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The thread on keto (and low carb) diet

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The idea of a reset of glucose homeostasis came from a few podcasts I listened to (I remember: Peter Attia, Valter Longo speaking about this concpet), but no clinical trials were mentioned, nor I'm aware of any. The length of time required supposedly varies, so this is an unconvenient variable. 

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18 hours ago, Dean Pomerleau said:

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?

No.  The largest studies and best quality evidence suggesting low carb diets can benefit metabolic health are focused on weight loss.  Based on a lot of anecdotal evidence my belief is it would be highly unusual for a low carb diet by itself to produce a substantial lasting metabolic reset without significant weight loss.  Small improvement seems possible though especially when low carb is an adjunct to things such as improved sleep hygiene, stress management,  exercise and reduction of smoking, alcohol and other toxins.

I don't believe carbohydrates are inherently toxic or a root cause of impaired carbohydrate metabolism and carbohydrate restriction mainly addresses downstream effects such as the morbidities of hyperglycemia and hyperinsulinemia.  I also think caloric restriction in most any form is the most powerful tool for addressing chronic hyperinsulinemia.  I think those who find carbohydrate restriction helps with appetite regulation are the ones who realize the most benefit from low carb diets.  McCoy's FMDs and other dietary practices suggest suggest excess appetite and insulin are not major issues for him. I'm fuzzy on the details of McCoy's glycemia issues and don't have a sense of what is driving it.

Two possibilities which are not mutually exclusive are diminished insulin production and diminished response to insulin.  Many T1Ds are finding carbohydrate restriction valuable for managing their condition although I'm unaware of reversal of T1Ds with complete loss of insulin production.  I have heard of multiple cases of people with very low c-peptide tests seeing small gains of c-peptide while eating low carb.  Obesity may be the most common driver of insulin resistance.  One flavor of obesity "skinny fat" sometimes called TOFI for thin outside fat inside is increasingly recognized as nearly as bad as FOFI.  McCoy could be pre-TOFI if his minimal subcutaneous fat is composed of a few large adipocytes instead of lots of small ones.  Adipocytes have an average lifespan of about 10 years and aging and being male are both risk factors for diminished capacity to replace and grow new adipocytes.  There are genetic predispositions and probably environmental factors as well.  Although fat is demonized having diminished capacity to store fat and buffer energy can be problematic irregardless of how fat or lean one is.

Low expression of PPAR-gamma has been found in my disease SBMA and I suspect this contributed to my metabolic decline and severe TOFIness.  I took the drug pioglitazone for one month with dramatic effects.  It made me ravenous and I regained 15 lbs mostly as subcutaneous fat.   After stopping the drug as I lost the regained weight I had rapid large improvements in metabolic health resulting in improved tolerance for carbs and protein.  I increased my protein intake by roughly 50% and expect I could eat several more apricots daily if I went back to a recommended level of protein. 

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Thanks Todd. That is really interesting and aligns with my own understanding. A low carb diet can help some people to lose weight quite effectively, but there doesn't seem to be evidence that eating low carb provides any unique advantage with respect to fixing impaired glucose metabolism apart from the improvement that come from weight loss and the obvious benefit of reduced exposure to glucose spikes while one is sticking to the low carb diet.

As you suggest, it seems possible that mccoy could have a issue with too much visceral fat impairing his ability to metabolize glucose. Or he could have an excess of intramyocellular lipids (ICMLs) impairing his glucose metabolism. Or both. Regardless of which it is, it seems like aerobic exercise (but probably not strength training) could be of considerable benefit [1][2][3], while going low carb without losing weight is unlikely to do (much) to fix the problem except to bring down glucose while he is sticking to the diet.

Another potential cause I discussed earlier is beta cell dysfunction impairing mccoy's ability to synthesize and release insulin to facilitate glucose clearance. But this seems unlikely given his observation that yogurt (a potent insulin secretagogue) effectively blunts the glucose spike after a high carb meal. So his beta cells can pump out sufficient insulin when called upon to do so.

--Dean

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[1] Obes Rev. 2012 Jan;13(1):68-91. doi: 10.1111/j.1467-789X.2011.00931.x. Epub 2011 

Sep 26.

A systematic review and meta-analysis of the effect of aerobic vs. resistance 
exercise training on visceral fat.

Ismail I(1), Keating SE, Baker MK, Johnson NA.

Author information:
(1)Discipline of Exercise and Sport Science, University of Sydney, Sydney, New 
South Wales, Australia.

