Polyunsaturated fats cause diabetes?


(Bunny) #6

Only when you hydrogenate (interesterified fat) or partially hydrogenate (trans fat) a polyunsaturated vegetable oil/fat or any fat for that matter?

Interesterified Fat? Who knows how this will go?

Maybe this[1] will kill us faster than trans fats[2]?

And maybe chemical extracted and processed fats/oils[3] are not so good either other than extra virgin cold pressed (no heat; not missing electrons; oxidation)?

Thought this video was interesting:

Virgin olive oil and liver meet hydrogen peroxide.

Wanted comment further on this rather crude example in the video above of some students playing around in a school lab.

Notice those giant bubbles forming at the bottom of the cup with the raw liver when it is hit with hydrogen peroxide, now imagine those giant bubbles at the bottom are your adipose fat tissue swelling up from inflammation? Much like Dr. Michael Eades MD, PhD, describes here? Now throw some High Fructose Corn Syrup HFCS on top of those trans fats and you get obesity and diabetes…eventually?

References:

[1] Interesterified Fat – Is it Worse Than Trans Fat?

[2] Hydrogenation & Industrial Application: “…partially hydrogenated vegetable oils are cheaper than animal fats, are available in a wide range of consistencies, and have other desirable characteristics (such as increased oxidative stability and longer shelf life), they are the predominant fats used as shortening in most commercial baked goods. A side effect of incomplete hydrogenation having implications for human health is the isomerization of some of the remaining unsaturated carbon bonds to their trans isomers. Trans fats (resulting from partial hydrogenation) have been implicated in circulatory diseases including heart disease.[26] The conversion from cis to trans bonds is chemically favored because the trans configuration has lower energy than the natural cis one. At equilibrium, the trans/cis isomer ratio is about 2:1. Many countries and regions have introduced mandatory labeling of trans fats on food products and appealed to the industry for voluntary reductions.[27][28][29] The food industry has moved away from partially hydrogenated fats (i.e. trans fats) and towards fully hydrogenated fats and interesterified fats in response to bad publicity about trans fats, labeling requirements, and removal of trans fats from the FDA list of foods Generally Recognized as Safe.[30][31][32] …”…More

[3] The Dangers of Vegetable Oil Extraction and Processing: An inside look at the nutritional and health problems associated with vegetable oil extraction and refining. By Paul Hawken and Fred Rohe November/December 1971


Fat cells live for 10 years, where is the science
Source for rendered fats resulting in increased triglycerides
(Full Metal KETO AF) #7

One might also expect that lifestyle and eating habits are suspect here, the way parents eat and live could lead to them developing diabetes and eating habits and activity habits are learned from parents. We tend to like the foods we grew up with. Two obese parents will usually have obese children because kids learn eating habits from parents. So I think it’s a learned habit more likely than actual genetics. If both parents have diabetes but their child were to eat and live differently, say they were adopted at birth I believe the surrogate parents would have more influence on whether that child would be prone to T2 developing. It’s just my theory, I don’t have any evidence but it seems to me anyone can develop T2 with a bad diet and lifestyle. :cowboy_hat_face:


#11

Haven’t finished reading through that, but interesting that they are targeting “added sugars” rather than “any sugar” which is the claim about T2D-Sugar association that I have heard (granted with more blame usually on Fructose molecules in particular, though whether they show up in Sucrose, Glucose, HFCS, organic grapes, whatever, doesn’t seem to make a huge difference except for the presence of Fiber which may or may not change the situation).

I’d imagine that’s because the more popular discussion of late, at least with any government action in the U.S., has been around Added Sugars, with labels not expected to list added sugars separately, treating them as categorically different and worse than ‘natural sugars’ for whatever reason.


#12

I largely agree with this, though there is something to be said about the ratio when it comes to the associated cholesterols actually being used for their purposes of inflaming and anti-inflammation in response to an injury, and whether you have enough of the one to counter the response of the other.

I would say though that there are a few other problems than just seed oils, but perhaps that depends on how narrowly you define a seed oil (Corn and soybean oil don’t have seed in the name and aren’t often thought of as seeds, though technically they serve a similar purpose).


