Have the keto experts talked about negative effects of "intramyocellular lipids" (IMCLs)

(charlie3) #1

I’m listening to a doc named Garth Davis on youtube who promotes plant based eating and criticizes keto. His version of the problem with keto is it tends to CAUSE insulin insensitivity and he mentions a mechanism for that. It didn’t take long for me to find a study in support. https://www.ncbi.nlm.nih.gov/pubmed/16648604

Part of the study abstract reads “the uptake into skeletal muscle may have negative consequences on insulin sensitivity. Besides the evaluation of the various methods to quantify IMCLs, this perspective describes IMCLs as valuable energy stores during prolonged exercise, which, however, in the absence of regular physical activity and with overconsumption of fat, can have detrimental effects on muscular insulin sensitivity.”

Has anyone seen an informed response to this?

(Leslie) #2

I only read the abstract but I always find sketchy any study that uses words like ‘might’ and ‘suggest’ more than once when building the argument to support their hypothesis

(CharleyD) #3

The peripheral insulin resistance is due to fat adaptation and adaptive glucose sparing not metabolic syndrome. Exercise improves that sensitivity.

To really know for sure if overconsumption of fat is bad get your 23andme with Promethease or others and see how your FTO gene SNPs are. If you have bad ones, then maybe high saturated fats aren’t the best.




(charlie3) #4

Thanks for the response. I’ve got the exercise covered (25 miles walking, 2 hours cardio, and 3 hours lifting per week). I like to exercise.

Something else you mention that I don’t have covered the way I would prefer is blood tests. I’d like there to be some place that will do the blood tests I request for a price that’s disclosed without needing to argue with some doc about it. Then I might take that to a doc that’s prudent How can I find a lab that will do this, for me, and how should I go about deciding which things to test. It might be nice to have a more detailed baseline for going forward.

(Todd Allen) #5

From the full paper:

Alternatively, high‐fat feeding promotes overfeeding and a positive fat balance. The surplus of fat is mainly stored in adipose tissue but also in non‐adipose tissue such as skeletal muscle. In this respect, the increase in IMCLs on a high‐fat diet could also simply be seen as an excessive storage of a surplus of circulating FAs. In that respect, it is interesting to note that obese subjects are characterized not only by increased adipose tissue but generally also by increased plasma lipid concentrations and by high IMCL content and low fat oxidative capacity (28). Additionally, in obese subjects with normal fat oxidation, IMCL content was normal too (99). This further suggests that the increase in IMCLs may be simply due to a mismatch between delivery to and oxidative capacity of skeletal muscle.

I don’t agree with the statement that high-fat feeding promotes overfeeding, at least not in the context of a low carb/keto diet, though it seems to be a common misconception outside the low carb community.

But if you are overeating and gaining fat some of that fat will end up in your muscles. And if you are sedentary that fat will accumulate and eventually cause trouble. What this paper didn’t go into is that it is high blood triglycerides that promotes fat uptake in muscle. Eating fat does spike triglycerides just as eating sugar spikes blood glucose. Overeating sugar chronically also raises fasting triglyceride levels. Get it high enough such as seen in metabolic syndrome and type 2 diabetes and you will still drive fat into muscle even if you aren’t “over eating fat”.

(Todd Allen) #6

If you live in the US what tests you can order directly without a doctor’s orders depends on which state you live in. Another complication is that many places play pricing games such as having a list price of say $500 for a test that insurers negotiate down to $50. Without the insurer middleman you have to be very careful to not ridiculously overpay for anything medical.

(CharleyD) #7

My doc is cool with me asking for anything within reason, but there’s always requestatest.com.

(Ken) #8

It looks like the potential negative effects are within a lipogenic nutritional pattern, with carb-fat combinations causing synergistically increased insulin secretion. I may have missed it, but it doesn’t appear to address a lipolytic pattern based on glucagon.

(Candy Lind) #9

I’m wondering if it’s a moot point for anyone on keto, since the test subjects were more than likely carbivores, and we all know that high-carb high-fat is the worst combination there is. Show me the same stats with Ketonian subjects and I’d take notice.