It is increasingly recognized that the location of excess adiposity, 
particularly increased deposition of visceral adipose tissue (VAT), is important 
when determining the adverse health effects of overweight and obesity. Exercise 
therapy is an integral component of obesity management, but the most potent 
exercise prescription for VAT benefit is unclear. We aimed to evaluate the 
independent and synergistic effects of aerobic exercise (AEx) and progressive 
resistance training (PRT) and to directly compare the efficacy of AEx and PRT 
for beneficial VAT modulation
. A systematic review and meta-analysis was 
performed to assess the efficacy of exercise interventions on VAT content/volume 
in overweight and obese adults. Relevant databases were searched to November 
2010. Included studies were randomized controlled designs in which AEx or PRT in 
isolation or combination were employed for 4 weeks or more in adult humans, 
where computed tomography (CT) or magnetic resonance imaging (MRI) was used for 
quantification of VAT pre- and post-intervention. Of the 12196 studies from the 
initial search, 35 were included. After removal of outliers, there was a 
significant pooled effect size (ES) for the comparison between AEx therapy and 
control (-0.33, 95% CI: -0.52 to -0.14; P < 0.01) but not for the comparison 
between PRT therapy and control (0.09, 95% CI: -0.17 to 0.36; P = 0.49).
Of the 
available nine studies which directly compared AEx with PRT, the pooled ES did 
not reach statistical significance (ES = 0.23, 95% CI: -0.02 to 0.50; P = 0.07 
favouring AEx). The pooled ES did not reach statistical significance for 
interventions that combined AEx and PRT therapy vs. control (-0.28, 95% CI: 
-0.69 to 0.14; P = 0.19), for which only seven studies were available. These 
data suggest that aerobic exercise is central for exercise programmes aimed at 
reducing VAT
, and that aerobic exercise below current recommendations for 
overweight/obesity management may be sufficient for beneficial VAT modification. 
Further investigation is needed regarding the efficacy and feasibility of 
multi-modal training as a means of reducing VAT.

© 2011 The Authors. obesity reviews © 2011 International Association for the 
Study of Obesity.

DOI: 10.1111/j.1467-789X.2011.00931.x
PMID: 21951360 [Indexed for MEDLINE]

 

-----------

[2] Int J Obes (Lond). 2021 May;45(5):982-997. doi: 10.1038/s41366-021-00767-9. Epub 

2021 Feb 8.

Effect of exercise intervention dosage on reducing visceral adipose tissue: a 
systematic review and network meta-analysis of randomized controlled trials.

Chang YH(1)(2), Yang HY(1), Shun SC(3).

Author information:
(1)School of Nursing, College of Medicine, National Taiwan University, Taipei, 
Taiwan.
(2)Department of Nursing, National Tainan Junior College of Nursing, Tainan, 
Taiwan.
(3)School of Nursing, College of Medicine, National Taiwan University, Taipei, 
Taiwan. scshun@ntu.edu.tw.

BACKGROUND: Visceral adipose tissue (VAT) are deleterious fat deposits in the 
human body and can be effectively reduced by exercise intervention. Despite 
well-established exercise prescriptions are available, the effective dosage of 
exercise for reducing VAT requires verification.
OBJECTIVES: The aims of this systematic review and meta-analysis were to 
determine the most effective exercise dosage (modality, intensity, duration, and 
amount) for decreasing VAT.
METHODS: Nine databases (EMBASE, Medline, Cochrane Central Register of 
Controlled Trial, PubMed, CINAHL, Scopus, Web of Science, Airiti Library, and 
PerioPath) were systematically searched for randomized controlled trials that 
objectively assessed VAT. The arms of included studies covered with different 
exercise modalities and dosage. Relevant databases were searched through 
February 2020.
RESULTS: Of the 34 studies (n = 1962) included in systematic review, 32 
(n = 1900) were pooled for pairwise or network meta-analysis. The results 
indicated that high-intensity interval training (SMD -0.39, 95% CI -0.60 to 
-0.18) and aerobic exercise (SMD -0.26, 95% CI -0.38 to -0.13) of at least 
moderate intensity were beneficial for reducing VAT. By contrast, resistance 
exercise, aerobic exercise combined with resistance exercise, and sprint 
interval training had no significant effects.
No difference in VAT reduction was 
observed between exercising more or less than 150 min per week. Meta-regression 
revealed that the effect of VAT reduction was not significantly influenced by an 
increase in the duration of or amount of exercise in an exercise program. The 
effective dosage of exercise for reducing VAT was three times per week for 12 to 
16 weeks, while duration per session for aerobic exercise was 30-60 min, and 
either less than 30 min or 30-60 min of high-intensity interval training 
accomplished sufficient energy expenditure to impact VAT.
CONCLUSIONS: These results can inform exercise prescriptions given to the 
general population for improving health by reducing VAT.

