Most vegetable oils are bad for you!

I've said it before but rather than saying it again, I'm going to let this article do it for me.

Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis

http://www.bmj.com/content/346/bmj.e8707

It shows that most of the vegetable oils that we have been told are healthy not only are not but are, in fact, harmful. If you have consistently been reading this blog then you know I addressed this with this post some while back.

http://ketosisprone.blogspot.com/2011/07/thinking-about-western-technology-food.html

I won’t gloat. I reached my differing conclusions because as a Ketosis Prone Type 2 diabetic the advice that was given to me about health was an unmitigated disaster. This type of diabetes, makes us the knockout mice of diabetics. We always seem to stand outside the standard dogma and, because we do, we point at other answers that have been obscured or forgotten. This is why I say our type of diabetes should be studied and studied, hard. Of course, till that day comes, you’ve still got me. ; )

Anyway, I’ve no intention of reinventing the wheel. What I’ve done is gone off and found some very good discussions of this paper that you can read at your leisure.

http://stan-heretic.blogspot.com/2013/02/us-study-double-mortality-after.html

http://barrygroves.blogspot.ca/2013/02/heart-attack-risk-in-healthy-spreads.html

http://hopefulgeranium.blogspot.co.nz/2013/02/the-results-show-that-omega-6-linoleic.html

http://anthonycolpo.com/research-update-polyunsaturated-vegetable-fats-are-not-heart-healthy/ 

 

I want to add this brief addendum. Note that the reduction in cholesterol did not change the rate of mortality. This maybe the first nail in the coffin of the cholesterol hypothesis.

Here's some more on the same topic over at the "Heretic".

http://stan-heretic.blogspot.com/2013/03/more-animal-fat-less-veg-oils-longevity.html 

 

Ethnic minorities in the U.S. have nearly twice the risk of diabetes even with low BMI's

This came across my desk from Medscape. http://www.medscape.com/viewarticle/779072?src=nl_topic

Recently, the Excellence in Diabetes 2013 conference was held in Turkey. One of the big statements to come out of it was this: “ type 2 diabetes, usually associated with obesity, can occur in many seemingly thin people from ethnic minorities.”

 

"Diabetes risk is higher in all ethnic groups than in whites, and of course some of this is just due to body weight, but evidence is now building that people of many races may be at increased risk of diabetes and cancer before they are even considered conventionally overweight."

Meanwhile, Chittaranjan Yajnick, MD, from King Edward Memorial Diabetes Unit, Pune, India, also gave a talk on what makes Indians so susceptible to diabetes. "We have seen that Indians are often diagnosed with diabetes 10 years earlier and 5- to 10-units BMI thinner than whites," he noted.
Both believe the explanation lies in "hidden" visceral fat found inside the body, between organs, in Asians and probably other ethnic groups too, but not in whites. This in turn affects the levels of adipokines secreted, such as leptin and adiponectin, which can have adverse metabolic effects.

The knowledge that Asians and other ethnic groups are at much greater risk for diseases associated with obesity, such as diabetes and many cancers, than whites, is not new, Dr. Maskarinec explained. But more recently, researchers have begun to show that nonwhites who are not even particularly overweight or who are of "normal" weight are at much higher risk than whites.

"People have talked about some kind of adaptation for white people, who have had a greater number of years to adjust to the type of food we are eating now," she postulated.

What they aren’t saying is that the connection between weight gain and diabetes isn’t as tight as they thought. Most of all prescriptions for holding off diabetes suggest that the key is healthy eating and exercise. This, I think, is largely due to how Americans view being overweight, which is strongly associated with diabetes in this country. People become fat because they over eat and don’t exercise. It is the same old “gluttony and  sloth“ line.

This attitude has pervaded the science as well. The first suggestion is that thin diabetics are secret fat people. Their fat is hidden because of its visceral nature.  So the relationship still holds even if only by the slimmest of margins.

There is one thing which does, however, come through loud and clear.

