The thread on keto (and low carb) diet

[mccoy]

3 hours ago, Sibiriak said:

Are you talking only about significant amounts of whole grains eaten separately,  or does that also apply to a modest amount of whole grains combined with lower glycemic,  slower-digesting foods in a moderately low calorie meal?  Where's the data?

In any  case,  there doesn't seem to be too much disagreement that for " diabetics and prediabetics a keto diet might be a useful tool to reset glucose homeostasis. "

Sibiriak, since my wife has a family history of T2 and T1 diabetes, she's measuring her glycemia pretty often after whole meals. Her fasting glucose is all right but after meals she often displayed 2 hours peaks at the border of frank diabetics according to teh ADA guidelines 2018 (> 140 mg/dL).

It turns out that, always within a meal context, some vegetables which I wouldn't have associated with high glycaemia, like zucchini, have actually spiked blood glucose. Also, pumpernickel bread, which everyone says it's the best, low GI bread. Whole grains of farro wheat caused similar spikes. Pasta, which should cause lesser peaks than ground cereals, spiked gluocse just the same. The quantity is of course relevant, but I'm speaking usual portions here.

Whereas surprisingly melba toast with jam at breakfast did not cause significant spikes, as well as low-calories ice cream (with carbs). One Apples, legumes, most vegetables even in hearty protions, did not spike blood glucose.

The above measures have been repeated multiple times so they are not the result of random events.

It would seem that Segal and Elinav have it right, the response to carbs ingestion is apparently an highly individual issue and general rules are often reversed. Unfortuntately those accurate, continuos glucometers dispensed to T1 diabetics are not available to the public in general (that I know); that would be a formidable tool to monitor one's glycemic signal throughout the day and design one's regimen accordingly.

We also know that a strong confounding factor here may be due to cortisol peaks, which apparently inhibit pancreas insulin production and are sometimes seen even at night, or in particular stressful situations. They might cause anomalous glycemic peaks not seen in more quiet conditions. 

Takehome lesson seems to be that glucose homeostasis is a pretty complex issue, function of individual repsonse and individual hormonal status , as complex after all as everything else in the body. Hard to define in a single, general rule.

After all Shawn Baker, the zero-carbs carnivore, displayed fasting glucose at the verge of pure diabetes...

 

Edited April 20, 2019 by mccoy

[mccoy]

5 hours ago, Todd Allen said:

I ate all of those foods today.  And it was damn good, it was mostly fat and I'm deep in ketosis.

My meal was a salad with red leaf lettuce, kale, spinach, avocado, eggplant sauteed in EVOO, sous vide beef heart, parmesan cheese, broccoli sprouts, fenugreek sprouts, olives,  black bean natto, pecans, sunflower seeds,  almond butter, tahini, dried tomatos,  ACV, ground flax, garlic, mustard, cumin, seaweed and salt followed by a desert of kefir'd heavy cream and chia, a raw egg and topped with cacao nibs and shredded coconut.

Todd, yours is an example of healthy keto diet, with a regimen designed after careful study of the literature and you are often monitoring your blood values.

From the Longo-Hyman conversation it is evident that many of the objections raised by Longo are due to the fact that the general public is not so well learned and is not followed by qualified professionals.

Do you remember Jerry Brainum's video, he starts recounting about the boy in the gym who said he was following a keto diet. When Jerry asked him if he was in ketosis, the boy didn't know what to answer. That's an example applicable probably to a high percentage of teh public.

[mikeccolella]

Lower carbohydrate diets and all-cause and cause-specific mortality: a population-based cohort study and pooling of prospective studies. 
Mazidi M, Katsiki N, Mikhailidis DP, Sattar N, Banach M. 
Eur Heart J. 2019 Apr 19. pii: ehz174. doi: 10.1093/eurheartj/ehz174. [Epub ahead of print] 
PMID: 31004146 
Abstract

thank you Al, does not look good for low carb diets based on the above. In fact if a comparison was made between a healthy carb diet and lcd I am sure it would be even more damning, however this one looks bad enough!

[Todd Allen]

15 hours ago, mikeccolella said:

thank you Al, does not look good for low carb diets based on the above. In fact if a comparison was made between a healthy carb diet and lcd I am sure it would be even more damning, however this one looks bad enough!

