is truly talking bout a medically supervised ketogenic diet, but rather more of an Atkins model. A truly ketogenic diet must be carefully managed by a medical team and is extrememly difficult to maintain. It is not a weight management tool.

    Your comments seem to imply that my “approach” is somehow high carb and further, that it is possible to lose significant weight without regard to calories–thus defying the laws of physics. I eat EVERYTHING that I eat in moderation and limiting calories means not wasting them on sugars. It’s not so much counting calories as CONTROLLING PORTIONS. I tell people to eat what they like (and they perk right up); then I tell them only 4 oz or only one little piece of pizza. That’s when they lose interest. Look, I don’t care how you want to parse the balance of carbs, fat, and protein, but you cannot stuff your face with bacon and eggs drenched in olive oil all day and hope to lose weight.

    The support people need is to accept that they will have a struggle in an obesogenic, food-obsessed culture. They need to develop a very big skepticism for ALL faddish approaches and learn to eat at home. They need to understand the pervasiveness of marketing and the difference between something marketed as “healthy” and what is actually healthy. Those “organic” chips will make you just as fat as the “conventional” ones. And it’s losing the fat that helps your diabetes, so when someone says (s)he controlled the diabetes with this or that diet, my question is how much weight did you lose? Then, how long can you maintain this diet?

    Once you learn to eat sensibly, it isn’t that difficult to maintain it. And of course there are bumps in the road. I recently had to go on a strict reset after thinking I could stop weighing myself every week! Several pounds accumulated very quickly indeed!

    I don’t understand why people fight my method and go on about “approaches” instead of spending the energy helping people accept the simple truth. A balanced diet that meets your own caloric requirements–that’s it. Exercise is good too, and can be covered by walking–as briskly as your physical limitations allow. But understand that you will have to walk very far and very briskly to work off a bacon cheeseburger with or without the nutritionally useless bun.

    And please, do clarify your use of the term ketogenic diet, because I get the feeling you (an others) are talking about something that is simply higher fat than usual, not the medical diet used in rare and extreme cases of epilepsy that cannot be controlled with medication.

    And Dr Scher, let me know when you have publishable results that are better than my “approach”. It takes a strong person indeed to stand up to the food culture, but it really is the only way.

    1. Toad, I think we agree on almost all fronts. Clarifications:

      – A ketogenic style of eating can cause dramatic blood sugar improvement immediately, before any significant weight has been lost. But in the long run, weight loss using just calorie restriction will probably achieve similar results. So even there, we sort of agree.

      – I think your approach is the most sensible of all approaches, hands down. But what we know about that sensible approach is that lots of people fail at it – repeatedly. So why not try something new, if it resonates for them? The KD may make it easier for some people to lose weight without as many cravings, though obviously that is a subjective statement.

      – The KD is a high-fat, low-moderate protein, very low-carb diet, in general. But any diet that results in nutritional ketosis could be called a KD. I agree that it looks really hard to stick with, but some people out there seem to like it and do well with it. More power to them.

      – I agree it is not realistic to think that one will lose weight by eating more calories than one burns through resting metabolic rate, exercise, and the thermic effect of food. We agree on that. But I do think that people with significant insulin resistance/diabetes, in general, will see better weight loss results by focusing on a lower carb approach. KD is just one of those approaches.

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