DOI: 10.1038/s41366-021-00767-9
PMID: 33558643

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

[3] The Journal of Clinical Endocrinology & Metabolism, Volume 86, Issue 12, 1 December 2001, Pages 5755–5761, https://doi.org/10.1210/jcem.86.12.8075
Published: 01 December 2001 Article history

Skeletal Muscle Lipid Content and Insulin Resistance: Evidence for a Paradox in Endurance-Trained Athletes 

Bret H. Goodpaster, Jing He, Simon Watkins, David E. Kelley

We examined the hypothesis that an excess accumulation of intramuscular lipid (IMCL) is associated with insulin resistance and that this may be mediated by the oxidative capacity of muscle. Nine sedentary lean (L) and 11 obese (O) subjects, 8 obese subjects with type 2 diabetes mellitus (D), and 9 lean, exercise-trained (T) subjects volunteered for this study. Insulin sensitivity (M) determined during a hyperinsulinemic (40 mU·m−2min−1) euglycemic clamp was greater (P < 0.01) in L and T, compared with O and D (9.45 ± 0.59 and 10.26 ± 0.78 vs. 5.51 ± 0.61 and 1.15 ± 0.83 mg·min−1kg fat free mass−1, respectively). IMCL in percutaneous vastus lateralis biopsy specimens by quantitative image analysis of Oil Red O staining was approximately 2-fold higher in D[iabetics] than in L[ean subjects] (3.04 ± 0.39 vs. 1.40 ± 0.28% area as lipid; P < 0.01). IMCL was also higher in T[rained endurance athletes] (2.36 ± 0.37), compared with L[ean subjects] (P < 0.01). The oxidative capacity of muscle determined with succinate dehydrogenase staining of muscle fibers was higher in T, compared with L, O, and D (50.0 ± 4.4, 36.1 ± 4.4, 29.7 ± 3.8, and 33.4 ± 4.7 optical density units, respectively; P < 0.01). IMCL was negatively associated with [insulin sensitivity] (r = −0.57, P < 0.05) when endurance-trained subjects were excluded from the analysis, and this association was independent of body mass index. However, the relationship between IMCL and M was not significant when trained individuals were included. There was a positive association between the oxidative capacity and M among nondiabetics (r = 0.37, P < 0.05). In summary, skeletal muscle of trained endurance athletes is markedly insulin sensitive and has a high oxidative capacity, despite having an elevated lipid content. In conclusion, the capacity for lipid oxidation may be an important mediator of the association between excess muscle lipid accumulation and insulin resistance.

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Hi Todd.

I looked up SBMA;  I hope you've had some success in coping with this disease.  You have my sympathies.

  --  Saul

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2 hours ago, Dean Pomerleau said:

A low carb diet can help some people to lose weight quite effectively, but there doesn't seem to be evidence that eating low carb provides any unique advantage with respect to fixing impaired glucose metabolism

Dean, I think this might be the closest example of a scientific study showing metabolic benefits of carbohydrate restriction without weight loss.  The cohort was obese and there was no attempt to show a lasting metabolic reset.  It suggests without weight loss carbohydrate restriction can favorably impact biomarkers of metabolic syndrome and risk factors for CVD.  The study appears to me as a well controlled intervention but like most such studies was both small and brief.  All of the diets used high fat cheese as the primary source of saturated fat. Carbohydrates came in part from processed grains.  With those limitations I don’t think it sheds much light on whether McCoy can achieve his goals or what dietary tweaks will best serve him.  Perhaps the discussion of tracked markers might be of value for McCoy’s efforts to evaluate the pros and cons of his choices.


Dietary carbohydrate restriction improves metabolic syndrome independent of weight loss

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Thanks Todd,

That is an interesting study. 

1 hour ago, Todd Allen said:

 All of the diets used high fat cheese as the primary source of saturated fat. Carbohydrates came in part from processed grains.

You forgot to mention all the fruit juice, fig Newton cookies and marshmallow fluff that were part of the high carb diet - for a total of 150g of refined sugar! Plus bizzarely all three diets, including the low fat, contained the same 200g of high-fat cheese. As a result, even the so called "low fat" diet contained 34g/day of saturated fat and very little PUFA.

You are right that none of the diets look anything like mccoy's.

