What happens to carbs/sugars when in keto/fat adapted


(Bunny) #21

This subject is very vast when getting into diabetes, macrophage infiltration of adipose fat cells and mitochondrial damaged adipose cells (…or the few existing ones inside it?); and starts expanding out into BAT:

Question: ”…Fat cells and glucose. How does it work? Sometimes it is claimed there is no glucose uptake by fat cells. However, brown adipose tissue does this. So? …” …More

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image link (above two): Note: notice how the lipid droplets are smaller and tinier and floating freely within the brown adipose tissue (BAT) with lots of iron rich mitochondria surrounding the smaller lipid droplets compared white adipose tissue (WAT)? (something is not right about that, considering the recent time frames of history like the invention of the microscope to peer in to see what it (…lipids, mitochondria etc.) looks like and recent inclusion of junk food or highly refined and processed carbohydrates (empty calories) and its impact on the health of human beings?) - Bunny (see also my post on OCT 3)

Notes:

[1] “…Studies using phospholipase C digestion of red blood cell membranes have been used to demonstrate that the major portion of the *phospholipids and proteins in membranes can change physical and chemical structure independently, and this has been interpreted as evidence for the mosaic pattern model of biological membranes (15, 21). The present studies indicate that some important properties (binding function) of the insulin receptor of liver and fat cell membranes are not affected by removal of membrane lipids. It will be important to determine whether the properties of the isolated and solubilized insulin receptor will closely resemble those of the receptor in its normal environment in the cell membrane. These studies are currently in progress. …” …More

[2] “…The concentrations of IGF-II required for half-maximal and maximal stimulation of glucose transport in human adipocytes are 35 and 100 times more than that of insulin. The possibility of IGF-II stimulating glucose transport by interacting predominantly with the insulin receptor is suggested by the following: 1) the concentration of IGF-II that inhibits half of insulin binding is only 20 times more than that of insulin; 2) the lack of an additive effect of IGF-II and insulin for maximal stimulation of glucose transport; 3) the ability of monoclonal insulin receptor antibodies to decrease glucose transport stimulated by submaximal concentrations of both IGF-II and insulin; and 4) the ability of IGF-II to stimulate insulin receptor autophosphorylation albeit at a reduced potency when compared with insulin. …” …More

[3] Inhibition of glucose transport in fat cells and activation of lipolysis by glucocorticoids.

[4] “…Researchers discovered that when the LRP1 receptor was active, adipocytes absorbed more fat and triggered a series of cell-signaling activities that caused the body to increase overall fat storage. Although both groups of mice were fed the same low-fat diet, the LRP1 knockout mice stored less fat and experienced no significant weight gain. “This shows that LRP1 is a critical regulator of lipid absorption in fat cells. Functional disruption leads to fewer lipids being absorbed into the cells and transported throughout the body,” explains Susanna Hofmann, first author of the study and pathology research instructor at UC. “Preventing these interactions in our model prevented the onset of obesity and diabetes.” …” …More

[5] infographic image links:

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image link (must be a lot of sugar {highly refined and processed carbohydrates} in that mouse chow?)

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#22

A great study about the differenence in healthy vs. unhealthy adipose tissue. So, the numbers CMJ came up with for that video graphic are kind of cherry-picked towards the extreme case.

…which contains this chart, among other things.


(Mark Rhodes) #23

Happened to me according to DXA, which of course is an approximation based on an algorithm based on a mouse study of mouse adipose tissue. Still the TREND was what got my attention. My VAT went from 3/4 pound to 2 1/4 during the weight gain I had after the nicotine cessation ( even with choline supplementation which you and I discussed last Oct? Nov?)

It has been trending downward since January, along with everything else


(Mark Rhodes) #24

I suggested you were rude. This is a community and we share our sources, our information and our frustrations. We try to link similar questions and comments to each other. We attempt to never be forgetful of a post we placed in cyber land. To say never mind and just stop was, in my opinion, just that.

If you had the question, others have too, they just haven’t asked. Plus reviewing material gives all of us a deeper understanding of our own health. We do this because we strive to be considerate of others. That you had the question means others did as well.

You joined in April of this year it looks like. Welcome!! I meant no insult.


#25

“I meant no insult” Well — calling someone rude pretty well disqualifies you from the “no insult” team albeit I assume no ill intent. It is by its very nature an insult.

There certainly is a way to suggest sharing links (again, which I didn’t keep because I meant to kill off the post) without insulting people (regardless of your intent). My “never mind” was because it seemed the topic has been well covered. While it probably has, there is certainly some new (at least to me) discussion in the post.

The good news is that the post lead to radically better explanations and discussions than anything I would have posted as a link.


(Bunny) #26

The question then becomes; what were you eating for this weight gain to occur? e.g. Junk Food (Highly Refined Carbohydrates; including HFCS mixed with maltose and sucrose?) vs. Whole Foods (excluding grains)?

Another question are you absorbing the choline you are supplementing with or eating in the absence of other nutrients required to absorb it[1] and is it being processed in the gut and your individual ability to absorb it correctly?

