World-leading breakthrough in diabetes research : Dr.Bernstein & Diabetes Forum : Active Low-Carber Forums

#1 ^

Sun, Nov-22-15, 13:09

Turtle2003 Turtle2003 is offline

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World-leading breakthrough in diabetes research

I do not understand something in this article. Why do they say that Type 2 diabetes is due to a lack of insulin production by the pancreas? I've read over and over that Type 2 is not a matter of a lack of insulin but is because of increased resistance to its effects by the body's tissues. Still, once in a while there will be an article like this that points to a lack of insulin being causal for Type 2.

Are these guys just flat out wrong? Am I mis-reading this?

Quote:

University of Melbourne researchers have pinpointed a gene that directly causes defective insulin secretion that results in the high blood sugar levels of type 2 diabetes.

The breakthrough gives investigators and people affected by the condition reason for renewed hope.

Understanding the mechanics of how this gene affects insulin secretion enables targeted therapeutics to be developed that will significantly correct the defect.

“The importance of this discovery is that it enables us to affect insulin secretion in a targeted and specific manner with the durability required to treat diabetes long term without causing cell damage,” says lead researcher and President of the Australian Diabetes Society, Associate Professor Sof Andrikopoulos.

Quote:

Associate Professor Andrikopoulos, who is based at the Austin Hospital, says 33 percent of patients over the age of 54 admitted to the Austin Hospital have diabetes.

Ninety percent of those are type 2 which is caused by a relative deficiency in the pancreatic hormone insulin, while 10 percent are type 1 which is caused by an absolute deficiency in insulin. Both forms of the disease are related to gene disorders that cause diabetes in a conducive environment.

Link to article

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#2 ^

Sun, Nov-22-15, 13:22

ojoj

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I think its both. In some cases insulin ceases to be produced in enough quantities and in other cases its produced but becomes useless??!! Thats my understanding.

Either way, eating carbs aint gonna help

Jo xxx

#3 ^

Sun, Nov-22-15, 13:24

Liz53

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Maybe by "relative deficiency" they mean the body *thinks* it has a deficiency? On the opposite hand, T1 is an absolute (real) deficiency....

I agree with you it is a stupid way to phrase it.

#4 ^

Sun, Nov-22-15, 13:34

Nicekitty

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Here's my understanding of diabetes--it starts with insulin resistance, the pancreas secretes more and more insulin to override the resistance, eventually the pancreas is "worn out" and cant' produce enough insulin to keep blood glucose levels at a safe level for the body. That is the point at which someone is actually diagnosed a diabetic. It is the end result of a process which has gone on for years, culminating in reduced insulin secretion.

The approach that these scientists are taking is all wrong on so many levels. What is the primary cause of diabetes? it is NOT a defective pancreas. It's NOT solved by throwing more drugs at "defective genes". The genes in our bodies are not "defective"--they are there for a reason. They have been perfected over thousands of years of evolution to keep out body as healthy as possible, though we often aren't able to deduce why or how they work. Flagging the poor pancreas to produce more insulin is not the answer, giving it a rest by reducing glucose intake is.

#5 ^

Sun, Nov-22-15, 16:14

MickiSue

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The wiggle word is the "relative". Insulin resistance leads to a need for even more insulin, if the body is to try to process all the BG. But it's a stupid way to describe it, I agree.

ANY actual lack of insulin, whether the pancreas has completely shut down production, or is just producing significantly lower amounts than is normal--for a normal diet, not one chronically high in glucose--is T1D.

Two of our nephews, brothers, developed T1D within a week or two of each other. One's pancreas had completely shut down. The other's was trickling out insulin.

#6 ^

Sun, Nov-22-15, 19:25

Justin Jor Justin Jor is offline

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The pancreas being worn out per se has never been proven or demonstrated to the best of my knowledge. What appears to be happening is that over time, the cells get increasingly more insulin resistant, and eventually the pancreas can't keep up, and the increased blood sugar levels do destroy beta cells (for sure, this happens) and it becomes a vicious cycle.

The idea of overclocking the pancreas, either with insulin resistance or drugs that cause it to secrete more, is logical but I'm not sure has been shown to actually happen.

#7 ^

Mon, Nov-23-15, 08:50

MickiSue

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The beta cells can, however, be destroyed by disease. It may have been coincidence, but both of the brothers I mention had had viruses a few weeks before.

The parts of the body that can be attacked by pathogens are more numerous than we imagine. I, myself, had a viral infection in my thyroid, about a decade ago. Now, that was weird!