Mike, one must read a study to make an informed judgement of its worth.  Here's a link to the full paper:
http://sci-hub.tw/https://doi.org/10.1093/eurheartj/ehz174

Here are a few of the study's weaknesses as identified by the authors.

Quote

In conclusion, despite the usual limitations of observational data (and so causality impossible to determine), our study highlights an unfavourable association of LCD with overall and cause specific mortality, based on both individual data and pooling previous cohort studies.

...as with other observational studies, some degree of measurement error in reporting dietary and other lifestyle characteristics is inevitable.

...we had no information on the dietary intake of the participants during the Follow-up which might have had an impact on the final results. Also, recall bias cannot be overcome as in such similar studies. Finally, as with many other observational study, reverse causality or residual confounding may potentially explain some findings. 

Studies based on epidemiological data are notoriously weak and inconsistent.  In the intro and discussion they point out other studies of this type with conflicting findings. 

Quote

The effectiveness of diets low in carbohydrate and high in protein and fat to promote weight loss and reduce the cardiometabolic risk was
reported in systematic reviews and meta-analyses.9,10

Nakamura et al. 11 found a lower risk of CVD mortality in Japanese individuals with a higher score of LCD, while they observed no association between LCD score and all-cause death. Another study that involved US women reported null results for the association of LCD with both overall and CVD mortality.14

In the recent analysis of the prospective urban rural epidemiology (PURE) study up to 70% of energy intake was due to refined carbohydrates.45 Of note, the results of the PURE study45 (n= 135 335, aged 35–70 years in 18 countries with a median follow-up of 7.4 years) showed that a higher carbohydrate intake was associated with an increased risk of total mortality [highest vs. lowest category: HR 1.28 (95% CI 1.12–1.46)] but not with the risk of CVD mortality.

 

This study based on admittedly inaccurate data focused on dietary composition of carbohydrates versus non-carbohydrates.  They lump fiber in with carbohydrates as if there was no difference between fiber and sugar.  Most consider fiber healthy and refined sugar unhealthy, including the authors.  Regardless of where one stands on the question of the healthfulness of fiber and sugar there is no questioning that fiber by definition is complex carbohydrates that we do not directly digest.  Our digestion of fiber is mostly limited to fermentation by gut microbes resulting in short chain fatty acids such as acetate, butyrate and propionate.  Equally stupid is lumping everything non-carbohydrate together.  Proteins and fats have very different properties and roles in a thoughtful diet.  There doesn't appear to be any consideration given to dietary quality, to how food was produced, processed or prepared, or to whether diets were nutritionally complete.

This study's cohort are not practicing caloric restriction.  They aren't attempting to optimize nutrition for longevity or any other purpose.  I fail to see how it has any relevance to myself or any other person who prioritizes health when choosing what to eat.  This is a study for people who think taking a daily multivitamin is a good alternative to a nutritionally complete diet.

 

Edited April 23, 2019 by Todd Allen

[srid]

On 4/12/2019 at 3:51 PM, mccoy said:

tedious (especially if no meat-fish nor dairy is eaten)

Speaking of which, there is a specific variation of keto called Paleolithic Ketogenic Diet, which is basically 2:1 fat:protein ratio (in grams) including animal foods only (some people can include minor amount of low-carb plants). 

https://www.reddit.com/r/PaleolithicKetogenic/

https://www.paleomedicina.com/paleolithic-ketogenic-diet/

An average person can live off on no more than 400g of meat per day, which is interesting from CR perspective. In fact, I'm in the process of transitioning from a carnivore diet to this one currently.

[Gordo]

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2737919?fbclid=IwAR0ZqeCQCWxCsD728uZyJ0-eY9XFYxxKubeJMuefwN43ZAXhWp_Sy_gYRhI

July 15, 2019

The Ketogenic Diet for Obesity and Diabetes—Enthusiasm Outpaces Evidence

Shivam Joshi, MD^1,2; Robert J. Ostfeld, MD, MSc³; Michelle McMacken, MD^1,2

Author Affiliations Article Information

JAMA Intern Med. Published online July 15, 2019. doi:10.1001/jamainternmed.2019.2633

[mccoy]

I read the comments below the article, from many physicians working in the field. Quite a few protest that in the 'trenches' the keto diet appears to exhibit good results especially so in T2D patients. I cannot believe that all those doctors are blinded by enthusiasm. It's still a pretty controversial field.

