Mexican Town Only Drinks Coke-Diabetes Deaths Up 30%

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ALS

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I lived with a Mexican family once in Mexico City. They cook the beans with a lot of vegetable oil added. PUFA consumption is high there. Sopes or something similar is also deep fried in vegetable oil - it's just cheaper oil.
 

michael94

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If Coca-cola would put in more effort to show ppl sugar is not that bad and take over the production of coconut oil and made it cheap, they can save Mexico's health and get richer in the process. Then the locals can work in the CC factory and there you have a win-win situation.
its a nice thought
 
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A documentary I had seen years ago related the change of life of a particular region of Mexico located in the mountains ( maybe the one mentioned here) and famous for being one the country's biggest water reservoir. Well, coca-cola implanted factories over there (the former coca-cola representative in Mexico became president and started using the water, they confiscated it so much over time that now people don't have running water, they use cokes for their religious/traditional rituals instead of water, and cokes is way cheaper than water, the very water which was theirs . Not to mention this guy who worked for coca-cola mexico and was elected president later on : Vicente Fox - Wikipedia . I had also posted this https://raypeatforum.com/community/...-like-a-six-year-old.16440/page-2#post-223618 .

I can't believe this isn't a bad joke
 

Wagner83

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I can't believe this isn't a bad joke
I know, my English was terrible! I don't remember writing the bits about the former coca cola representative - then president abusing his power to help coca cola simply because I don't know if that's true, I do think they had tried to manipulate the viewer into making the association (success, but I linked to the guy's wiki) . I had watched it years ago and was more naive back then. The documentary is pretty terrible,
anti - sugar and biased, over emotional and all : most of it was annoying to watch, so it isn't a source to be trusted but the information on the water was interesting nonetheless. The possibility coca cola doesn't disclose all of its ingredients (read, the potential use of coca leaves) is intriguing as well. I doubt anyone would believe such a dominant industry, for so long, everywhere, can make it to the top and maintain their position without breaking eggs. I can't find the documentary (-ies) in English.

Is it true that to make a liter of coke one needs 3 liters of water?

By the way, I wonder how good "A material manufactured by heating sugars with a sulphite and ammonia or ammonium compounds," can be, maybe @Travis has some thoughts on e150d?
 
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Travis

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I've long suspected that the very high obesity and insulin resistance rate of both the US and Mexico is due to a high consumption of both high PUFA seed oils (soy bean, cotton seed, etc) and fructose. I think the seed oils especially when fried damage metabolism including the liver and so high fructose consumption leads to fatty liver and other dysfunctions especially when a person is not currently athletic.

Many Mexicans fry everything in seed oils, while many Americans eat lots of processed food that contain seed oils as main ingredients. We could probably reduce a lot metabolic dysfunction in North America by eliminating the use of seed oils in the food supply. I don't think fructose would usually be a problem otherwise.

Yes, I was thinking insulin resistance was caused by improper membrane lipids. It has been proven with reconstructed micelles that ω−3 DHA increases glucose flux. Omega−6 arachidonic and osbond acids displace this membrane lipid, lowering glucose flux in vitro. This is shown by the most reliable method: the trapping of glucose molecules inside of micelles as they form, with the subsequent determination of the amount leaked out—the assumption of course being that influx is proportional to outflux.

Insulin resistance could merely be the inability of the cell to quickly take-in glucose, caused by a top-heavy dietary ω−6/ω−3 ratio. Having ω−6 fatty acids as membrane lipids also increases membrane cholesterol, also experimentally proven, which could further cause more glucose resistance than that shown in vitro with reconstituted micelles.

Does the epidemiological data support this mechanism?
 

Travis

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I know, my English was terrible! I don't remember writing the bits about the former coca cola representative - then president abusing his power to help coca cola simply because I don't know if that's true, I do think they had tried to manipulate the viewer into making the association (success, but I linked to the guy's wiki) . I had watched it years ago and was more naive back then. The documentary is pretty terrible,
anti - sugar and biased, over emotional and all : most of it was annoying to watch, so it isn't a source to be trusted but the information on the water was interesting nonetheless. The possibility coca cola doesn't disclose all of its ingredients (read, the potential use of coca leaves) is intriguing as well. I doubt anyone would believe such a dominant industry, for so long, everywhere, can make it to the top and maintain their position without breaking eggs. I can't find the documentary (-ies) in English.