Ethnic minorities that come to the U.S. and take up the standard American diet are at a very high risk of diabetes. There is something toxic in our food/environment that isn’t as widespread in the rest of world. It is becoming so though as we see in the rising rates of diabetes around the world.

People here who aren’t part of ethnic minorities tend to discount problem but they should view this as a “canary in a coal mine” situation. On some level, this is affecting everyone. We really need to quit looking at fat and start looking at what in our environment forces our bodies to put on fat.

Thinking about Diabesity 3

These “Thinking about “ pieces are my highly speculative way of working out diabetes  using the KPT2 perspective, right now I’m wondering about obesity and whether it really is what we’ve been told it is.

First of all I believe there is something in our food that can be toxic at a fundamental level, especially with constant exposure, which causes our bodies to compensate in ways that cause problems down the line.

Essentially, I’m saying that body processes go awry and instead of helping, begin to hurt. The result of this is what I’m calling inflammation, basically slightly misaligned processes that are rubbing each other the wrong way. These processes go awry do to cumulative trauma. Cumulative trauma is actually a term for injury caused by repetitive actions. I use it here because it captures the idea of repeated exposures causing small amounts of damage that can lead to chronic and disabling consequences.

Here’s a useful analogy. A highly skilled boxer blocks or slips most punches but still some get through and take an effect. This tells in the later rounds when the coordination is missing and the punches are neither hard nor crisp, systems are now misfiring due to the accumulated damage caused by punches.

Robert Scheinman on A Sweet Life used this description for IR, which I’m now stealing for my own purposes. You have a satellite disk on the roof and through the actions of wind and rain, it slowly, over time, shifts. It becomes misaligned and the reception begins to suffer. You can boost the signal many times to get reception but for the most part you’re going to get a lot more static as well. Think of this static as an interference that disrupts or skews signaling in the body.

Okay, I almost said it. Now I’ll state it concisely. Fat is largely protective in our modern toxic environment. Think of it as the body’s storage facility, a place where the effects of toxicity can be sequestered. Notice that I said “the effects of toxicity”. I don’t doubt that some toxins do get stored in the body, but here I’m talking about the compensations that the body makes when it comes into contact with a toxin

Toxicity is a very specific thing for any given individual; some of us are sensitive to some things and not to others and some vary in how much exposure will cause a response. There is a general area under the curve where our behavior clusters given any input but we are talking KPD here.  It is widely known that people of color have a disproportionate rate of diabetes and KPD is found at a higher rate in peoples of color. So for the sake of keeping this short, I’m going with the idea that KPD’s basically have around the same sensitivities.

Now I can give you the idea of “fat carrying capacity”. One of the papers mentioned on this blog referred to the fact that the heaviest KPD’s kept their blood sugars in check far better than the thinner diabetics even as they continued to gain weight.

http://ketosisprone.blogspot.com/2010/06/increased-weight-and-insulin-resistance.html

This situation continued until eventually the people relapsed. Their blood sugars rose sharply       . My position on this is that they reached the end of their carrying capacity. This is where the body can no longer put on body fat as a response to a continual toxic challenge because body fat, in itself, becomes toxic. Without this ability, the toxicity (which in this case may be the high blood sugars) can not be stored and the blood sugars rose until they, once again, went out of control.

I’m using blood sugars here but what is body putting on fat in response to?  It could be almost anything, that it has a strong correlation to stabilized blood sugars in this case doesn’t mean that they are linked. There could be a myriad of things triggering it. What this is about is that this is a response to something internal not to caloric intake or goodness of food.

This carrying capacity runs largely between the two poles of skeletal muscle  and fat tissues both which can be used to draw down toxicity effects and depending on the person this storage will be on a line between these two poles.

For example, I put on muscle easily but fat is nearly impossible for me to maintain. In this case, I would be down near the muscle part of the spectrum. I actually think this is rare. There is a very strong evolutionary advantage to putting on weight since it gives you something to fall back on in lean times. I would suspect that most people would shade more towards fat storage.