My detached personal impression is that across the board and barring some very specific cases, the keto diet is good, probably as a relatively short term emergency measure, to manage obesity and diabetes, whereas on the long term the trade off may be negative.

Longevity: not optimized by the keto diet.

Muscle hypertrophy: not optimized by the keto diet. 

Also, a strict medical supervision seems to be necessary since the genetic makeup may control detrimental reactions (hyperlipidaemia, inflammation).

A lot in some cases may also depend whether the keto diet is rich in saturated fats or if saturated fats are limited and monounsaturated fats are prevailing (EVOO, avocados, nuts). In a few words, if the keto diet is plant-based and relatively rich in fibers it may provide some layers of protection against possible unfavourable outcomes.

Edited August 7, 2019 by mccoy

[Todd Allen]

On 8/6/2019 at 8:06 AM, Gordo said:

The Ketogenic Diet for Obesity and Diabetes—Enthusiasm Outpaces Evidence

Virta Health has been racking up impressive results coaching patients in using a ketogenic diet to get off medications for diabetes, obesity and numerous comorbidities.  Enough so that they have been signing contracts with the Veterans Administration, the state of California, Blue Cross Blue Shield and numerous other organizations.  They adopted  a policy of only taking payment for services less than the savings on their patients previous health care costs.  This is fueling rapid growth and within a few years I expect they will have published sufficient data to silence most critics other than those whose livelihoods are threatened by Virta's success.  If Virta's stock was publicly traded I'd dump a lot of my other investments to take a major stake.

[Sibiriak]

 

The Italian bodybuilder and actor Franco Columbu, whom Arnold Schwarzenegger called his “best friend” in a moving tribute on social media, has died aged 78

https://www.theguardian.com/film/2019/sep/01/arnold-schwarzenegger-pays-tribute-to-best-friend-franco-columbu-who-dies-aged-78

Italian bodybuilder Franco Columbu, who has died aged 78, on a podium with Arnold Schwarzenegger.

Columbu with Schwarzenegger

 

[Todd Allen]

From his wikipedia page:

Quote

 

On August 30, 2019, after experiencing a sudden illness while swimming off the coast of San Teodoro, Sardinia, Columbu drowned and later died during the transportation by helicopter to the hospital in Olbia.[15] He was 78 years old.[16][17]

 

 

[mccoy]

Franco Columbu's was renowned for his physical strength notwithstanding his small stature. I used to read his course on bodybuilding, and what I remember impressed me were his guidelines on nutrition (he was a Phd in this field), outlining a simple and pretty healthy diet (many vegetables, fruit, fish, lots of yogurt, avoid isolated protein, eat natural...), similar to what I was already eating.

I also improved significantly my strength based on his suggestions, although my constitution was not that of a strongman and suffered for it, eventually having to quit weightlifting for 25 years, until a few years ago.

He was famoust for his world recors in blowing water bottles, 25 in a row, and there is a youtube video in which he  does that at the age of 66

 

 

[mccoy]

lll

Edited December 28, 2019 by mccoy

[mccoy]

This is the best unbiased presentation on fat loss diets for healthy people that I saw. From the master of muscle hypertrophy, Brad Schoenfeld himself. Includes extensive coverage on keto diet. Very simple and clear, and strictly evidence based.

 

 

Edited December 28, 2019 by mccoy

[Todd Allen]

22 hours ago, mccoy said:

From the master of muscle hypertrophy, Brad Schoenfeld himself.

I've read a couple of his books on muscle hypertrophy.  I hadn't seen him before and imagined him to be very fit.  Kind of shocked to see him in a video and see he is also a master of abdominal fat hypertrophy.

 

[mccoy]

LOL, Todd, you are perhaps going a little overboard with it. He's the n°1 recognized authority, probably, in research and practical applications on muscle hypertrophy, that doesn't mean he's the n°1 fittest guy in the world. I did not notice that he has much abdominal fat, although I noticed that he's not so big, that does not bother me, he's not training much these days.

Edited December 29, 2019 by mccoy

[Todd Allen]

18 hours ago, mccoy said:

LOL, Todd, you are perhaps going a little overboard with it.

