Nitrites contribute to Type II diabetes?

[Beerina]

Hot Dogs May Contribute To Causing Type II Diabetes?

...due to the nitrites in it, used as a preservative. Apparently they break down in the stomach to chemicals that kill pancreas cells.


Well, I would be one data point in severe evidence of it, as I got it, got it strongly and relatively young (late 20s), and chugged tons of bologna sandwiches over the years.

But...does it? There seem to be cross-purpose problems here.

There's this other theory that big belly fat, intra-abdominal, gives off some chemicals that cause insulin resistance in cells, and that this, not poor pancreas function, causes the Type II diabetes -- your pancreas spits out insulin, but your cells just can't use it very well.

So there would be two separate issues here:

1. Insulin resistance
2. Poor pancreas function


Ironically, (some?) Type I, the classic diabetes, apparently is caused by a particular infection that chemically resembles the cells in the Islets of Langerhans, so your body fights it off (it seems similar to a bad case of the flu) and in the process slowly destroys its own insulin-producing cells in the pancreas.

So...is Type II halfway related to Type I in that there's pancreas destruction?


You'd think enough people with Type II would have died in car crashes and had their pancreases analyzed -- are they healthy or weak or almost dead?

And why is this insulin resistance so hard to track down and counteract with a drug? Or just surgically remove the fat blob, or whatever it is (is it the entire blob? The cells? A clump somewhere that can be removed?)

 

[Beerina]

Why it's an issue is some years ago I lost weight, getting to around 220 pounds, and essentially got rid of my diabetes. I gained back weight to about 270, then went down to 245-ish for about 8 years. Now I'm back down to 200 but still have bad blood sugar control. Why?

The fat blob is much smaller than it was when I was 220 8 years ago -- the only difference must therefore be pancreas destruction, right? And I have been eating lots of turkey sandwiches for dinner in lieu of baloney or whatnot, since turkey is very low-fat. But most brands have nitrites in it! Oh my god.

Or could it be that I now have much more severe insulin resistance? But if that's the case, the fat blob can't be the only cause, or even the primary one. Unless if cell de-insulin-resistancing (if you follow that) takes a long time. I have only been about 200 pounds for about 4 months now.


Any ideas?

 

[casebro]

Sounds like my own history.

A few years ago, I dropped from 325 to 265, didn't need insulin. So far this year, I've dropped from 294 to 247, but still needed insulin when at 265. Though not now. I'm guessing the we are getting old, so need more________ ? work? weight loss? fiber? magnesium? I dunno.

Low carb and busting my ass at restoring an old truck. I call it the Power Wagon weight loss plan, a combination of Pumping Power Wagon Iron, and Power Wagon Yoga. Works for me.

Low carb helps with appetite control, and lowers sugars. Plus a large glass of wine with dinner helps too. But lately there is less Casebro to soak up the wine, I've had to cut back on that. Same prob with coffee.

 

[enjoytheview]

Type I diabetes (a.k.a. "insulin dependent diabetes mellitus") is an autoimmune disease. The body makes T cells (a type of immune cell) that bind to the beta cells in the Islets of Langherhans of the Pancreas and destroy them. Beta cells are the only cells in the pancreas that produce insulin, and therefore when they're destroyed the body does not make insulin. What exactly it is on the beta cell that the T cell binds to is poorly understood.
One thing that makes a person more likely to get type I diabetes is how their T cells are made. The "building blocks" of the T cell receptor are proteins called HLAs. A person with HLAs DR3 or DR4 are especially susceptible. In caucasians, 90-95% of people with Type I diabetes have one or both of these HLAs, compared to ~40% in the normal population.

In contrast, type II diabetes is known as "non insulin-dependent diabetes mellitus". This disease is still genetic (perhaps even moreso than type I) but it is not an autoimmune condition. People with this condition may have beta cell dysfunction, but not destruction in the same way as in type I diabetes. Typically though, most people with type II diabetes make an adequate amount of insulin and their body just doesn't respond well enough to it. i.e. type II diabetes is typically an "insulin resistance" disease.

