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  #1   ^
Old Fri, Aug-23-19, 08:02
teaser's Avatar
teaser teaser is offline
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Default What causes inflammation? Not glucose...

https://www.sciencedaily.com/releas...90821082238.htm


Quote:
What drives inflammation in type 2 diabetes? Not glucose, says new research

To date, the underlying causes of inflammation in obesity and type 2 diabetes mellitus (T2DM) have been poorly understood, which has hampered efforts to develop treatments to prevent complications from a disease that is the third leading cause of death in the United States.

But new research at the University of Kentucky shows that changes to mitochondria -- the powerhouse of cells -- drive chronic inflammation from cells exposed to certain types of fats, shattering the prevailing assumption that glucose was the culprit.

Chronic inflammation fuels many of the devastating complications of type 2 diabetes, including cardiovascular, kidney, and periodontal diseases, and is thus one of the key targets for therapy development. This new data may enlighten the conversation about tight glycemic control as the dominant treatment goal for people with diabetes.

The research was recently published in Cell Metabolism by a team led by Barbara Nikolajczyk (UK Barnstable Brown Diabetes Center, Department of Pharmacology and Nutritional Sciences) and Douglas Lauffenberger (MIT Department of Biological Engineering).

Nikolajczyk and Lauffenberger didn't set out to disprove the glucose-inflammation causation theory. Based on the importance of glycolysis -- a 10-reaction sequence that produces energy -- in other types of inflammation, the team hypothesized that immune cells from patients with type 2 diabetes would produce energy by burning glucose. "We were wrong," Nikolajczyk said.

"We exclusively used immune cells from human subjects for all of the work, " Nikolajczyk explained, noting that humans, but not animal models of type 2 diabetes, have the specific pro-inflammatory T cell profile her team had identified in earlier research.

The team was surprised to find that glycolysis wasn't driving chronic inflammation. Instead, a combination of defects in mitochondria and elevated fat derivatives were responsible.

Nikolajczyk said she sees applications for this research in both basic and clinical sciences. She hopes to precisely define pro-inflammatory lipid types and explore associations between circulating and/or tissue-associated lipids and insulin resistance, one key feature of Type 2 diabetes. She is also interested in contributing to the development of new analytical approaches, spearheaded by Dr. Lauffenburger's team, that leverage ongoing lipid-related findings into a new understanding of pathology in type 2 diabetes.

"Aggressive blood glucose control to lower the risk of diabetic complications has been the goal for most people with Type 2 Diabetes for decades," Nikolajczyk said. "Our data provide an explanation for why people with tight glucose control can nonetheless have disease progression."


So... this is true, but it's also nonsense in its way. Also not particularly new. Various lipid derivatives, ceramides etc. are implicated in the cellular damage that occurs in the liver, pancreas, etc. in diabetes. Beta cells in a very high glucose solution do okay, also in a high palmitic acid/low glucose solution. When the glucose is high and free fatty acids are also high--the cells start treating the free fatty acids differently, churning out these damaging lipid molecules, that can lead to beta cell dysfunction and death.


Forcing glucose into cells that don't need it and forcing them to do something with it--metabolizing the glucose itself, maybe that's not harmful. Filing my nails is harmless. Unless I'm really bad at it. Filing my nails when the boat is sinking and I could have been bailing, that could be a problem. I can't very effectively do both at the same time.
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  #2   ^
Old Fri, Aug-23-19, 08:20
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Ms Arielle Ms Arielle is offline
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Quote:
Filing my nails when the boat is sinking and I could have been bailing, that could be a problem. I can't very effectively do both at the same time.


ROFL Thanks for the image-- got my laugh in for the day!!

What bothers me is that the information is still rather vague. Reading this folks will think: Ok to guzzle sugar again.

Another point missing is that some inflammation can be a good thing. Chronic inflammation no. But inflammation is part of the protect and fix system of the body. That inflammation is at the cellular level and just part of the basic mechanism, thats new and interesting. BUt does it cause disease? Is it a problem or is it "normal"?