Perhaps, depending in part on the frame of reference.  Compared to the average American adult Brad looks great.   But I've seen plenty of older power lifters with more impressive muscles and older body builders with narrower waists, flatter bellies and straighter backs.

[mccoy]

Todd, now that I 'm thinking back to what I wrote and blaming my defective knowledge of the English language, I notice I should have written as follows:

He's a master of the research on hypertrophy

He's not a bodybuilder any longer, he trains once a week just for maintenance and he's fully committed to his research, seminars, consultancies and so on.

By reading his books and listening to his podcast, I can list a few of his undeniable merits:

• All his suggestions are based on peer-reviewed research, many of which have been led by himself
• He fully understands individual variability and warns against applying the results of research literally
• He proves to be absolutely unbiased. What he suggests is what has been proven by research so far to work
• His suggestions are relevant exclusively to natural bodybuilding. He does not discuss hormones, insulin and other drugs.

The bottom line, if we want to develop or maintain muscle mass, he's the n°1 reference. No doubt about it. After reading his book, I'm reviewing some details I gave for granted. I'll try to summarize a few relevant points in the thread of exercise optimization. They may not apply rigorously to your condition, but sure are the best set of suggestions I'm aware of.

[Sibiriak]

Keto diet works best in small doses, Yale researchers find   January 23, 2020

Quote

A ketogenic diet — which provides 99% of calories from fat and protein and only 1% from carbohydrates — produces health benefits in the short term, but negative effects after about a week, Yale researchers found in a study of mice.

 

[Todd Allen]

On 2/17/2020 at 7:32 AM, Sibiriak said:

Keto diet works best in small doses, Yale researchers find  

 

Feeding lab mice an unnatural diet of highly refined lab chow ingredients is a poor basis upon which to generalize effects in other species such as free living humans of diets only sharing similar macronutrient ratios but composed of completely different foods.  Stories such as this mainly serve to suggest to me the stupidity of the researchers and journalists and the gullibility of their followers.

In this case much of the blame goes to the journalist as this is the referenced paper and its initial paragraph and much of what follows suggests a different story:

Ketogenesis activates metabolically protective γδ T cells in visceral adipose tissue
 

Quote

Diets with limited carbohydrate content induce a metabolic switch to fatty acid metabolism whereby the host produces and uses ketone bodies to meet energetic demands. The KD is an extremely high-fat, very low-carbohydrate diet in which ~90% of calories come from fat and <1% of calories from carbohydrate, thus limiting glucose availability and forcing this metabolic adaptation towards fatty acid oxidation. Despite its very high caloric density, the consumption of KD is linked to weight loss and improved metabolic health in obese individuals1,2 and reduced inflammation in mouse models3–5. In contrast, it is established that caloric excess, especially the high-fat, high-carbohydrate western-type diet, is the main cause of obesity and its associated chronic inflammatory diseases. Obesity is a growing global epidemic that is associated with increased risk of numerous chronic diseases, including stroke and cardiovascular diseases, diabetes and certain cancers6. According to the World Health Organization, nearly 2 billion people worldwide are overweight and approximately one-third of these individuals are obese7. Thus, weight-loss diets, including KD, that force the host to be driven into fatty acid oxidation and production of ketone bodies represent a potential strategy to alleviate obesity-associated diseases. It is, however, unclear how a calorically rich KD affects adipose tissue inflammation.
 

 

Edited February 19, 2020 by Todd Allen

[Gordo]

[Note: I moved this and the next few posts from a thread on the recipe forum to here since they are about low carb diets.- DP]

On 7/28/2021 at 12:55 PM, mccoy said:

low-carb diet,

 

[mccoy]

Gordo, whatever dr. Garth, Dan Buettner, the various epidemiological studies may say, I must, unfortunately, stick to my objective individual evidence of a trend toward increased fasting BG.

My diet was in between the costa Ricans and the Sardinians, so as a whole within the blue zones parameters. There may be various reasons to my increased BG, but I'm not sure that a high-carb, normocaloric diet will improve that. 

From what I heard, a few months of lowcarb should suffice to reset glucose homeostasis, so I'll be hopefully able to resume eating healthy carbs, maybe choosing foods and combos which avoid excessive spikes/stimulation of beta cells.