And as you point out, the key is that the glucose improvement in the low carb group was measured via fasting glucose while the group was following the diet and thus exposed to little glucose (the same sort of fasting glucose drop that mccoy has already seen on low carb). It didn't address whether they were better able to process glucose after following the diet for a while (i.e. achieved a metabolic reset) or what happens when the started eating (healthy) carbs again.

--Dean

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3 hours ago, Dean Pomerleau said:

You forgot to mention all the fruit juice, fig Newton cookies and marshmallow fluff that were part of the high carb diet - for a total of 150g of refined sugar! Plus bizzarely all three diets, including the low fat, contained the same 200g of high-fat cheese. As a result, even the so called "low fat" diet contained 34g/day of saturated fat and very little PUFA.

I didn't bother to open up the supplemental document as limitations I mentioned found in the methods and discussion were sufficient to rule this out from speaking in any meaningful way to McCoy's situation.  But you prompted me to look for the sample diets and my statement "It suggests without weight loss carbohydrate restriction can favorably impact biomarkers of metabolic syndrome and risk factors for CVD."  at a minimum needs to be changed to "restriction of fruit juices and highly processed junk food carbohydrates can favorably ...".

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So far, after one month, I can say that my adiposity remained the same or decreased a little, but nothing dramatic such as becoming very ripped. Muscle mass is about the same. As I've written, the glucose setpoint decreased by about 10 mg/dL and of course glucose spikes are absent. 

As to the adiposity, I remember I've always been sensitive to a decrease of dietary fats and calories, thereby losing weight and adiposity. The only previous time I tried lowcarb it was actually low carb-low protein, with more saturated fats. It resulted in a pronounced weightloss, muscle mass and adiposity, even if training (rather obviously, missing either significant glucose and  BEAAs signals, mTOR went in relative inhibition).

Exactly one year ago my fasting BG was 84 mg/dL and insulin very low, below the lab range minimum. HOMA-IR was consequently very low. Last month, when wearing the CGM, the glucose spikes were pretty short-lasting, which is supposed to be a sign of insulin sensitivity.

So, I have no clue why my FG increased by 15-20 mg/dL . Maybe by increasing bodyweight (I reached +5 kg at a point, from 68 to 73 kg), by drinking often cacao with honey and eating so many oranges first time in the morning during the winter, plus many smoothies with bananas, milk, honey and sometimes whey. Plus sweet bites after meals. Even if I exercised and practiced CE, beta-cells may have been excessively stimulated.

 

Edited by mccoy

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34 minutes ago, mccoy said:

Exactly one year ago my fasting BG was 84 mg/dL and insulin very low, below the lab range minimum. HOMA-IR was consequently very low. Last month, when wearing the CGM, the glucose spikes were pretty short-lasting, which is supposed to be a sign of insulin sensitivity.

So, I have no clue why my FG increased by 15-20 mg/dL .

My guess is an upregulation of one or more stress hormones.  Cortisol in particular but also epinephrine, norepinephrine, CRH & ACTH and even growth hormone can all raise blood sugar.   If so it can quickly resolve.  Sometimes the triggers are obvious such as concerns producing anxiety but a wide range of things such as infections, injuries, mold and other toxins can also produce stress responses which can be challenging to identify.

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20 hours ago, Saul said:

I looked up SBMA;  I hope you've had some success in coping with this disease.  You have my sympathies.

 

Thanks Saul, it was bad several years ago when I felt like a passenger on a doomed airliner as my health and fitness plummeted despite my efforts.  Now I feel more like a sailor attempting a solo ocean crossing.  There are strong unpredictable forces at play but I know the decisions I make matter.  The past few years have been exciting and satisfying and I expect an interesting and hopefully long journey.

I've challenged my father-in-law to a 1 mile foot race 7 years from now on his 100th birthday.  Each time we meet we discuss our training efforts and most recent best times.  I'm the underdog but I have been closing the gap.  If I'm victorious I'll need new  challenges.  Have you got plans for your 100th and is sidewalk racing with canes or poles allowed in your neighborhood?

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1 hour ago, Todd Allen said:

My guess is an upregulation of one or more stress hormones.  Cortisol in particular but also epinephrine, norepinephrine, CRH & ACTH and even growth hormone can all raise blood sugar.   If so it can quickly resolve.  Sometimes the triggers are obvious such as concerns producing anxiety but a wide range of things such as infections, injuries, mold and other toxins can also produce stress responses which can be challenging to identify.

Todd, yes that's another possibility, maybe cortisol, considering how my sleep quality is going downhill. One of my choices eventually, if no final resolution occurs,  might be to consult an endocrinologist.