Is it true that to make a liter of coke one needs 3 liters of water?

By the way, I wonder how good "A material manufactured by heating sugars with a sulphite and ammonia or ammonium compounds," can be, maybe @Travis has some thoughts on e150d?

Sounds like an interesting food additive. The caramelization of sugars occurs naturally in the cooking of many foods, and 'caramel' appears to be merely a polymer of glucose. However, I am not sure why they bring ammonia into this; this could be done for flavor, but I would guess that it's actually done for color. I would speculate further that the glucose polymers are sulfated to increase their ζ-potential, allowing them to repel each other while preventing aggregation/precipitation in Coca-Cola™ and its premix syrup. We do have sulfated polysaccharides in the brain, called condriotin, and the loss of it's sulfate groups—i.e. from acetominophen overuse—can lead to: (1) a reduction in ζ-potential, (2) a collapse of the chains, and (3) the formation of the β-amyloid deposit. Behind the neurofibrillary tangle caused by aluminum, the β-amyloid is 'the other' classic Alzheimer's disease inclusion body. Besides aluminum and profound sulfate deficiency, I would nominate low folates as the third leading cause of dementia. I think speaking of something as 'the cause of Alzheimer's' today is impertinent because it's really just come to mean 'dementia,' and there are many causes for that. I believe the ALCOA had something to do with the re-broadening of this condition's classification, of course helping obscure and dilute any correlations with aluminum.
 
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I know, my English was terrible! I don't remember writing the bits about the former coca cola representative - then president abusing his power to help coca cola simply because I don't know if that's true, I do think they had tried to manipulate the viewer into making the association (success, but I linked to the guy's wiki) . I had watched it years ago and was more naive back then. The documentary is pretty terrible,
anti - sugar and biased, over emotional and all : most of it was annoying to watch, so it isn't a source to be trusted but the information on the water was interesting nonetheless. The possibility coca cola doesn't disclose all of its ingredients (read, the potential use of coca leaves) is intriguing as well. I doubt anyone would believe such a dominant industry, for so long, everywhere, can make it to the top and maintain their position without breaking eggs. I can't find the documentary (-ies) in English.

Is it true that to make a liter of coke one needs 3 liters of water?

By the way, I wonder how good "A material manufactured by heating sugars with a sulphite and ammonia or ammonium compounds," can be, maybe @Travis has some thoughts on e150d?

No your english is fine. Vincente fox working for coke and being responsible for stealing the water from mexico and now being president of mexico is shocking to me.
 

Kartoffel

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No your english is fine. Vincente fox working for coke and being responsible for stealing the water from mexico and now being president of mexico is shocking to me.

Luckily for Mexicans, he is no longer President.
 

Wagner83

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No your english is fine. Vincente fox working for coke and being responsible for stealing the water from mexico and now being president of mexico is shocking to me.
I think he was either presented as an example of things being suspicious (I mean the role of coca cola in Mexico in general ) or it was an accusation more or less implied in the documentary which of course had a goal in mind, however it doesn't mean it's wrong, and this guy did work for coca cola before becoming president. His name is a bit fishy too lol.
 

Mito

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Yes, I was thinking insulin resistance was caused by improper membrane lipids.
Chris has explained it in terms of cellular energy overload and reactive oxygen species in the mitochondria.

“So the effect of reactive oxygen species on glucose uptake is antagonizing insulin. The effect of reactive oxygen species at the mitochondrial membrane to reject free fatty acids coming in – that’s actually doing what insulin would have done if the cell were responding well to insulin.”

“So when it comes down to it, in my opinion, what makes the cell stop responding to energy? It’s not all about carbs, it’s not all about insulin, and it’s not all about reactive oxygen species. Reactive oxygen species are central mediators of the process, but it is the context that drives the response to those reactive oxygen species. And that context is one of cellular energy overload.”

https://chrismasterjohnphd.com/2016/08/24/insulin-resistance-isnt-all-about-carbs-and-insulin/

I would guess having higher ω−6 in the mitochondria membranes would lessen the cells capacity to take in energy and probably generate more reactive oxygen species?
 