 

[Dean Pomerleau]

12 hours ago, mccoy said:

From what I heard, a few months of lowcarb should suffice to reset glucose homeostasis, so I'll be hopefully able to resume eating healthy carbs, maybe choosing foods and combos which avoid excessive spikes/stimulation of beta cells.

 

mcccoy,

Is there actual evidence that a few months of low carb eating can reset glucose metabolism and enable pre-diabetic to go back to eating heathy carbs if they aren't overweight to start with and either don't lose any weight or lose mostly muscle mass on the low carb diet? It seems like someone should have done a trial to test the hypothesis of improved glucose metabolism from low carb eating in the absence of weight loss.

--Dean

[Dean Pomerleau]

If prediabetes is caused by damaged / dysfunctional beta cells in the pancreas being unable to deliver the insulin the body needs to shuttle glucose into cells, then it seems plausible that following a low carb diet for a few months would give your beta cells time to rest and recover. But it is not clear beta cell damage is the (primary) cause of prediabetes. 

An alternative plausible cause is intermyocellular lipids (ICMLs), that is, fat accumulation in skelatal muscles that prevents the proper disposal of glucose. Evidence of this hypothesis include [1], which found that the level of ICMLs correlated strongly with HbA1C in pre-diabetic and [2] which found ICMLs were elevated in the lean, prediabetic offspring of diabetics, but not in those offspring who were lean with normal glucose metabolism. And this meta-analysis [3] found that high fat diets increase ICMLs.

If this second hypothesis were true and it is fat in skelatal muscles that results in prediabetes, then it would be bad news for a normal weight prediabetic to go low carb since it might gum up their muscles with more fat, impairing rather than improving their already-shaky glucose metabolism, even if fasting glucose drops while on the low carb diet from the acute reduction in glucose to process. 

That is why it would be so interesting to see evidence one way or the other of a low carb diet's impact on glucose metabolism in normal weight prediabetics who don't lose weight on the diet.

--Dean 

-----------

[1] European Journal of Clinical Nutrition volume 73, pages1373–1381 (2019)Cite this article

Evidence of higher intramyocellular fat among normal and overweight Indians with prediabetes

S. Sucharita, R. Pranathi, M. Correa, P. Keerthana, L. J. Ramesh, G. Bantwal, H. M. Venkatappa, K. P. Mahadev, T. Thomas, R. J. Bosch, S. D. R. Harridge & A. V. Kurpad A

Abstract

Background
The rise in prevalence rates of Type 2 Diabetes among Indians is well recognized. The research focus has been primarily to understand the changes in insulin sensitivity and beta cell dysfunction among Indians with Type 2 Diabetes. However, no data are available on the role of peripheral tissue, in particular intramyocellular lipid (IMCL) content and its impact on glucose homeostasis among Indians with prediabetes.

Methods
28 male subjects (20–40 year) were studied. 13 with prediabetes (BMI ranging from 25.4 ± 2.9 kg/m2) and 15 controls (BMI ranging from 24.6 ± 2.8 kg/m2) were recruited. Body composition by dual energy X-ray absorptiometry (DXA), insulin sensitivity, insulin secretion rates were derived using the minimal model of C-peptide secretion and kinetics rates and skeletal muscle strength of the lower limb (quadriceps) was assessed using Isokinetic dynamometry. From muscle biopsy samples of the vastus lateralis, IMCL fat content (Oil red O staining) was determined.

Results
The prediabetes group were older compared to controls (P < 0.01), but had similar BMI. The muscle to fat ratio, plasma Insulin, C peptide, HOMA-IR and HOMA % B were also comparable between the groups. IMCL fat content (%) was significantly higher in the prediabetes group compared to controls (7.0 ± 0.7% vs. 2.0 ± 0.3%, P < 0.01). This difference persisted even after controlling for age. Overall the IMCL fat content (%) was positively and significantly associated with HbA1c (r = 0.76, P < 0.01). HOMA-IR was significantly correlated with central (android, trunk) adiposity (kg) (r = 0.71, P < 0.01) but not with IMCL (%).

Conclusions
This is the first direct evidence of existence of significantly higher lipid levels within skeletal muscle cells among normal and overweight young Indians with prediabetes. However, there was no association between IMCL and HOMA-IR among the prediabetes group.