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Ketogenic diets inhibit mitochondrial biogenesis and induce cardiac fibrosis

Abstract
In addition to their use in relieving the symptoms of various diseases, ketogenic diets (KDs) have also been adopted by healthy individuals to prevent being overweight. Herein, we reported that prolonged KD exposure induced cardiac fibrosis. In rats, KD or frequent deep fasting decreased mitochondrial biogenesis, reduced cell respiration, and increased cardiomyocyte apoptosis and cardiac fibrosis. Mechanistically, increased levels of the ketone body β-hydroxybutyrate (β-OHB), an HDAC2 inhibitor, promoted histone acetylation of the Sirt7 promoter and activated Sirt7 transcription. This in turn inhibited the transcription of mitochondrial ribosome-encoding genes and mitochondrial biogenesis, leading to cardiomyocyte apoptosis and cardiac fibrosis. Exogenous β-OHB administration mimicked the effects of a KD in rats. Notably, increased β-OHB levels and SIRT7 expression, decreased mitochondrial biogenesis, and increased cardiac fibrosis were detected in human atrial fibrillation heart tissues. Our results highlighted the unknown detrimental effects of KDs and provided insights into strategies for preventing cardiac fibrosis in patients for whom KDs are medically necessary.

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4 hours ago, Ron Put said:

This was a rat study using a terrible diet that happens to be keto.  One could just as easily construct a terrible vegan diet that gives rats heart disease and then title it "vegan diet causes heart disease".

They fed rats a diet that was 60+% cocoa butter.  This is considered an acceptable fat source for keto diets but not one that should be the main source.  The only other source of fat was a few percent soybean oil widely considered a fat to be avoided on keto diets.  The only source of protein was casein.  100g of cocoa butter has 0.1g of omega 3s, essentially zero of the essential alpha-linolenic acid and the derivatives EPA, DPA and DHA which are important for both mitochondria and heart health.  Casein is widely considered a highly inflammatory protein source especially A1 which is far more common than A2.  A cocoa butter and casein diet is highly deficient in micronutrients. Here is a review that addresses other aspects of the paper such as speculations about cardiac fibrosis in humans:

https://ketonutrition.org/ketones-and-heart-health/

Edited by Todd Allen

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If the whole point of being on a keto diet is the ketones, then for those who aren't aware, time-restricted feeding every day provides a modest amount (not that this is necessarily helpful for you, Todd).

After fasting for say 10-12hrs iirc you are essentially in a state of ketosis until you re-feed.  I aim for TRF of 8hr feed, 16hr fast and hope that gives me perhaps 4hrs of ketosis daily.  Rhonda Patrick mentions this and I've seen it in other literature as well.

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2 hours ago, Clinton said:

If the whole point of being on a keto diet is the ketones, then for those who aren't aware, time-restricted feeding every day provides a modest amount (not that this is necessarily helpful for you, Todd).

I am eating more protein than recommended for keto so a good fraction of my ketones, which isn't a lot, is due to TRF as I mostly stick to a 9 AM to 3 PM feeding window.

I transitioned from low carb to keto chasing better blood sugar.  Also I lost a lot of fat in the first few months of low carb and then stalled out and found it a bit easier to skip meals and keep a lower average caloric intake eating keto.  The neurotrophic potential of ketones was of interest when I had severe issues with neuropathy but it is negligible now and only if it comes back would there be incentive to prioritize higher ketones to see if it helps.

Physical performance and body composition are my current top priorities.  I did a 3 month test with high ketones 3+ mmol/l with a daily breakfast of whey protein concentrate in 1/3 cup of MCT oil, a couple eggs and some kefir and a lunch of red meat or fish with small amounts of low carb vegetables.  I felt and performed well.  I gained about 5 lbs and thought I was gaining mostly muscle but DEXA scans showed the gain was more than half fat and I feared much of it was intramuscular based on skin fold measures.  Both DEXA and skin fold measurements have enough error that I would need to repeat this to have high confidence in the results and perhaps some day I will retest but I turned to trying variations of what appears to give better results for me which is slower bulking phases emphasizing protein, 160 to 200 g, with low ketones 0.2 to 0.3 mmol/l and maintaining weight stability with 1 week a month at about 50% of calories eating only breakfast or lunch and ketones stay moderate as protein is fairly high at 100+ g.

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Clinton, thanks for the bit about intermittent fasting and ketones -- I did not know that.

Tod, it's clear that your diet works well for you, and of course, your points about rats are valid. But the point is that that humans generally use glucose, and populations that are generally long-lived consume higher amounts of starches and fiber than others. There is some evidence that ketosis results in oxidative stress and metabolic acidosis in the long run, and the one population that consumes a high-fat diet, the Innuits, is genetically adapted to not enter into a permanent state of ketosis, which may be of significance.