So how does insulin resistance work? One theory is that free fatty acids (FFAs) are in excess in overweight people, and therefore get deposited into muscle and the liver (these are the tissues that insulin acts on). FFAs are known to be potent inhibitors of insulin signalling and therefore can create an insulin resistance.

Another theory relates to Leptin. Leptin is a hormone released by the body that essentially tells a person to stop eating. Studies* with animals have shown that if they are leptin deficient, they demonstrate severe insulin resistance. If you administer those same animals leptin, the insulin resistance disappears. One cause of obesity is a lack of leptin (hence excessive food consumption) and therefore the cause of the obesity may also be the cause of the diabetes.

The two theories above are likely both true, and there are heaps of other possible causes as well. Basically, the causes of type II diabetes isn't particularly well understood at the moment. It looks like it's a combination of genetics, environment and lifestyle.
Given that it looks like it's a multifactorial problem and that we know less than we'd like to about the causes, a simple cure is still a long way away. There's no "site" in the body where the insulin resistance occurs, so it's not something you could remove surgically or anything like that.



*See: "Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystropy" published in Nature 401(6748), 1999

 

[Astrodude]

Perhaps the same bacteria that attacks insulin producing cells also converts nitrates to nitrites.

 

[Beerina]

Why hasn't the leptin thing been given to type IIs to see what happens?

 

[Beerina]

Perhaps the same bacteria that attacks insulin producing cells also converts nitrates to nitrites.

Don't know about that, but it's apparently the stomach itself that converts nitrites to whatever it is that kills pancreas cells. Whether those chemicals get into the bloodstream, past the liver, and make it all the way to the pancreas and do non-trivial damage, even over long periods of time, is another issue. That link I gave at the beginning didn't get into that bit, because it's probably not known.

Hence my question as to whether type IIs have crappy pancreases or not. Certainly some must have been studied in minutia by now.

 

[Pantaz]

I can't find the study mentioned in the linked article. I checked all the other pages linked in the article, but there is no mention of nitrites/nitrates, or of the Harvard study.

The Harvard page for researcher An Pan, has a list of his published papers, but none of the titles seem related to this topic. (Although, he has several papers concerning diabetes and depression.)

 

[enjoytheview]

Why hasn't the leptin thing been given to type IIs to see what happens?

Hormones are pretty dangerous. You can't just inject hormone x into a person and see what happens. They're all very tightly regulated in the body.

Plus, a human with leptin deficiency is very easy to spot. (see here) They're very very large from a young age.
A person who was a skinny or normal sized youth and then got larger during adolescence or adulthood is probably not leptin-deficient because leptin deficiency is largely genetic. Most type II diabetics are probably more likely to be leptin-resistant than leptin-deficient (although it's entirely possible that they have perfectly normal leptin levels and just simply eat too much or eat the wrong food) so there'd be as much point in giving them leptin as there is in giving them insulin.

Children with actual leptin deficiency are treated with leptin though.

I'd advise anyone with a real interest in this topic to check out papers written by Joseph Proietto. He's an Australian researcher at the Austin Hospital in Melbourne and most of the stuff I'm saying is regurgitated from lectures that he's given us at uni. If I understand correctly, his lab are at the forefront of this kind of research.

 

[casebro]

My personal thought? It ain't the nitrate, it's the sodium phosphate. Basically a soap, it keeps the added water dispersed through the cheap meats. And probably does the same to people. It is also injected into those rotisseried 'deli roasted chickens'. Notice how moist they are? It's in many sausages, hams, cold cuts...

But without any study specs, we don't know whether it was an epidemiological study, where commonality is not caus-ality. Might be that diabetics crave more meat, so the meat may not be cause but effect. I'm type II, and need extra carnitine. Beef is the best source. So, did the beef give me CAD? Or the lack of carnitine casued a craving for beef, as well as heart disease? (carnitine is even recommended for heart muscle health. I take it particularly for myopathy)

 

[enjoytheview]

Just out of curiosity, how exactly do you think something like sodium phosphate would make a person insulin resistant or insulin deficient?