---

[2] Diabetes 1999 May; 48(5): 1113-1119. Https://doi.org/10.2337/diabetes.48.5.1113

Association of increased intramyocellular lipid content with insulin resistance in lean nondiabetic offspring of type 2 diabetic subjects.

S Jacob, J Machann, K Rett, K Brechtel, A Volk, W Renn, E Maerker, S Matthaei, F Schick, C D Claussen and H U Häring

Abstract

Insulin resistance plays an important role in the pathogenesis of type 2 diabetes; however, the multiple mechanisms causing insulin resistance are not yet fully understood. The aim of this study was to explore the possible contribution of intramyocellular lipid content in the pathogenesis of skeletal muscle insulin resistance. We compared insulin-resistant and insulin-sensitive subjects. To meet stringent matching criteria for other known confounders of insulin resistance, these individuals were selected from an extensively metabolically characterized group of 280 first-degree relatives of type 2 diabetic subjects. Some 13 lean insulin-resistant and 13 lean insulin-sensitive subjects were matched for sex, age, BMI, percent body fat, physical fitness, and waist-to-hip ratio. Insulin sensitivity was determined by the hyperinsulinemic-euglycemic clamp method (for insulin-resistant subjects, glucose metabolic clearance rate [MCR] was 5.77+/-0.28 ml x kg(-1) x min(-1) [mean +/- SE]; for insulin-sensitive subjects, MCR was 10.15+/-0.7 ml x kg(-1) x min(-1); P<0.002). Proton magnetic resonance spectroscopy (MRS) was used to measure intramyocellular lipid content (IMCL) in both groups. MRS studies demonstrated that in soleus muscle, IMCL was increased by 84% (11.8+/-1.6 vs. 6.4+/-0.59 arbitrary units; P = 0.008 ), and in tibialis anterior muscle, IMCL was increased by 57% (3.26+/-0.36 vs. 2.08+/-0.3 arbitrary units; P = 0.017) in the insulin-resistant offspring, whereas the extramyocellular lipid content and total muscle lipid content were not statistically different between the two groups. These data demonstrate that in these well-matched groups of lean subjects, IMCL is increased in insulin-resistant offspring of type 2 diabetic subjects when compared with an insulin-sensitive group matched for age, BMI, body fat distribution, percent body fat, and degree of physical fitness. These results indicate that increased IMCL represents an early abnormality in the pathogenesis of insulin resistance and suggest that increased IMCL may contribute to the defective glucose uptake in skeletal muscle in insulin-resistant subjects.

----------------

[3]  Front Nutr. 2018 Feb 20;5:7. doi: 10.3389/fnut.2018.00007. eCollection 2018.

The Effects of Diet on the Proportion of Intramuscular Fat in Human Muscle: A Systematic Review and Meta-analysis
Sara Ahmed 1, Dhanveer Singh 2, Shereen Khattab 1, Jessica Babineau 3, Dinesh Kumbhare 4

Abstract
Background: There is an increasing trend in the consumption of poor-quality diets worldwide, contributing to the increase of non-communicable diseases. Diet directly influences physiological composition and subsequently physical health. Studies have shown that dietary macronutrient and energy content can influence the proportion of intramuscular fat (IMF), which mediates various metabolic and endocrine dysfunction. The purpose of this systematic review was to identify evidence in the literature assessing the association between different dietary interventions on the proportion of IMF in humans.

Methods: Three medical databases were investigated (Medline, EMBASE, and Cochrane) to identify studies assessing changes in IMF after dietary interventions. The primary outcome measure was the change in IMF proportions after a dietary intervention. The effects of high-fat, high-carbohydrate, low-calorie, and starvation diets were assessed qualitatively. A meta-analysis assessing the effect of high-fat diets was conducted. Follow-up sensitivity and subgroup analyses were also conducted.

Results: One thousand eight hundred and sixty-six articles were identified for review. Of these articles, 13 were eligible for inclusion after a full screening. High-fat diets increased IMF proportions, standardized mean difference = 1.24 (95% confidence interval, 0.43-2.05) and a significant overall effect size (P = 0.003). Diets with an increased proportion of carbohydrates decreased IMF proportions; however, increasing caloric intake with carbohydrates increased IMF. Starvation diets increased IMF stores, and hypocaloric diets did not result in any IMF proportion changes.