Keto diets are a viable alternative for people who have impaired glucose function, but it doesn't mean that they are good for one's health in the long run. They help people lose weight while eating a more "palatable" to them diet than vegetables and whole grains, but the loss for most is to a significant extent loss of water and muscle mass. Muscles just work better with glucose.

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I don't think we've discussed this 2019 study [1] before. It involved 23 young, normal weight (BMI ~21), healthy and moderately trained young women from a nutrition program in Sweden. They logged all their food for one week prior to the low carb dietary intervention followed by three weeks of a low carb diet. Here is their dietary composition before and after the intervention:

Screenshot_20210807-142025_Chrome.jpg

 

As you can see, their baseline diet averaged to about 45% carbs (only 5% added surgar) and 35% fat (10% of calories from saturated fat). Not a bad diet to start with, and already pretty high in fat. They went up to 78% fat (30% of energy from saturated fat) during the three week intervention and spent a lot of time in ketosis.

The diet was supposed to be isocaloric to prevent weight loss, but nevertheless the subjects lost a couple pounds of mostly water and lean mass. Their LDL and triglycerides went up 39% and 20% respectively after only 3 week mccoy - it didn't take months.. LDL went from a healthy 77 mg/dL to 124 mg/dL (p < 0.001). Ouch. Triglycerides went from 60 -> 72 mg/dL (p = 0.035). 

Regarding glucose metabolism - fasting glucose dropped a little while on the low carb diet (4.7 -> 4.4 mmol/L, or 85 -> 80 mg/dL - i.e. these women were already in good shape fasting glucose-wise).

But unfortunately, if anything glucose metabolism got a little worse and most notably the beneficial effects of exercise on glucose metabolism seemed to be dramatically blunted by three weeks on a low carb diet.

Here are the curves of four glucose tolerance tests on these women. The first two (circles) were at baseline (before three weeks of low carb) either after having not exercised for 48 hours, or having exercised the afternoon before the OGTT. The other two curves (triangles) are the OGTT results after the 3 weeks of low carb dieting, rested or the morning after an afternoon bout of exercise:

Screenshot_20210807-104901_Chrome.jpg

Screenshot_20210807-105005_Chrome.jpg

As you can see, the glucose levels in response to the glucose load appears slightly worse after the low carb diet (closed triangles) than at baseline (closes circles). And exercising prior to the OGTT didn't help after the low carb diet (open triangles) in fact it appeared their glucose spiked more in response to an OGTT the morning after a bout of afternoon exercise. The AUC for insulin was actually higher during the OGTT after exercise subsequent to the 3 weeks of low carb, indicating apparent insulin resistance, which the authors speculated may be a result of increased circulating free fatty acids blunting the effects of insulin.

This contrasts with their baseline. before the three weeks of low carb. In that case, exercising the afternoon before dramatically reduced the glucose levels during a morning OGTT the next day (open circles) relative to the rested OGTT (solid circles), and the insulin release during the post-exercise OGTT was lower too.

Here are the glucose AUCs for the four OGTT tests shown above, with statistically significant differences indicated:

Screenshot_20210807-143417_Chrome.jpg

 

Overall, not at all a ringing endorsement for a period of low carb dieting having beneficial effects on glucose metabolism (or cholesterol) in the absence of (much) weight loss in healthy people. Of course the young women were metabolically healthy to begin with and were still on the low carb diet at the time of the OGTTs so their bodies may have shifted to burning fat and not handling glucose well (having not seen much glucose for a while). This study did not address how long this relative glucose intolerance lasts after a period of low carb dieting.

--Dean 

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[1] Front. Physiol., 19 December 2019 | https://doi.org/10.3389/fphys.2019.01499

Effect of a Low-Carbohydrate High-Fat Diet and a Single Bout of Exercise on Glucose Tolerance, Lipid Profile and Endothelial Function in Normal Weight Young Healthy Females


Thorhildur Ditta Valsdottir1,2*†, Christine Henriksen3, Nancy Odden4, Birgitte Nellemann2, Per B. Jeppesen5, Jonny Hisdal6, Ane C. Westerberg4,7 and Jørgen Jensen2