(Carl Keller) #13

I won’t say that sugar is the entire problem but I wouldn’t say that it’s not a large part of the problem. I base this belief mainly on how Jason Fung reverses T2D in many of his patients:

" How to Reverse Diabetes

Once we understand type 2 diabetes, then the solution becomes pretty bloody obvious. If we have too much sugar in the body, then get rid of it. Don’t simply hide it away so we can’t see it. There are really only two ways to get rid of the excessive sugar in the body.

  1. Don’t put sugar in.
  2. Burn it off.

That’s it. That’s all we need to do. The best part? It’s all natural and completely free. No drugs. No surgery. No cost."

https://idmprogram.com/reverse-type-2-diabetes-the-quick-start-guide/

Isn’t their shift in diet proof enough? There’s quite a few indigenous populations who ate lots of highly unrefined carbs and never even heard of diabetes until they had regular access to processed foods. Sure it’s correlation but it’s covincing enough for me.

And this is how science is supposed to work. Challenging everything, even your own beliefs and trying to disprove them is the best way to get the entire picture.

BTW, I really liked the Hindu fable in the first study you posted:

An ancient Hindu fable tells of six learned blind men who approach an elephant. All are highly esteemed, but all are blind. The first blind man approaches the elephant and happens to bump up against its broad and sturdy side and declares “the elephant is very like a wall!” The second blind man feels the tusk and cries an elephant is “very much like a spear!” The third happens to grab the elephant’s squirming trunk in his hands and boldly declares the elephant is “very like a snake!” The fourth blind man palpates the leg of the elephant and declares “it is clear the elephant is very like a tree!” The fifth blind man who happens to touch the elephant’s ear declares “even the blindest man can tell that the elephant is very like a fan”. The sixth blind man happens to grasp the swinging tail and declares to his comrades the elephant is “very like a rope!”

What then ensues is a long, passionate argument filled with heated dispute amongst these learned men which gets them nowhere. Although each is partly right, none of them has seen the whole picture (while learned, they are blind, after all!). This fable has been utilized in many different eras and many different cultures to recount arguments in areas as diverse as theology and politics. It illustrates the inaccuracy of seeing only a part of a subject and assuming that it is the whole. It is a cautionary tale that even learned men can sometimes be misled by their preconceived notions or only seeing a portion of the whole.


(Bunny) #14

Hmmm? If you eat fat with sugar that would be not so good? Eat only fat with little to no sugar and you will be in ketosis? (you will find no human study that would show a “relative” or “same risk”)

If you were to eat 20 teaspoons of table sugar (beet/cane) and 20 teaspoons of High Fructose Corn Syrup a DAY? No exercise? I wonder what your individual chances of developing a fatty liver (NAFLD) would be within 18 days? I would wager a pretty good chance? (important caveat: don’t try this at home folks because it just might work…)


(Full Metal KETO AF) #15

I still have a problem with this, even if you’re genetically predisposed to developing diabetes it’s still contingent on a poor diet and lifestyle. Otherwise everyone who has that genetic pattern would probably get it. It may increase the likelihood that you’re going to develop it on the SAD but if it was all about genetics then the keto diet wouldn’t fix it. I can’t I believe that sugar and carbs don’t lead you down the path towards diabetes. Too many folks have reversed their conditions by just eating keto to not believe that eating a ketogenic diet will keep pretty much everyone from developing diabetes if they don’t have it already and in case they do it’s a fix. Seems like the most reasonable explanation to me. Common sense. :cowboy_hat_face:


(Full Metal KETO AF) #18

I started my autistic son on keto a month ago. He’s older and not in school anymore. You can hope your eating habits will rub off on him. :cowboy_hat_face:


#19

From what I understood from various presentations and writings of Drs. Lustig, Phinney, Volek and Fung, and others, @alexelcu has the predisposition from parents idea correct in that genetics, early exposure, habits, and perhaps epigentics are major factors, and environment is, in a way, secondary.

But, that is to say: the environment can trigger the response of the predisposition, and practically is the only thing we can do anything about right now (can’t change your parents or the past, dna manipulation isn’t really very viable and available for humans at the moment, though epigenetics could potentially be tweaked in what I would consider still crude ways, though that also can involve changes in diet and other environmental factors).