References:

[1] “…Together with several B-vitamins (i.e., folate, …” “…vitamin B6, and riboflavin), choline is required for the…” “…by the relationship between choline and other …” …etc. …More


(Bunny) #27

That’s some pretty fascinating stuff:

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Here is another one that expands on looking for an algorithm on impaired glucose metabolism and obesity:

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”…“Our proposed algorithm could be useful in identifying subjects with a high risk of becoming overweight or obese,” says senior author Mikael Ryden of Karolinska Institutet. “This information could be used by clinicians to determine who would benefit the most from intensified lifestyle interventions such as physical activity, which enhances hormone-stimulated lipolysis and may therefore prevent fat accumulation and metabolic disturbances.”

Rydén and his team took biopsies of subcutaneous fat tissue from 89 women, all of whom were initially healthy and non-obese, and followed up 13 years later. The women who gained weight in the interim showed a 50% increase in spontaneous lipolysis and a 50% decrease in hormone-stimulated lipolysis compared with weight-stable individuals. Moreover, lower expression of genes involved in regulating lipolysis was associated with later weight gain.

“The findings suggest that insufficient lipolysis, that is, high basal lipolysis which cannot be adequately accelerated by hormone stimulation, may shift the balance in lipid turnover towards uptake, which facilitates fat mass growth,” says first author Peter Arner of Karolinska Institutet. …” …More

Ketogenic Diet & Macrophage Biology; Further Reading By Title:

[1] Subcutaneous Adipose Tissue Macrophage Infiltration Is Associated With Hepatic and Visceral Fat Deposition, Hyperinsulinemia, and Stimulation of NF-κB Stress Pathway

[2] Liver-associated macrophage infiltration and altered cellular signaling in SIV-infected macaques.

[3] Exercise training inhibits inflammation in adipose tissue via both suppression of macrophage infiltration and acceleration of phenotypic switching from M1 to M2 macrophages in high-fat-diet-induced obese mice.

[4] Palmitoleate Reverses High Fat-induced Proinflammatory Macrophage Polarization via AMP-activated Protein Kinase(AMPK)

[5] Macrophage-directed Therapies Summit

[6] Anti-Oxidant and Anti-Inflammatory Activity of Ketogenic Diet: New Perspectives for Neuroprotection in Alzheimer’s Disease

[7] Ketogenic diet in endocrine disorders: Current perspectives

[8] Ketogenic Diet Impairs FGF21 Signaling and Promotes Differential Inflammatory Responses in the Liver and White Adipose Tissue

[9] Fat cell filling, ketogenic diet, and the history of biochemistry

[10] Obesity-Related Perivascular Adipose Tissue Damage Is Reversed by Sustained Weight Loss in the Rat.

[11] Regulation of Microvascular Function by Adipose Tissue in Obesity and Type 2 Diabetes: Evidence of an Adipose-Vascular Loop


(PSackmann) #28

If this is the case, then does this mean that weight swings are a natural part of life? Eating ancestrally, weight would have gone down in the winter and spring, then starting rising in the summer to really top off in the fall? I read a lot about the body eventually getting to a stable weight and naturally regulating, I wonder if instead we should look at a stable weight range, and what that would look like, based upon the amount of fat that would need to be stored to support basic life functions during a famine.
Thoughts?


(Mark Rhodes) #29

A typical keto diet for myself. I have not had a single cheat day in 33 months. I don’t eat any of the crap you mention. As I said though my VAT has come down. It is still higher at 1.5 pounds. I expect it has gotten lower and I will know this Saturday after my next scan.

Never fell out of ketosis. Glucose became elevated from 4.8 mmol to about 5.3. It ALL had to do with how insulin is affected by nicotine.

As to the choline which we discussed here ,I am sure that if nothing else I took them alongside of my coffee which included heavy cream. Lacking that my morning fare would have been sausages made with no preservatives by my local butcher.

Besides the choline I took B vitamins, L-Arginine , Acetyl-L carnitine etc.


#30

Well if @marklifestyle has it right then the keto woe is surely not the right plan for healthiest… but why would the approach that suited our ancient ancestors have been healthiest? I don’t think evolution works that way at all. people around the world have always had radically different food sources and adapted to available regional foods. And what does that mean for today when I can buy a banana or a ribeye any day of the year? Sure some of our ancestors were hunter/gatherers…I ask so what? They didn’t have particularly long lives or even necessarily very healthy ones. Pretty sure they evolved to pass on the genes as efficiently as possible like all the rest of the mammals. What that meant for the ones who survived past 40 is hard to say but I doubt it is nearly as relevant to optimal health today as many would make it out to be. Just my $0.02


(Mark Rhodes) #31

YES!! I have thought that for health reasons ( not aesthetics ) that adding a couple pounds as winter approaches is very reasonable. The hard winter and it’s uncertainty are approaching. Having a “pudge” would help ensure survival through some harsher times.

I think the notion of stable weight is very misleading. Anything within a 30 pound range when eating seasonally would be stable in my viewpoint and welcome if resources fell low. Natural fasting would take off the weight as it should. No chance of diabetes or the other metabolic diseases as the time spent under any one condition .