Low-carbohydrate-high-fat (LCHF) diets are efficient for weight loss, and are also used by healthy people to maintain bodyweight. The main aim of this study was to investigate the effect of 3-week energy-balanced LCHF-diet, with >75 percentage energy (E%) from fat, on glucose tolerance and lipid profile in normal weight, young, healthy women. The second aim of the study was to investigate if a bout of exercise would prevent any negative effect of LCHF-diet on glucose tolerance. Seventeen females participated, age 23.5 ± 0.5 years; body mass index 21.0 ± 0.4 kg/m2, with a mean dietary intake of 78 ± 1 E% fat, 19 ± 1 E% protein and 3 ± 0 E% carbohydrates. Measurements were performed at baseline and post-intervention. Fasting glucose decreased from 4.7 ± 0.1 to 4.4 mmol/L (p < 0.001) during the dietary intervention whereas fasting insulin was unaffected. Glucose area under the curve (AUC) and insulin AUC did not change during an OGTT after the intervention. Before the intervention, a bout of aerobic exercise reduced fasting glucose (4.4 ± 0.1 mmol/L, p < 0.001) and glucose AUC (739 ± 41 to 661 ± 25, p = 0.008) during OGTT the following morning. After the intervention, exercise did not reduce fasting glucose the following morning, and glucose AUC during an OGTT increased compared to the day before (789 ± 43 to 889 ± 40 mmol/L∙120min–1, p = 0.001). AUC for insulin was unaffected. The dietary intervention increased total cholesterol (p < 0.001), low-density lipoprotein (p ≤ 0.001), high-density lipoprotein (p = 0.011), triglycerides (p = 0.035), and free fatty acids (p = 0.021). In conclusion, 3-week LCHF-diet reduced fasting glucose, while glucose tolerance was unaffected. A bout of exercise post-intervention did not decrease AUC glucose as it did at baseline. Total cholesterol increased, mainly due to increments in low-density lipoprotein. LCHF-diets should be further evaluated and carefully considered for healthy individuals.

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6 hours ago, Dean Pomerleau said:

Their LDL and triglycerides went up 39% and 20% respectively after only 3 week mccoy - it didn't take months..

I suppose like it regularly happens in the nutrition literature, some people show one thing, the others are ready to show the opposite.

Edited by mccoy

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6 hours ago, Dean Pomerleau said:

Of course the young women were metabolically healthy to begin with and were still on the low carb diet at the time of the OGTTs so their bodies may have shifted to burning fat and not handling glucose well (having not seen much glucose for a while). This study did not address how long this relative glucose intolerance lasts after a period of low carb dieting.

IT is a well-known fact that people on keto should not undergo an OGTT during keto, but (empirically) only after a few days of carb-adaptation. 

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On 8/6/2021 at 2:05 PM, Ron Put said:

There is some evidence that ketosis results in oxidative stress and metabolic acidosis in the long run

Ron, how long do you expect it takes for these issues to become problematic?  F2-Isoprostanes is considered a good indicator of oxidative stress and in particular of lipid peroxidation.  It is considered a strong indicator of cardiac risk which my doc ordered out of concern over my cholesterol rising on every single test with TC=400 most recently.  Over 5 years keto, the year prior has been very high in red meat, eggs, butter plus a little coconut oil to boost my saturated fat ratio and my test results are below.  Other than LDL all other indicators of cardiac risk have been equally excellent.  And no my urine was not dilute as other tests drawn from the same sample showed high values for ketones and several hormones.

f2-isoprostanes.jpg.5a0dfd850a903ae1a5e6019948735ca8.jpg

Metabolic acidosis when keto is no more difficult to manage than B12 deficiency eating vegan.  One can take the Dr. Terry Wahls approach of eating large amounts of leafy greens and low carb veg.  Or one can follow Dr. Paul Saladino's advice to eat a lot of bones, bone broth, egg shells, etc.  Or one can supplement with highly alkalizing forms of minerals such as citrates of sodium, potassium, magnesium and calcium.  Mild ketosis is only mildly acidifying and very easy to manage.  By contrast high protein such as when I'm eating 1.5 g per lb body weight is a bit more challenging but still very manageable if one simply pays a bit of attention to the issue.

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On 8/6/2021 at 2:05 PM, Ron Put said:

They help people lose weight while eating a more "palatable" to them diet than vegetables and whole grains, but the loss for most is to a significant extent loss of water and muscle mass. Muscles just work better with glucose.

Ron, I hope you can help these folks before they lose too much muscle.