Wagner83

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Sounds like an interesting food additive. The caramelization of sugars occurs naturally in the cooking of many foods, and 'caramel' appears to be merely a polymer of glucose. However, I am not sure why they bring ammonia into this; this could be done for flavor, but I would guess that it's actually done for color. I would speculate further that the glucose polymers are sulfated to increase their ζ-potential, allowing them to repel each other while preventing aggregation/precipitation in Coca-Cola™ and its premix syrup. We do have sulfated polysaccharides in the brain, called condriotin, and the loss of it's sulfate groups—i.e. from acetominophen overuse—can lead to: (1) a reduction in ζ-potential, (2) a collapse of the chains, and (3) the formation of the β-amyloid deposit. Behind the neurofibrillary tangle caused by aluminum, the β-amyloid is 'the other' classic Alzheimer's disease inclusion body. Besides aluminum and profound sulfate deficiency, I would nominate low folates as the third leading cause of dementia. I think speaking of something as 'the cause of Alzheimer's' today is impertinent because it's really just come to mean 'dementia,' and there are many causes for that. I believe the ALCOA had something to do with the re-broadening of this condition's classification, of course helping obscure and dilute any correlations with aluminum.
Do you think the ammonia or reaction with ammonia could be meaningful healthwise?
 

Travis

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Do you think the ammonia or reaction with ammonia could be meaningful healthwise?

It could, but in addition to the sulfated polysaccharides in the body we also have N-containing polysaccharides. The most well-known example of these is of course N-acetylglucosamine, yet simply glucosamine is also found (glucose + amine). Could this modified caramel material be almost like a glucosamine macromolecule with sulfate groups attached? added for color, increased solubility, and perhaps even flavor?

'This product we have here is not merely your run-of-the-mill glucose caramel, sir, what we have here is high ζ-potential color-enhanced glucosamine caramel.' ―Coca-Cola™ Sales Rep

Yet: despite this process perhaps forming some natural compounds, it almost certainly will form many more unnatural ones.

Vessby, Bengt. "Dietary fat and insulin action in humans." British Journal of Nutrition (2000)

'There are also indications from some studies that a high intake of fat is associated with impaired insulin sensitivity (Lovejoy & DiGirolamo 1992; Mayer et al. 1993; Parker et al. 1993; Marshall et al. 1997; Mayer-Davis et al. 1997) and an increased risk of developing diabetes (Marshall et al. 1991, 1994; Tsunehara et al. 1991), also independent of obesity. This risk may be modulated by the type of fatty acids in the diet (Marshall et al. 1991; Tsunehara et al. 1991; Colditz et al. 1992).' ―Vessby

'Borkman and co-workers (Borkman et al. 1993) were the first to demonstrate an association between the fatty acid composition of the phospholipids in the skeletal muscle cell membranes and insulin sensitivity in humans. They showed that the insulin sensitivity in healthy Australian men was directly related to the sum of the proportions of long-chain polyunsaturated fatty acids with 20–22 carbon atoms in the skeletal muscle phospholipids. [How would you think Chris Masterjohn would explain this?]' ―Vessby

'In another study in Pima Indians (Pan et al. 1995), similar results were achieved. It has been suggested that the n-6 : n-3 ratio might be important in determining insulin sensitivity (Storlien et al. 1996).' ―Vessby

'A detailed analysis of how variations of the fatty acid composition of the cell membrane may affect insulin sensitivity falls outside the scope of this review. Several explanations are possible, as discussed earlier (Storlien et al. 1996). Altered fatty acid composition of the cell membranes in the skeletal muscle will influence the physicochemical properties of the membranes with consequent effects, for example on receptor function, ion transport over the membranes, cell energy requirement and cell signalling. [What about simply glucose permeability of the membrane itself, which has been demonstrated by reconstituted liposomes?] A high proportion of [long-chained] saturated fatty acids in the cell membrane may impair insulin action by:

(1) altered insulin receptor binding/affinity
(2) altered ability to translocate/insert glucose transporters
(3) changes of phospholipid fatty acids – interaction with function of second messenger (protein kinase C)
(4) reduced ion permeability (membranes less ‘leaky’).' ―Vessby

[(5) increasing the density of the cell membrane and also its sterol affinity, thereby physically-modifying its inherent glucose permeability.] ―Travis
'The preliminary results indicate for the first time that a change of dietary fatty acid composition from more saturated to more monunsaturated fatty acids is associated with improved insulin sensitivity in humans (Vessby et al. 1999). [This also runs counter to Masterjohn's mitochondrial free radical explanation.]' ―Vessby
 
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MrSmart

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Chris has explained it in terms of cellular energy overload and reactive oxygen species in the mitochondria.