The Ancestral Health people have some good resources I particularly thought Miki Ben-Dor at this years Carnivory Con in Boulder was pretty informative.


#32

“I have thought that for health reasons ( not aesthetics ) that adding a couple pounds as winter approaches is very reasonable. The hard winter and it’s uncertainty are approaching. Having a “pudge” would help ensure survival through some harsher times.”

I agree on the notion of stable weight being misleading. Now as to hard winters, few of us need the pounds to make it through the winter months as access to food is not (generally) much of a problem!


(PSackmann) #33

True, but I don’t know if our bodies understand that or not. Just speculation, some of it could be tied to the number of daylight hours,with longer daylight hours triggering a craving for fruit. I wonder if there’s ever been a study comparing eating habits at the equator compared to the Arctic Circle, specifically looking at number of daylight hours?


(Mark Rhodes) #34

What an original thought!! I have looked at meal timing of the Mediterranean Diet…the sweets in the morning, larger meal mid day and light snack/meal at night usually comprised of some salad like food stuffs compared to similar ingredients in the States but reversing the meals. Light in the morning. Heavy in the afternoon or evening and then the sweets going to bed with a high insulinemic load.

But to consider then length of a day into that timing pattern? Wow. Great idea.


(Mark Rhodes) #35

Except evolution would not have caught up with this ability to not need food stuffs in the winter. I also firmly hold that evolution would have adjusted to carbohydrates as we became more agrarian IF we had not sped up that process through refinement of grains into dust ( flours) and made them super absorbent- its the difference between coca leaf and crack.

So if we could have slowly introduced and kept agrarian food stuffs our bodies would stop reacting to sugar as a toxin and actually treat it like a food stuff.


#36

I guess I didn’t make myself clear. I was addressing the “optimal health” issue. This involves some definitions. The WHO preamble defines health as a “state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.” I guess optimal should mean the best possible and presumably over a long period of time. Optimal health for me includes aging and functional ability well into my days (now) as a grandpa and who knows maybe much longer. Evolution doesn’t give a rat’s behind about old people. Optimal health isn’t just being able to pass on your genes to a generation capable of survival and doing the same. If that was optimal health I’d put more stock in the ancestral health/paleo concept. I think optimal health by any reasonable definition is not what evolution selects for. Well it makes for an interesting discussion.


#37

Question is, was that omental fat (which surrounds the intestines and is involved with immune system), ectopic fat (globs of fat attached to organs), or fatty infiltration of organs? I think you’d need an MRI or similar to distinguish the difference.
If the fat is inflamed and swollen it’s going to look like it’s “fatter”.

If you mean in humans, then probably not. There is some interesting data concerning hamsters (also squirrels) which are triggered by the number of daylight hours to shift their eating habits.

In summary, a natural programmed state of fat catabolism was associated with increased FGF21 production in the liver and BAT, consistent with the view that FGF21 has a role in adapting hamsters to the hypophagic winter state. https://www.sciencedirect.com/science/article/pii/S0018506X14000543


(Mark Rhodes) #38

As UN-luck would have it an CT & ultrasound was done…

First , for the uninitiated the DXA for VAT is based on mice. A single slice of the scan at a certain site is measured and an algorithm is applied. Then the mouse is autopsied and the measure is verified. This then is applied to humans .
This is accurate enough when looking at trends, not so much snapshots. Thus when I say I had an increase of 3/4 to over 2 this was a series of DXA.

No to the CT. I have had abdominal cramping since November 2018. I can no longer do abdominal exercises. Hard enough to not cramp doing ones that involve core. The cramping was so bad that once st work I cramped and passed out in my colleague’s office only to awaken to EMT s fiddling with EKG and a flight fir life called. Yo! It’s a cramp! Check my records…

Anyway after an ineffective ER visit I showed my doctor my nicotine cessation weight gain ( BTW he went keto because of my sucess & he is used to the fact I order my own blood labs) mentioned a worry about fatty liver & pancreas due to this and an elevated AST & bilirubin.

The tests were done. No fatty organs. Plus the VAT from DXA continues to trend down since December 2018.

All in all the 30 pound weight gain due to nicotine cessation took about 12 months to work though. I quit chewing as I stepped off the plane returning home from Ketofest 2018.

As to the cramps. Bro science led me to Taurine. Taurine supplements have decreased cramps. When I forget taurine I start to tingle the same way and immediately remember to take some.

This led me to at least 8 good papers on why Taurine is a CONDITIONAL Essential Amino Acid.


Dr. Katherine Chauncey is a low carb doctor specializing in cancer & taurine


#39

Niiice!

Excellent point. I was having a conversation about taurine and heart health after seeing the recent problems with dog food. Maybe some of my rib cramping is really a cry for more taurine?

https://www.walkervillevet.com.au/blog/grain-free-dog-food-dcm/
Spoiler alert: pea protein doesn’t have much taurine and lectins may block absorption.


(Mark Rhodes) #40

If you need heart health & Taurine ask @tdseest . Hes more on FB but think he cruises the forum once in awhile. He has to fight his cat for his Monster beverage which he claims is his taurine source.