#8 ^

Mon, Nov-23-15, 09:15

GRB5111

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I had seen a similar phrasing in a recent article posted on this forum; although, I don't believe the word "relative" was used. This forum is the last place that would let poor or incorrect wording get by, and rightly so! Whenever I read something like this, I think of others reading the same thing, but with a totally different interpretation. This is particularly dangerous when the article provides a quote that diabetes is a "lifelong disease" and implies that it cannot be controlled without medication or, now, genetic manipulation. What about giving the body what it needs to respond the way it's intended?

The closest this article came to a non-medical solution was the following:

Quote:

“We have become a lot more unhealthy than what we were 25 years ago – we don’t exercise as much and it is easier and cheaper to buy processed low quality and energy dense foods than to buy a piece of good quality protein to cook up with vegetables and salad.”

Yet, it sounds like it's no one's fault taking the easy way out and bearing no responsibility, and that we're all simply victims of life style changes that must be dealt with using brute force. Wow!

#9 ^

Sat, Jan-09-16, 13:46

nwlifter

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I gotta chime in on this, even though new here. I've been doing massive intense research on these mechanisms. The current, and supported idea, for 'Nutrition Induced' type 2 diabetes (the most common) is this...
Improper diet causes high levels of the fatty acid Palmitate. Whole foods, have a proper ratio of palmiate to oleic fatty acids
Oleic negates the bad effects of Palmitate
But high sugar levels cause the body to synthesize a lot more palmitate.
When palmitate is 'burned as feul' in organ (liver and pancreas) cells, and muscle cells, it causes no harm. But when blood glucose rises, and cells switch to glucose as a fuel (beta cells, liver, muscle), they must now package the palmitate instead of 'burning' it as they are now using glucose even though more palmitate is coming in. The repackaging is where the issue occurs, to make it into a trig, it has a left over called a ceramide, this is the nasty byproduct that stays in the cell and causes insulin and other resistances. It throws off the beta cells glucose sensing, throwing off insulin production/storing, etc. In the liver it causes IR which makes it continue to dump glucose and ignore insulin's suppressive effects. The alpha cells are insulin resistant and continue to 'over release' glucagon adding to higher resting BG's. The cycle progress, one begetting the other until fasting and post prandial bgs are way over normal.

So, it all starts with lipo-toxicity, namely palmitate in the presence of higher blood sugar levels.

I'm sure you guys have read the full text Newcastle study, if it's taken for what it is, rather than a proposed cure, it shows that intra cellular lipids in the liver and pancreas are the key instigator of over glucose production from the liver, lack of first phase insulin response, delayed and lower 2nd phase, and higher levels of glucagon.

#10 ^

Sat, Jan-09-16, 23:29

GRB5111

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nwlifter - Welcome. Here's a link that may address some of the previous posts in the thread you're responding to:

https://intensivedietarymanagement....pancreas-t2d-9/

What started this thread was a lack of rigor the journalist used in reporting the genetic impact on insulin availability. On top of that, a few of us were wondering whether this was yet again something that could more easily be corrected by adjustment of the diet rather than another complex human metabolism engineering attempt to chase symptoms over root causes.

If you've been on the Fung site already, you may have read the findings that pancreatic beta cells may not get burned out; rather, their function is now thought to be inhibited by fat. Losing visceral fat can restore beta cell functioning while diminishing IR.

#11 ^

Sun, Jan-10-16, 09:35

teaser

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Quote:

Improper diet causes high levels of the fatty acid Palmitate. Whole foods, have a proper ratio of palmiate to oleic fatty acids

Have you seen this?

http://www.ncbi.nlm.nih.gov/pubmed/12629214

Quote:

Triglyceride accumulation protects against fatty acid-induced lipotoxicity.
Listenberger LL1, Han X, Lewis SE, Cases S, Farese RV Jr, Ory DS, Schaffer JE.
Author information
Abstract
Excess lipid accumulation in non-adipose tissues is associated with insulin resistance, pancreatic beta-cell apoptosis and heart failure. Here, we demonstrate in cultured cells that the relative toxicity of two common dietary long chain fatty acids is related to channeling of these lipids to distinct cellular metabolic fates. Oleic acid supplementation leads to triglyceride accumulation and is well tolerated, whereas excess palmitic acid is poorly incorporated into triglyceride and causes apoptosis. Unsaturated fatty acids rescue palmitate-induced apoptosis by channeling palmitate into triglyceride pools and away from pathways leading to apoptosis. Moreover, in the setting of impaired triglyceride synthesis, oleate induces lipotoxicity. Our findings support a model of cellular lipid metabolism in which unsaturated fatty acids serve a protective function against lipotoxicity though promotion of triglyceride accumulation.