“So the effect of reactive oxygen species on glucose uptake is antagonizing insulin. The effect of reactive oxygen species at the mitochondrial membrane to reject free fatty acids coming in – that’s actually doing what insulin would have done if the cell were responding well to insulin.”

“So when it comes down to it, in my opinion, what makes the cell stop responding to energy? It’s not all about carbs, it’s not all about insulin, and it’s not all about reactive oxygen species. Reactive oxygen species are central mediators of the process, but it is the context that drives the response to those reactive oxygen species. And that context is one of cellular energy overload.”

https://chrismasterjohnphd.com/2016/08/24/insulin-resistance-isnt-all-about-carbs-and-insulin/

I would guess having higher ω−6 in the mitochondria membranes would lessen the cells capacity to take in energy and probably generate more reactive oxygen species?

It's pretty much impossible at this point to arrive at a decisive conclusion on the incidence of insulin resistance or diabetes. There are at least 80 good associations, and we can conclude so far is that it definitely has to do in a large part with (1) inflammation, (2) high caloric density, and (3) hypothyroidism.
 

Wagner83

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It could, but in addition to the sulfated polysaccharides in the body we also have N-containing polysaccharides. The most well-known example of these is of course N-acetylglucosamine, yet simply glucosamine is also found (glucose + amine). Could this modified caramel material be almost like a glucosamine macromolecule with sulfate groups attached? added for color, increased solubility, and perhaps even flavor?

'This product we have here is not merely your run-of-the-mill glucose caramel, sir, what we have here is high ζ-potential color-enhanced glucosamine caramel.' ―Coca-Cola™ Sales Rep

Yet: despite this process perhaps forming some natural compounds, it almost certainly will form many more unnatural ones.

Vessby, Bengt. "Dietary fat and insulin action in humans." British Journal of Nutrition (2000)

'There are also indications from some studies that a high intake of fat is associated with impaired insulin sensitivity (Lovejoy & DiGirolamo 1992; Mayer et al. 1993; Parker et al. 1993; Marshall et al. 1997; Mayer-Davis et al. 1997) and an increased risk of developing diabetes (Marshall et al. 1991, 1994; Tsunehara et al. 1991), also independent of obesity. This risk may be modulated by the type of fatty acids in the diet (Marshall et al. 1991; Tsunehara et al. 1991; Colditz et al. 1992).' ―Vessby

'Borkman and co-workers (Borkman et al. 1993) were the first to demonstrate an association between the fatty acid composition of the phospholipids in the skeletal muscle cell membranes and insulin sensitivity in humans. They showed that the insulin sensitivity in healthy Australian men was directly related to the sum of the proportions of long-chain polyunsaturated fatty acids with 20–22 carbon atoms in the skeletal muscle phospholipids. [How would you think Chris Masterjohn would explain this?]' ―Vessby

'In another study in Pima Indians (Pan et al. 1995), similar results were achieved. It has been suggested that the n-6 : n-3 ratio might be important in determining insulin sensitivity (Storlien et al. 1996).' ―Vessby

'A detailed analysis of how variations of the fatty acid composition of the cell membrane may affect insulin sensitivity falls outside the scope of this review. Several explanations are possible, as discussed earlier (Storlien et al. 1996). Altered fatty acid composition of the cell membranes in the skeletal muscle will influence the physicochemical properties of the membranes with consequent effects, for example on receptor function, ion transport over the membranes, cell energy requirement and cell signalling. [What about simply glucose permeability of the membrane itself, which has been demonstrated by reconstituted liposomes?] A high proportion of [long-chained] saturated fatty acids in the cell membrane may impair insulin action by:

(1) altered insulin receptor binding/affinity
(2) altered ability to translocate/insert glucose transporters
(3) changes of phospholipid fatty acids – interaction with function of second messenger (protein kinase C)
(4) reduced ion permeability (membranes less ‘leaky’).' ―Vessby

[(5) increasing the density of the cell membrane and also its sterol affinity, thereby physically-modifying its inherent glucose permeability.] ―Travis
'The preliminary results indicate for the first time that a change of dietary fatty acid composition from more saturated to more monunsaturated fatty acids is associated with improved insulin sensitivity in humans (Vessby et al. 1999). [This also runs counter to Masterjohn's mitochondrial free radical explanation.]' ―Vessby
Thanks.