MeganMay.jpg.e9d82187cd9177615c938dd7ea3f20da.jpg

MarkBell.jpg.9a70c66015a48a5075063f8443bab534.jpg

evabirath.jpg.f0b38175f74489ae8d374b80d16f7387.jpg

https://www.instagram.com/evabirath__health/

RobertSikes.jpg.9efde9e7bfe4e998205ddb102135c6fe.jpg

ThomasDelauer.jpg.f34db02b5b4b9015bcdb70dfb3192813.jpg

https://thomasdelauer.com/blog/

BakerVsGreger.jpg.6d4a3ee90ab889809ab9da912423adda.jpg

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I've seen many bodybuilders over the years who died in their 50's.  Arnold  has gone on a vegan diet himself after his own heart issues.  

I would put Dr. Gregor's blood work against Dr. Baker's any day.  This video talks about Dr. Baker's  bloodwork.  Stick around until he gets to

Dr. Baker's risk for diabetes. 

https://www.youtube.com/watch?v=uxC_76sUIf8

 

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29 minutes ago, pete533 said:

I've seen many bodybuilders over the years who died in their 50's.  Arnold  has gone on a vegan diet himself after his own heart issues.  

I would put Dr. Gregor's blood work against Dr. Baker's any day.  This video talks about Dr. Baker's  bloodwork.  Stick around until he gets to

Dr. Baker's risk for diabetes. 

https://www.youtube.com/watch?v=uxC_76sUIf8

High mortality among bodybuilders is associated with high usage of performance enhancing drugs such as anabolic steroids.  I left Dave Palumbo out of the list of photos I posted despite his being perhaps the most massively muscled keto diet proponent because he has a reputation of being a heavy abuser of PEDs.

The people I posted are health conscious.  Mark Bell talks of having used PEDs and their necessity to be top level competitive but speaks openly about the health impacts and encourages natural bodybuilding as better for health and longevity.  Robert Sikes competes in drug tested natural body building competitions and is only moderately muscled by comparison but is able to achieve an exceptionally ripped low body fat physique and is a good example of what can be achieved on a keto diet.

The video is old.  Dr. Baker has since normalized his blood sugar by changing his approach to exercise and incorporating some lower intensity higher volume work in his routine.  He still eats the same. 

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What about his LDL or does that not matter to people who extol a high animal protein diet for health.  High blood sugar and high A1C for a person who doesn't eat carbs and he chalked that up to a deficiency of squats?  I started reading posts from the CR Society twenty years ago when people were cutting calories to lengthen their life span, not caring  about how buff they looked on the beach.  I guess it has changed.  Keto fanatics, anti-vaxxers, etc.  I don't think you can eat a carnivore diet (which Baker does)   and consider that "health conscious"  BTW "Dr." Baker lost his medical license in 2017 and has been banned from Twitter.  https://rationalwiki.org/wiki/Shawn_Baker

 

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On 8/8/2021 at 3:14 PM, pete533 said:

What about his LDL or does that not matter to people who extol a high animal protein diet for health.

I'm fine for now with my LDL of 287 which I expect will rise into the 400s maybe 500s if I attain my body composition goals.  I'm much more concerned about cardiovascular disease than I am about LDL.  But my heart works great and my docs have been unable to detect any sign of heart disease.  Shawn Baker being a cardiologist ought to have a decent sense of whether he is developing CVD and what to do about it if he is.

 

On 8/8/2021 at 3:14 PM, pete533 said:

I started reading posts from the CR Society twenty years ago when people were cutting calories to lengthen their life span, not caring  about how buff they looked on the beach.  I guess it has changed

I posted the photos of buff keto/zero carb practitioners not to suggest it as an optimal life extension strategy but as a counter point to Ron Put's assertion that carb restriction causes muscle wasting and inhibits performance.  I suggest there is more to muscle health than carbs or lack of carbs or how does one explain Dr. Baker vs Dr. Greger?

 

On 8/8/2021 at 3:14 PM, pete533 said:

I don't think you can eat a carnivore diet (which Baker does)   and consider that "health conscious" 

Plenty of others are following Dr. Baker's lead of prescribing meat for better health after first testing the diet on themselves.  Here are some of them which I expect most people would say look "health conscious".

DrPaulSaladino.jpg.bc97deca8d7ba59313a033d549ecc6d8.jpg

DrJaimeSeeman.jpg.a22e8a3043cfd4c2f91e41682d0f6242.jpg

DrTedNaiman.jpg.a769c458ee0a5ab2911bf1dd06edf581.jpg

DrGabrielleLyon.jpg.0492d582a04d0c8362c78ee63ff69864.jpg

And Dr. Dominic D'Agostino who I think is a PhD vs an MD but he runs a research lab that has been investigating keto diets for cancer, ALS and other conditions.

DrDominicDAgostino.jpg.9f2a19354ed964c7d76ace26a582e4ad.jpg

 

Edited by Todd Allen

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