How they work together? It’s generally considered that different people, genetically or otherwise, have different general levels of insulin resistance. While this can perhaps increase do to exposure over time, it’s also a matter of some appear (at this time) to start with higher or lower resistance, and it seems to be on a kind of sliding scale (rather than binary of high and low resistance or something), which seems to be likely genetics related, though it may involve other early development factors as well. This doesn’t entirely mean anyone in this group will necessarily develop T2D, obesity, etc., but the likelihood increases with increased and continual exposure to insulin over time (which may itself also increase resistance over time). What this boils down to is there is a subset of the population that is highly unlikely to develop these problems because of their genetics, regardless of what they eat (or, at least, they won’t develop them specifically due to insulin/sugar, which right now is our primary consideration), another subset that is highly prone to these problems based on what/how they eat (if what they eat triggers an insulin response, or a high insulin response, and frequently enough), and several other subsets that fall somewhere between the two, and are likewise influenced by how much insulin over a period of time they are exposed to based on various factors of what/how they eat.

Very likely, the above should be caveated with “along with additional factors”, the problem is, those other factors, at the moment, appear to be even less clear.

The early womb exposure issue is actually more or less the same as eating though, as it’s usually attributed to the mother eating extra high insulin inducing foods and thus the child becoming exposed to the insulin in the blood earlier and developing a tolerance/resistance earlier.

All that said, no, this kind of exposure is not the only thing that can trigger a problem for anyone. Dr. Lustig, back before he was particularly involved with the ketogenic community and wouldn’t really endorse it, also had stories from his practice of young patients that rather suddenly developed obesiety and other problems in a short time due to a severe head injury which altered some hormone production, which I believe was treated with either drugs or surgery (or both) because of it’s particular nature, and one can imagine something like could show up in a person without an injury due to genetics/mutations. Radiation can also screw stuff up in odd ways, though generally we’d consider that an environmental problem as well.

And, all that said, there are other, perhaps less understood, hormones that can come into play here. Insulin and sugar exposure just, at the moment, appears to be the most common trigger for many people. That doesn’t mean it’s the only one. Even Dr. Fung and several others who generally promote a ketogenic diet will talk about working with a particular person and not recommending a ketogenic diet for their particular situation, but rather address some other problem (cortisol levels, for instance, which is the most common other hormone blamed for issues, but again perhaps not the only other).

These are indeed complex systems we’re dealing with, and there is, at this time, no “one size fits all” solution (despite how some like to hype things). When I started the ketogenic diet, I honestly wasn’t looking for much, and hadn’t been convinced of every claim, I was merely convinced this was “not dangerous” and had potential for health benefits, and simply the easiest way to get away from things I was convinced were unhealthy.


(Bacon is a many-splendoured thing) #20

Dr. Lustig discusses brain damage as a cause of obesity, both to illustrate the mechanisms involved, and to dismiss the idea of “it’s your fault you’re fat.” Some of his stories are startling.

Here is his latest contribution to the discussion:


(Bacon is a many-splendoured thing) #22

Such a bummer, huh? :grin::grin::grin:


(mole person) #23

Coconut oil is derived from the meat of the coconut which resides within the endocarp (seed of the coconut drupe). It’s still a seed oil, but it’s a fruit seed oil.


(Bacon is a many-splendoured thing) #26

I hope he’s right, because I do enjoy an apple from time to time, lol!

It was Dr. Lustig’s lecture, “Sugar: The Bitter Truth,” that got me eating this way. Scared the crap out of me, and helped me admit I’m a sugar-addict. It worked, too, because even though diabetes runs rampant through both sides of the family, my bloodwork is now all normal.


#27

That’s what got me interested as well. I became convinced of that side of things first, and after doing additional research became convinced Keto was the easiest way to get away from sugar, or whatever was the real problem, and was safe. Though, technically, I started keto as a test to ensure it was safe while continuing to restrict the sugar my kids ate. (I’m not one that ever had diabetes or anything, though I was a bit overweight by the time I started).