Conclusion: This systematic review suggests that high-fat diets and diets with caloric intake increased above the amount required to maintain BMI with carbohydrates, and short-term starvation diets are associated with increases in IMF content. Further studies are needed to assess the effects of macronutrient combinations on IMF and the influence of diet-induced IMF alterations on health outcomes. In addition, IMF poses a possibly effective clinical marker of health.

PMID: 29516003 PMCID: PMC5826234 DOI: 10.3389/fnut.2018.00007

[Todd Allen]

6 hours ago, Dean Pomerleau said:

An alternative plausible cause is intermyocellular lipids (ICMLs), that is, fat accumulation in skelatal muscles that prevents the proper disposal of glucose. Evidence of this hypothesis include [1], which found that the level of ICMLs correlated strongly with HbA1C in pre-diabetic and [2] which found ICMLs were elevated in the lean, prediabetic offspring of diabetics, but not in those offspring who were lean with normal glucose metabolism. And this meta-analysis [3] found that high fat diets increase ICMLs.

 If this second hypothesis were true and it is fat in skelatal muscles that results in prediabetes, then it would be bad news for a normal weight prediabetic to go low carb since it might gum up their muscles with more fat, impairing rather than improving their already-shaky glucose metabolism, even if fasting glucose drops while on the low carb diet from the acute reduction in glucose to process. 

I was a morbidly obese by body fat although of normal BMI and I'm fairly certain my prediabetes was driven by ectopic lipid accumulation both intramuscular lipids and visceral fat.  These are considered standard findings of my disease SBMA and are correlated with severity and rate of progression.  I've been getting regular DEXA scans which give measurements of visceral fat  and total body fat.  I also track body fat using skin fold calipers and a tape measure which always report I am leaner than by DEXA.  I assume much of the difference is due to intramuscular fat which DEXA sees but doesn't report separately while the other methods are based on statistical data.  Thus the greater amount of body fat reported by DEXA is probably largely attributable to the amount of fat in my muscles in excess of the statistical average for men of my age, height and weight.  Through nearly quarterly DEXAs for the past 4 years while experimenting with various approaches to diet I've been chipping away at the intramuscular fat which is still pretty bad in my legs but approaching normal in my torso and arms.  By contrast my visceral fat went away extremely fast and has been exceptionally low for men of my age for the past 3 years.

The typical research high fat diet which commonly produces scary results is a very unnatural highly processed diet with carbohydrates up to 40% of calories often 10% of calories from sucrose alone and a lot more from refined starch, fat from refined seed oils and refined casein for protein with powdered vitamins and minerals added for nutritional completeness.  I'm currently typically eating about 60% calories as fat the majority saturated, 35% protein and 5% carbs from natural whole foods mostly animal based minimally processed and gently cooked which is working exceptionally well for me.

My tolerance for sugar is much improved.  We spent the past couple weeks harvesting our apricot tree and I was able to eat up to 6 daily while maintaining good blood sugar something unthinkable a few years ago.  But I would not make an extended habit of eating that much carbohydrate and have no desire to return to a "normal" diet and become diseased again.

[Dean Pomerleau]

Thanks Todd,

Interesting anecdote. Given your disease and your (former) morbid obesity, I'm not sure your experience tells us very much about the effects of a low carb eating in lean prediabetics who are otherwise healthy and trying to maintain their current weight.

I don't think anyone questions the fact that a low carb diet can produce substantial weight loss and thereby improve insulin sensitivity. And I think it's pretty obvious that eating very few carbs will reduce serum glucose for as long as you continue to eat that way. The question is whether low carb eating can have lasting benefits for glucose metabolism in the absence of weight loss relative to a balanced diet - i.e. deliver the kind of "metabolic reset" mccoy is hoping for so he can go back to eating healthy carbs like fruit. While it it clearly a big win for you relative to the way you were, eating up to 6 apricots daily without your blood sugar going through the roof doesn't sound too impressive (no offense).

Since you seem pretty knowledgeable about the low carb lifestyle, do you know of any scientific evidence that a low carb, weight-maintaining diet can restore someone's ability to effectively metabolize glucose?

--Dean