@Amazoniac had linked to a paper which explained the same things, more PUFAs in muscles increased insulin sensitivity. In general MUFAs seemed like the best bet for insulin sensitivity. I think tyw and others had interesting posts on PUFAs, this thread looks worth checking:
https://raypeatforum.com/community/...s-insulin-resistance.12212/page-3#post-169127
 
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Travis

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Thanks.

@Amazoniac had linked to a paper which explained the same things, more PUFAs in muscles increased insulin sensitivity. In general MUFAs seemed like the best bet for insulin sensitivity. I think tyw and others had interesting posts on PUFAs, this thread looks worth checking:
https://raypeatforum.com/community/...s-insulin-resistance.12212/page-3#post-169127

I just read like . . . eleven studies on this, and also that physicochemical one on liposomal glucose flux a few days ago. I think the most enlightening one is this:


I am under the impression that unsaturation leads to increased membrane glucose permeability, generally, and thus increased insulin sensitivity. However, the feeding of safflower oil and other ω−6 fatty acids very often lead to type II diabetes. Docosahexaenoic acid ostensibly provides the highest glucose flux in vivo as well as in vitro, and ω−6 fatty acids inhibit ω−3 elongation. So the beneficial effect of ω−6 fatty acids could really only be apparent, or only 'conditionally helpful:' While it's true that ω−6 fatty acids appear to increase glucose flux when compared against certain saturated fatty acids, they appear weak by contrast to DHA—which they inhibit. In the study cited above, it had been the 'DHA + Sat' rats having the best glucose sensitivity despite their high intake of saturated fatty acids. So just as with all other parameters of cell membrane physiology, the longed-chained ω−6 fatty acids fail to perform as well as the more natural ω−3 analogues.

But then again, this is only glucose flux. A person eating a low starch diet while not bolting-down soda cans doesn't need the highest glucose permeability achievable. Glucose flux says nothing about a cell's ability to metabolize short-chained fatty acids, such as those found in coconuts and goat cheese, nor is it correlated with amino acid uptake. I think there are many things to consider when it comes to lipids, but ω−6 fatty acids still appear harmful in every way conceivable.
 
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Wagner83

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I just read like . . . eleven studies on this, and also that physicochemical one on liposomal glucose flux a few days ago. I think the most enlightening one is this:


I am under the impression that unsaturation leads to increased membrane glucose permeability, generally, and thus increased insulin sensitivity. However, the feeding of safflower oil and other ω−6 fatty acids very often lead to type II diabetes. Docosahexaenoic acid ostensibly provides the highest glucose flux in vivo as well as in vitro, and ω−6 fatty acids inhibit ω−3 elongation. So the beneficial effect of ω−6 fatty acids could really only be apparent, or only 'conditionally helpful:' While it's true that ω−6 fatty acids appear to increase glucose flux when compared against certain saturated fatty acids, they appear weak by contrast to DHA—which they inhibit. In the study cited above, it had been the 'DHA + Sat' rats having the best glucose sensitivity despite their high intake of saturated fatty acids. So just as with all other parameters of cell membrane physiology, the longed-chained ω−6 fatty acids fail to perform as well as the more natural ω−3 analogues.

But then again, this is only glucose flux. A person eating a low starch diet while not bolting-down soda cans doesn't need the highest glucose permeability achievable. Glucose flux says nothing about a cell's ability to metabolize short-chained fatty acids, such as those found in coconuts and goat cheese, nor is it correlated with amino acid uptake. I think there are many things to consider when it comes to lipids, but ω−6 fatty acids still appear harmful in every way conceivable.
Do you think the ability to burn short-chained fatty acids is ever impaired? I was under the general impression that fatty acids oxidation was mostly frowned upon and seen as perpendicular to glucose use, however short chained fatty acids appear to be in a league of their own. Why do you think someone drinking soda cans would need maximum glucose flux ? Does it have anything to do with how quickly the glucose part of sucrose has to be processed? I don't know if anyone ever suggested that the glucose part of liquid sucrose could be an issue.
I do like feta cheese* and it appears that sheep milk might also be high in mct but I can't see the details': https://onlinelibrary.wiley.com/doi/abs/10.1002/9781119110316.ch3.2 . The claims about higher PUFAs do not bother me, see the table under "nutrition by comparison", if sheep milk indeed yields more cheese per liter of milk then the concerns diminish further.