ETA: for anyone interested in reading what I'm reasonably certain is the study the article in the OP is talking about, you can find it here

 

[Tatyana]

Type I diabetes (a.k.a. "insulin dependent diabetes mellitus") is an autoimmune disease. The body makes T cells (a type of immune cell) that bind to the beta cells in the Islets of Langherhans of the Pancreas and destroy them. Beta cells are the only cells in the pancreas that produce insulin, and therefore when they're destroyed the body does not make insulin. What exactly it is on the beta cell that the T cell binds to is poorly understood.
One thing that makes a person more likely to get type I diabetes is how their T cells are made. The "building blocks" of the T cell receptor are proteins called HLAs. A person with HLAs DR3 or DR4 are especially susceptible. In caucasians, 90-95% of people with Type I diabetes have one or both of these HLAs, compared to ~40% in the normal population.

In contrast, type II diabetes is known as "non insulin-dependent diabetes mellitus". This disease is still genetic (perhaps even moreso than type I) but it is not an autoimmune condition. People with this condition may have beta cell dysfunction, but not destruction in the same way as in type I diabetes. Typically though, most people with type II diabetes make an adequate amount of insulin and their body just doesn't respond well enough to it. i.e. type II diabetes is typically an "insulin resistance" disease.

So how does insulin resistance work? One theory is that free fatty acids (FFAs) are in excess in overweight people, and therefore get deposited into muscle and the liver (these are the tissues that insulin acts on). FFAs are known to be potent inhibitors of insulin signalling and therefore can create an insulin resistance.

Another theory relates to Leptin. Leptin is a hormone released by the body that essentially tells a person to stop eating. Studies* with animals have shown that if they are leptin deficient, they demonstrate severe insulin resistance. If you administer those same animals leptin, the insulin resistance disappears. One cause of obesity is a lack of leptin (hence excessive food consumption) and therefore the cause of the obesity may also be the cause of the diabetes.

The two theories above are likely both true, and there are heaps of other possible causes as well. Basically, the causes of type II diabetes isn't particularly well understood at the moment. It looks like it's a combination of genetics, environment and lifestyle.
Given that it looks like it's a multifactorial problem and that we know less than we'd like to about the causes, a simple cure is still a long way away. There's no "site" in the body where the insulin resistance occurs, so it's not something you could remove surgically or anything like that.



*See: "Leptin reverses insulin resistance and diabetes mellitus in mice with congenital lipodystropy" published in Nature 401(6748), 1999

There is always a genetic component to type II diabetes, but it is agreed by the medical community that 80% of type II diabetes is lifestyle related.

The fatty acid profile of cellular membranes of muscles is strongly related to the fatty acid profile of the diet, and if someone is eating a lot of processed meats, it is likely the fatty acid profile of their diet is not ideal (saturated and trans fats).

Insulin resistance has another hypothesis which relates to this fatty acid profile of the cellular membranes.

Insulin has receptors on various cells that require glucose, and when insulin binds to a receptor, a conformational change or 'shift' in the receptors sets off a cascade of other molecules that result in glucose transporters being moved to the cellular membranes to transport glucose into the cells.

There are quite a few different glucose tranporters (something like GLUT 1-10) that occur on different tissue that operate at various levels of glucose (and therefore insulin) in the bloodstream.

It is thought that the 'bad' saturated fatty acids (too many saturated or trans fats), make the membranes inflexible so the conformational 'flex' cannot happen.

Why hasn't the leptin thing been given to type IIs to see what happens?

Leptin has been given to obese patients, the results haven't been disappointing.

Deranged leptin metabolism is only going to be a part of the issue in type II diabetes.

I wouldn't be surprised if there is a clinical or has been a clinical trial.

 

[casebro]

Just out of curiosity, how exactly do you think something like sodium phosphate would make a person insulin resistant or insulin deficient?

ETA: for anyone interested in reading what I'm reasonably certain is the study the article in the OP is talking about, you can find it here

In their 'discussion', they do mention sodium as the possible link, of several.

There is no stronger emphasis on nitrates, sodium, or just plain weight gain in their discussion. Though I didn't see any stats on weight gain's relative risk as compared to red meat. I suspect they have data mined the red meat scare, and ignored the huge weight gain RR?