(Bacon is a many-splendoured thing) #28

Just be aware that, as any dietician can tell you, keto is unsustainable and will kill us. I plan for keto to kill me at age 106 while sky-diving, lol! :rofl::rofl::rofl:


(Bunny) #30

Dr. J. Fung did a little review on Dr. Robert Lustig’s 2009 video called: “The Deadly Effects of Fructose” what is so scary is how silent HFCS is…the liver turning it directly into visceral fat, no insulin needed? I do wonder if that’s possible without insulin? Dr. Lustig said himself in one of his presentations that: “…glucose blood sugar levels are not the same-thing as insulin levels or chronically elevated levels of insulin? …” I would think the chronically elevated levels of insulin (i.e. HOMA-IR?) would be from the fatty liver (NAFLD) and fatty pancreas? Two different types (WAT & VAT) of fat storage going on? Insulin type of fat storage and the HFCS type?

After burner affect?

“…Fructose, which neither raises blood glucose nor insulin was considered more benign than other sweeteners for many years. An all-natural sweetener found in fruit that didn’t raise the Glycemic Index sure sounded healthy. But it had a hidden dark side, one that was not obvious for many decades.

The toxicity of fructose could not be seen by looking at the blood sugars, only by looking at the slow accumulation of fat in the liver. The key was the fatty liver. …” - Dr. J. Fung
image image image

Note: ”…Free fructose vs. naturally occurring: So, too much fructose is no good. However, it is important to differentiate between free or added fructose over the fructose packaged into whole foods. It is generally agreed that consuming fructose when encased in its natural form, such as in fruit and vegetables, isn’t of concern. …” …More


Fat cells live for 10 years, where is the science
More new studies to counter
#32

5.2 mmol/L so quickly actually sounds rather concerning to me, particularly along with your other symptoms. You’re not a Type 1 Diabetic are you (or something with a similar ketone affect)? I suppose if you can’t move the ketones into where they are needed for use that might also result in them hanging around in the blood more. I’m guessing if you have all these numbers and info you are working with a doctor on this one.

But yea, that illustrates the point that there isn’t really a one size fits all. A ‘well formulated ketogenic diet’ (as Phinney likes to say, distinguishing from a hap hazard one which can cause problems due to deficiencies and other issues) seems to be great for a large chunk of the population, perhaps even most, but with anything there’s always some subset of the population that is different for one reason or another and needs to do things differently.


(Scott) #33

I often wonder if a part of the genetic connection is that the kids will likely have a similar diet as the parents.


#35

I haven’t heard from many people getting that high even on some extended fasts, nor with daily deficits. I have heard of people getting that high, yea (may have done so myself but my measurements weren’t definitive enough to say), but it usually takes a while and they aren’t eating as much carbs in between as you mentioned.

But hey, everyone’s bodies act differently.


(Carl Keller) #37

Type 2 diabetes

A combination of insulin resistance and an inadequate capacity to secrete insulin leads to the development of type 2 diabetes, with adiposity a critical risk factor. Prospective studies report little association between total fat consumption and risk of diabetes but an association may exist, as with cardiovascular disease, for type of fat. The findings of a few short term feeding trials (usually lasting four weeks, with some up to 16 weeks) that assessed intermediate endpoints support this evidence. Evidence from randomised controlled trials suggests that industrially produced trans fats increase inflammatory factors and adversely affect lipid levels, but no inconclusive evidence was found for an effect on markers of glucose homoeostasis.3839 Evidence from prospective studies suggests that intake of industrially produced trans fats is positively associated with the incidence of type 2 diabetes, while the intake of polyunsaturated fatty acids is inversely associated.440 More specifically, a blood biomarker of the most abundant omega 6 fatty acid, linoleic acid, is inversely associated with the incidence of type 2 diabetes.4142Despite promising studies in animals, diets rich in marine omega 3 fatty acids have not been shown in humans to reduce insulin resistance or the incidence of type 2 diabetes. However, biomarker studies point to an inverse association between blood omega 3 fatty acids (alpha linolenic acid) derived from plants and type 2 diabetes.4143Because the type of dietary carbohydrate may also affect the risk of diabetes, any relation between dietary fat and type 2 diabetes may depend on the quantity and quality of carbohydrate as well.

https://www.bmj.com/content/361/bmj.k2139