There's a similar study using arachidonic acid instead of oleic, that was also effective.

Oleic acid might protect from the consequences of fatty pancreas--but at least potentially, by exacerbating triglyceride accumulation. There's a maybe related thing that happens in a mouse model of diabetes. By making the rodents choline deficient, diabetes is prevented--but their livers get very fatty. The theory there is the same, the byproducts of free fatty acid metabolism cause the damage, while the stored triglycerides are more or less inert, relatively harmless. I've wondered for a while what happens in the pancreas with the choline deficiency, whether there's an increase in triglyceride accumulation there as well, but I haven't stumbled over anything looking at that yet.

#12 ^

Sun, Jan-10-16, 11:12

nwlifter

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Quote:

Originally Posted by GRB5111

Yes for sure, I had started researching that from the Newcastle Study, the one that got all these researching going on the lipo-toxicity deal. Then I kept digging, they now know the path for lipo-toxicity, and how one 'gets to that point', via the fatty acid palmitate. It explains why people can go keto / VLC, get their numbers down, but if they return to a high sugar diet, they slip back to type 2 symptoms (they put back that pancreatic fat), very interesting stuff!

Yes, I've read quite a bit too on beta cells, in fact, even the ones they have seen that they assumed were 'dead' in autopsy, are actually either just 'insulin negative', or have been so resistant to glucose, they returned more back to a stem type cell, as if waiting for reactivation.

#13 ^

Sun, Jan-10-16, 11:19

nwlifter

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Quote:

Originally Posted by teaser

Have you seen this?

http://www.ncbi.nlm.nih.gov/pubmed/12629214

There's a similar study using arachidonic acid instead of oleic, that was also effective.

Oleic acid might protect from the consequences of fatty pancreas--but at least potentially, by exacerbating triglyceride accumulation. There's a maybe related thing that happens in a mouse model of diabetes. By making the rodents choline deficient, diabetes is prevented--but their livers get very fatty. The theory there is the same, the byproducts of free fatty acid metabolism cause the damage, while the stored triglycerides are more or less inert, relatively harmless. I've wondered for a while what happens in the pancreas with the choline deficiency, whether there's an increase in triglyceride accumulation there as well, but I haven't stumbled over anything looking at that yet.

Yes, have read that and a few others on that subject, very cool stuff!

In more detail....

When BG is low, beta cells are running more on internal and supplies fats, when BG rises, the cells switch to glucose metabolism, at that point, incoming FFA's are repackages to trigs for storage. When palmitate is repackaged, it leaves behind a nasty byproduct, called a ceramide. It causes the signaling/sensing/other issues we see with beta cell disfunction. Oliec acid, if present in a good enough quantity, protects from this effect.
Now interestingly, a member on a diabetis forum I post at pointed out that most natural foods, even meats, have a good ratio of palmitate to oleic acid. so where is this surplus of palmitate coming from that starts this whole process? Carbs, and sugar is the worst, or bodies create fatty acids (fat storage from high glucose) and sugar --> palmitate. So if we eat a nornal bad diet that is so common, we end up elevating our BG all day, with tons of sugar (palmitate) the higher BG causes the beta, alpha, liver and muscle cells to store it, accumulating ceramides and causing this whole issue.

I now make darned sure I get olive oil in my diet, every day now, AND keep my BG's low with low carb eating.

I know choline is huge for helping the liver empty internal lipids, so I have been taking that supplement for a couple months now. Almost since I started this 'reset process'. So far, so good I've come a long ways in just over 2 months gearing my lifestyle to fit the theory of ectopic fat reduction.

From 'just under' T2 BG numbers to normal range now

#14 ^

Sun, Jan-10-16, 11:37

nwlifter

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#15 ^

Sun, Jan-10-16, 11:39

teaser

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I find the choline part interesting in that making an unquestionably positive change in the diet--at least for these mice--has the potential to actually temporarily induce diabetes, at least over the period of "defatting" of the liver. Dr. Davis of WheatBelly has some posts where he writes about patients who experience a temporary increase of triglycerides and blood glucose--even to diabetic levels--early on with a low carb diet. Maybe the process of clearing fat from the liver (or even the pancreas) is what causes this temporary "diabetes?"