And by the way, their overall risk of developing type II was only about 1:300 years. Eating red meat made the risk 1:270. Not exactly "THE CAUSE".

 

[Beerina]

I can't find the study mentioned in the linked article. I checked all the other pages linked in the article, but there is no mention of nitrites/nitrates, or of the Harvard study.

The Harvard page for researcher An Pan, has a list of his published papers, but none of the titles seem related to this topic. (Although, he has several papers concerning diabetes and depression.)

This is all I can find on it, from the primary link:

This analysis, appearing Aug. 10 online in the American Journal of Clinical Nutrition, is based on data from three major studies encompassing more than 200,000 adults, some of whom have been followed for nearly 30 years.

Read more: http://www.foxnews.com/health/2011/...icantly-increase-diabetes-risk/#ixzz1VKpfWxsQ

Still, both the effect (parts of pancreas destruction) and the intermediate state (feed someone a pound of bologna, look in their bloodstream for the chemicals that kill pancreas cells) should not be hard things to test.

 

[Beerina]

My personal thought? It ain't the nitrate, it's the sodium phosphate. Basically a soap, it keeps the added water dispersed through the cheap meats. And probably does the same to people. It is also injected into those rotisseried 'deli roasted chickens'. Notice how moist they are? It's in many sausages, hams, cold cuts...

I always thought they just infused a gelatin through the stuff.

I searched hard for a brand of deli turkey that didn't have it, as I hate it in turkey (slimy!). There was one brand with a low-salt turkey that also was more dry, almost as if it were carved from a turkey breast sans gel.

 

[Andrew Wiggin]

Hard to control for the influence of the all-hotdog diet on diabetes? Increased weight correlates with diabetes, and eating lots of hotdogs correlates with increased weight.

 

[Pantaz]

This is all I can find on it, from the primary link:...

I e-mailed An Pan (the researcher mentioned in the article) asking for the title of the study and where it can be found. I'll post when I hear from him.

 

[enjoytheview]

I e-mailed An Pan (the researcher mentioned in the article) asking for the title of the study and where it can be found. I'll post when I hear from him.

The study is this one:

http://junksciencecom.files.wordpress.com/2011/08/hu-meat-diabetes.pdf

 

[Pantaz]

The study is this one:

http://junksciencecom.files.wordpress.com/2011/08/hu-meat-diabetes.pdf

Great! Thank you!

So... that study cites another that actually looked at processed meat additives:

The RR [relative risk] of type 2 diabetes was 1.37 for processed meat (95 % CI 1.11, 1.71) in the multivariate model. The results were explained more by intakes of Na than by intakes of SFA, protein, cholesterol, haeme Fe, Mg and nitrate, and were not modified by obesity. No association was found between red meat, poultry and the risk of type 2 diabetes. In conclusion, reduction of the consumption of processed meat may help prevent the global epidemic of type 2 diabetes. It seems like Na of processed meat may explain the association.​

As casebro mentioned, it seems sodium is more likely the bad guy.

 

[casebro]

I've been thinking about this thread a bit. Not all thoughts about diabetes, soem abotu sat fat/clogged arteries.

Studies have shown a link between sat fat intake and clogged arteries. But other studies that look at stearic acid, the major sat fat in pork and beef, have shown no link. Another point is that coconut oil is totally saturated, yet places that eat lots of coconut oil have low rates of clogged arteries.

So, what if it is not the lard, it's the additives? Show me a guy that likes a steak, I'll show you a guy that likes his Bratwurst.

Would that explain the Mediterranean paradox too? Rich foods, but less additives? It's not the addition of olive oil, it's the absence of additives?

So far as my own anecdotal connection, I was hypertensive for 10 years before I turned diabetic. There is a "Syndrome X" or "Metabolic Syndrome" that connects hypertension, diabetes, high cholesterol numbers, and artery disease. Syndrome, not cause and effect.

And maybe it's not the sodium, but the nitrogens? Show me a man who went on a low salt diet, I'll show you a man who is eating less sodium nitrate.