(CharleyD) #10

I would wager that’s the confounder in 99% of the studies plant-based people use to say that keto is unhealthy.

(Bunny) #11

Other interesting bits:

  1. Docosahexaenoic Acid Protects Muscle Cells from Palmitate-Induced Atrophy “…5. Conclusions: Our data support the idea that the saturated fatty acid palmitate blunted myotube growth, markers of oxidative metabolism, increased intramyocellular lipid content, and caused unresponsiveness to very high concentrations of insulin. However, the omega-3 polyunsaturated fatty acid DHA restored insulin responsiveness, and cellular growth. This was shown in experiments, where the addition of DHA attenuated the palmitate-induced changes in myotube morphology and size, intramyocellular lipid content, and PGC1α and COX-IV protein abundance, and these changes were associated with improved basal and insulin-stimulated signaling. Storlien and colleagues first demonstrated a positive effect of fish oil on systemic insulin sensitivity in 1987 [10]. The data in the current study extend these observations and supports a novel hypothesis, that long-chain omega-3 fatty acids may improve insulin signaling in skeletal muscle in a high-fat environment at least in part, by maintaining PGC1α protein expression even in the presence of palmitate. However, recent work by Hessvik et al. [59] suggests that mitochondrial mass is independent of fatty acid treatment in myotubes, so the role of mitochondria mass and function on regulation of the beneficial effects in muscle is not yet clear. Future studies are needed to investigate whether omega-3 fatty acids promote oxidative metabolism and preserve mitochondrial mass and quality to prevent insulin resistance and prevent cellular atrophy in a high fat environment. …”
  1. Higher insulin sensitivity in vegans is not associated with higher mitochondrial density ”… Conclusions: Vegans have a higher IS, but comparable mitochondrial density and IMCL content with omnivores. This suggests that a decrease in whole-body glucose disposal may precede muscle lipid accumulation and mitochondrial dysfunction in IR development. …”

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  1. Effects of a Paleolithic diet and exercise
    on liver fat, muscle fat and insulin sensitivity     “…Contemporary hunter-gatherers like the Kitava Islanders and the Greenlandic Inuit eat a diet similar to that of the Paleolithic Era and have a strikingly low frequency of cardiovascular events. Detailed studies of the metabolic effects of the Paleolithic diet, with and without exercise, are therefore warranted. …”
  1. Revisiting the connection between intramyocellular lipids and insulin resistance: a long and winding road
(CharleyD) #12

Actually, my response is that we don’t complain about muscles keeping glycogen stores just for them. Should we complain about being fat adapted and muscles keeping some fat nearby? They’re already down-regulating their insulin receptors after all…

(charlie3) #13

More than once I’ve commented here that in my younger days worked muscles were stiff and sore after exercise. These days after workouts there is the predictable muscle fatigue but they feel warm and fuzzy, not stiff and sore. Is it the higher amount of fat stored in the muscle cells?

(CharleyD) #14

Warm and fuzzy is the proper post-exercise inflammation due to the hormetic stress. I get that after taekwondo classes as well, especially on the calisthenics/conditioning days. (whoever the hell came up with jump-squats and jump-lunges can go right to hell, imho)

I think the lack of stiffness and soreness is due to much less reactive O2 species burning down the place.

(Bacon is a many-splendoured thing) #15

@charlie3 @Dipper_Actual It’s also probably because your muscles produce less lactate when burning fat. Lactate is one of the by-products of the glycolytic metabolic pathway.

And to the OP, “intramyocellular lipids” are the fatty acids our muscles burn when we are fat-adapted. Remember that ketone bodies are inrtermediate products of lipolysis, and that muscles can burn fat just as well as they can burn ketones.

Dr. Attia goes into this in some detail in this presentation:

(charlie3) #16

I’ve changed my approach to lifting compared to 30 years ago. Back then I did bro splits and trained to failure. Today I do 3 whole body workouts a week.do 10 sets per exercise per week and stop a rep short of failure. Strength is improving with far less fatigue than 30 years ago.

(She had one feck to give and that feck is gone.) #17

Yes. Yes they can.