And let's not forget glucose intake increases insulin, which is good at inflammation; but it too has a multitude of jobs and is vital to good health beyond keeping blood glucose down.
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  #3   ^
Old Fri, Aug-23-19, 10:32
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GRB5111 GRB5111 is offline
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Quote:
Originally Posted by Ms Arielle
ROFL Thanks for the image-- got my laugh in for the day!!

What bothers me is that the information is still rather vague. Reading this folks will think: Ok to guzzle sugar again.

Another point missing is that some inflammation can be a good thing. Chronic inflammation no. But inflammation is part of the protect and fix system of the body. That inflammation is at the cellular level and just part of the basic mechanism, thats new and interesting. BUt does it cause disease? Is it a problem or is it "normal"?

And let's not forget glucose intake increases insulin, which is good at inflammation; but it too has a multitude of jobs and is vital to good health beyond keeping blood glucose down.

All valid points and underscoring that there's much more to learn. I typed this while I was not filing my nails . . .
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  #4   ^
Old Fri, Aug-23-19, 11:15
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Rofl........
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  #5   ^
Old Sun, Sep-15-19, 09:28
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mike_d mike_d is offline
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LOL I'll have to remember that one ... It's better than "Nero fiddled while Rome burned."
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  #6   ^
Old Sun, Sep-15-19, 09:52
M Levac M Levac is offline
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Yes, nonsense.

Reading carefully, I find that they didn't actually find the culprit: "She hopes to precisely define pro-inflammatory lipid types and explore associations..."

Hopes...explore? That doesn't sound like they figured it out. More likely they have exactly no clue, while still working under the lipid hypothesis. Conversely, we have a long-standing effective method to find a culprit: Remove it and see what gives. For example, all infections are proven to be caused by a pathogen, simply by removing this pathogen and looking at symptoms. Accordingly, in the case of diabetes type 2, the primary culprit is found to be dietary carbohydrates, simply by removing them from the diet and looking at the symptoms. Additionally, doing so allows us to find any other contributing culprit, as the case may be, again by looking at the symptoms.

Defects in the mitochondria? Highly unlikely, as in zero. What's the cause of these defects? Displacing the problem doesn't provide a solution. The likelihood of defective mitochondria is pitted against the global epidemic. How is it possible that a genetic defect gets in an entire world population, all at once, in the same generation? By contrast, we can certainly change everybody's diet, all at once, in the same generation, and we have. We could even imagine that if there are indeed defects in mitochondria, then the cause is most likely this world-wide change in our diet. After all, biology dictates diet, and the wrong diet invariably causes disorders.
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  #7   ^
Old Sun, Sep-15-19, 10:03
CityGirl8 CityGirl8 is offline
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Quote:
Originally Posted by M Levac
Defects in the mitochondria? Highly unlikely, as in zero. What's the cause of these defects? Displacing the problem doesn't provide a solution. The likelihood of defective mitochondria is pitted against the global epidemic. How is it possible that a genetic defect gets in an entire world population, all at once, in the same generation? By contrast, we can certainly change everybody's diet, all at once, in the same generation, and we have. We could even imagine that if there are indeed defects in mitochondria, then the cause is most likely this world-wide change in our diet.
Well said!
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  #8   ^
Old Sun, Sep-15-19, 10:11
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Ms Arielle Ms Arielle is offline
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Mitochondria.... there is evidence that our mitochindria cannot repair itself in a SAD environment. It is a point that led me to look more carefully at Dr Fung and dr bikmans work. Fung for fasting, bikman for insulin.

Apparently our cells cannot fix and repair as intended unless insulin is very low and body is in fasting state.

While DrFung advocates 24,36 and 42hr fasts especially for postmenopausal women, he tells the story of a man with a sore on his foot that would not heal and discussion of amputation was real
Dr fung is clear that longer fasts should be monitored by a health profressional, and in this case the man was to fast for seven days then do some fasting over two more weeks. The sore healed.