*as a major source of proteins in a meal it's probably too much salt and dehydration (and fat?) .
 
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haidut

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Do you think the ability to burn short-chained fatty acids is ever impaired? I was under the general impression that fatty acids oxidation was mostly frowned upon and seen as perpendicular to glucose use, however short chained fatty acids appear to be in a league of their own. Why do you think someone drinking soda cans would need maximum glucose flux ? Does it have anything to do with how quickly the glucose part of sucrose has to be processed? I don't know if anyone ever suggested that the glucose part of liquid sucrose could be an issue.
I do like feta cheese* and it appears that sheep milk might also be high in mct but I can't see the details': https://onlinelibrary.wiley.com/doi/abs/10.1002/9781119110316.ch3.2 . The claims about higher PUFAs do not bother me, see the table under "nutrition by comparison", if sheep milk indeed yields more cheese per liter of milk then the concerns diminish further.

*as a major source of proteins in a meal it's probably too much salt and dehydration (and fat?) .

Let's see what Travis has to say, but the SCFA were mentioned in the recent thread I posted. It is the decrease in those SCFA (and especially butyrate) through antibiotic therapy that improved glucose metabolism. So, they are definitely involved in insulin resistance, at least as far as the enterocytes are concerned.
https://raypeatforum.com/community/...ivity-by-reducing-fatty-acid-oxidation.24954/
 

Travis

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I cannot think of a reason why an insulin insensitive—or glucose impermeant—membrane would have a reduced fatty acid uptake, especially after coming across the statement that 'amino acid uptake had not been impaired.' You could even suppose, based on solubility considerations, that it might even be increased.

Diabetes type II a functional property of membrane lipids that will only manifest itself in 'everyday' conditions when glucose intake exceeds cellular uptake. Millions of people could have 'diabetes-like membranes,' yet suffer little since their glucose intake is moderate. The type-specific ability of certain fatty acids to cause diabetes type II has been well established, and is most often explained in the following ways:

• Randle Cycle Effects
• Eicosanoid–Receptor Effects
• Insulin Receptor Effects
• Physical Membrane Properties

All of these explanations are superficially plausible, yet it's my contention that the physical membrane properties exceed the others in prominence. Docosahexaenoic acid also appears to yield the highest glucose uptake rates in vitro as well as in vivo, a fact very hard to reconcile with Randle Cycle explanations. Studies taking muscle biopsies of Norwegian men indicate 'unsaturation index' to be most-correlated with glucose flux, and studies using rats indicate DHA is the most effective here. Have a look at the following two graphics from the study cited above:


rats.png

rats2.png


All rats had been fed varying fat/oil combinations on top of their basal diet, ostensibly high in ω−6 and low in ω−3 fatty acids. The group that'd been supplemented with cell membrane 'stiffening' tallow had led to the greatest insulin resistance, yet the group given tallow + α-linolenic acid had the least. This effect had been completely abrogated by the safflower oil in the 'Poly/short ω−3' group, and I would interpret this to mean that: The linoleic acid found in safflower oil is inhibiting Δ⁶-desaturase, an enzyme needed twice during the desaturation–elongation phase of DHA synthesis via α-linolenic acid. The 'Poly/long ω−3' group had been given pre-made DHA, so it's synthesis could not be inhibited by the ω−6 fatty acids also given. The 'Poly/long ω−3' group had good insulin sensitivity despite the safflower oil, nearly on par with the 'Sat/short ω−3' group. I believe the physicochemical membrane paradigm is realistic, and also the best way to reconcile all diabetes data published.
 

Wagner83

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Let's see what Travis has to say, but the SCFA were mentioned in the recent thread I posted. It is the decrease in those SCFA (and especially butyrate) through antibiotic therapy that improved glucose metabolism. So, they are definitely involved in insulin resistance, at least as far as the enterocytes are concerned.
https://raypeatforum.com/community/...ivity-by-reducing-fatty-acid-oxidation.24954/
Thanks for pointing this out, you made me realize I was thinking about MCFA not short ones (poor mistake):
https://raypeatforum.com/community/...usiasm-about-mct-oil.14506/page-2#post-282399
 
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