For me, this example drives home that our bodies are not getting what they need via SAD. AND the study above has missed the boat.
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  #9   ^
Old Mon, Sep-16-19, 13:29
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GRB5111 GRB5111 is offline
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Further thinking about this, could it possibly be likely that abundance of glucose thereby increasing blood insulin that we know increases storage of fat, also creates fats at ratios that impair mitochondira? Why do many of those on SAD have high triglycerides where many on LC have very low triglycerides? Looking for a single smoking gun causing inflammation and mitochondrial defects should not be the objective here. That's why it's called a metabolic system.

My hsCRP measurement indicating inflammation was very low, and this was after several years of eating strict low carb, keto. How come?
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  #10   ^
Old Mon, Sep-16-19, 14:08
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cotonpal cotonpal is offline
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Quote:
Originally Posted by GRB5111
Looking for a single smoking gun causing inflammation and mitochondrial defects should not be the objective here. That's why it's called a metabolic system.


That's what I was thinking. Why are people always looking for the singular cause when our bodies are complex systems?
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  #11   ^
Old Mon, Sep-16-19, 20:27
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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Quote:
Originally Posted by GRB5111
Further thinking about this, could it possibly be likely that abundance of glucose thereby increasing blood insulin that we know increases storage of fat, also creates fats at ratios that impair mitochondira? Why do many of those on SAD have high triglycerides where many on LC have very low triglycerides? Looking for a single smoking gun causing inflammation and mitochondrial defects should not be the objective here. That's why it's called a metabolic system.

My hsCRP measurement indicating inflammation was very low, and this was after several years of eating strict low carb, keto. How come?


Just the thing. With glucose-lipid toxicity in a petri dish, you can just decide which free fatty acids the cells will be exposed to, and whether or not glucose will be high. In a type II diabetic or somebody who's insulin resistant/insensitive? It's a little harder. Low fat enthusiasts will point out that a high carb, low fat diet can result in increased glucose tolerance and insulin sensitivity. It can push down free fatty acids, so cells aren't exposed to the toxic mix of elevated glucose along with elevated free fatty acids. This is fine and good and may be in operation in healthy populations around the world that do or did eat lower fat, higher carbohydrate diets.

But we carry quite a lot of fat on our bodies. Even those of us who are fairly lean still carry fat stores that dwarf what we're likely to eat in a day. If we can't do that trick of lowering systemic free fatty acids by just not eating much fat, and many of us can't, at least not to the extent that would be best for that insulin sensitizing effect, then the opposite approach of instead avoiding carbs and concentrating on fat for dietary energy sources makes more sense. I think it's good that both options exist, although I think it would be wrong to insist that both options exist for everybody.

Part of the problem with high triglycerides might be just that they don't occur unless the liver is exposed to both large amounts of glucose and high levels of free fatty acids--and that when that's happening, the liver is unlikely to be the only organ in the body for which this is the case.
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  #12   ^
Old Mon, Oct-07-19, 18:45
Ms Arielle's Avatar
Ms Arielle Ms Arielle is offline
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Popping in for a related comment.

Years ago when donating platelets, there is time to look around at the bags not filling withred whole blood but an entirely different fluid, everything but the red blood cells essentially. The bags of yellowy liquid, much like bees wax was of interest because my bag was rather white. Figured it was due to my vlc diet. Just makes made me think about hiw a vlc diet affected the blood profile.....
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  #13   ^
Old Tue, Oct-08-19, 07:09
tess9132 tess9132 is offline
 
Plan: general lc
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Quote:
here is time to look around at the bags not filling withred whole blood but an entirely different fluid, everything but the red blood cells essentially. The bags of yellowy liquid, much like bees wax was of interest because my bag was rather white. Figured it was due to my vlc diet. Just makes made me think about hiw a vlc diet affected the blood profile.....
That's interesting!
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  #14   ^
Old Tue, Oct-08-19, 14:52
Zei Zei is offline
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I wonder, had you eaten (a vlc high fat meal) recently before your donation? Seems like maybe the fats temporarily being distributed by the bloodstream for fuel might cause that?
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