The common view of fat storage is that it is a way to store energy for future uses. Here the idea takes a bit of a twist. Putting on fat is a way of offsetting problems caused by  blood sugars by quickly converting these sugars to fat and storing them in fat tissue. Obviously, this would have to do with the relative sensitivity of the two types of tissue to insulin. This is not a constant but I would say that those who tend to put on fat have more overall sensitivity there.

Let’s put this on a scale of 0 to 100. At “0”, a person has no ability to store fats while at “100” they have an endless ability to do so. Where a person sits on this scale determines the person’s carrying capacity.

I would assume that the need for such capacity would only come into play if the person needs it. If the environment doesn’t contain a lot of toxicity for an individual then there would be little or no reaction and little need to use this capacity.

Why do people feel better when the drop weight? Using this idea, it would be when they have exceeded their carrying capacity. The lose of weight would take them below the point where their weight becomes toxic. This would also seem to suggest that it should be very hard to lose and keep off weight since the fat isn’t about energy but a need to off set some imbalance. In this case, it serves a purpose in maintaining stability. The body would seek to put this weight back on and if it is truly protective, it would probably put back more to guard against any future losses.

This may seem absurd but I don’t find it any more absurd as believing that in the last forty years a third of the population has become lazy over eaters. There is also the fact that most of the people I know, who are obese, work pretty hard and do watch what they eat.

Slowly, I am being prodded up a path that says the strong correlation between diabetes and obesity is akin to that of smoke and heat to fire.

Traditional foods ... again

This popped up a few days ago and is very much in line with what I've been saying about diet and food.  Here.
  
This is a study done in Lebanon (KPD is well-documented in the Middle East). It should be noted that there was one other diet that was examined but it showed no association with diabetes. This diet would be close to a low carb diet.


The findings of this study demonstrate direct associations of the Refined Grains & Desserts and Fast Food patterns with T2D and an inverse association between the Traditional Lebanese pattern and the disease among Lebanese adults. 
 Dietary patterns and odds of Type 2 diabetes in Beirut, Lebanon: a case - a case study

What should be noted is that this diet maybe safe now but it too is subject to the substitution of ingredients as well so complacency, as regards ones diet, should be guarded against.

Diabesity 2

This is my rant taking my type of diabetes as the major form in the world. I make no apologies to anyone. We are forgotten but we are important because it gives a view of diabetes that is different and necessary.

 Diabetes is ultimately caused by the failure of the immune system due to inflammations introduced by environmental toxicity. An environment is toxic if it does not support the health of an organism. This can be toxins that are viral, bacterial, physical or chemical and it may also be the case that the environment is toxic if it doesn’t supply the necessary components for health. It is also true that almost anything can be toxic above a certain threshold. This is where long term genetic adaptation comes in.

Over time a successful organism will change in ways to suit that environment. It will develop the mechanisms to recognize then offset or neutralize toxins. What is important is the very systems that must cooperate are in some ways disrupted and can not complete their functions leading to more inflammation and less cooperation. We see autoimmune diseases, sensitivities and deficiencies as part of this.

The net effect of this is a some what continuous suboptimal functioning which forces the body to compensate. The outcome of all this is what we call “diabetes”. There are all kinds of toxins out there but the one I’m going to concentrate on has to do with diet.

Why diet, two things: diseases of civilization and obesity. “Diseases of civilization” have been noted for centuries and is caused when some previously unexposed culture adopts our diet. This occurred largely before we had the scientific sophistication to develop most of the chemicals that people say plague our environment today. It also precedes the wide spread manipulation of foods, both plants and animals, by industrial systems to increase yields and profits. The rise of diabetes and obesity seem to be moving hand in hand. Weight gain, no matter whatever else it is about, is about eating and eating is the port of our major exposure to the environment.

 I was an athlete and many of the people I’ve corresponded with were as well. A change of less workouts, for whatever reasons, but still the same eating pattern turned quickly into the abrupt onset of diabetes. How can you go quickly from athleticism to diabetes? On the face of it, this would seem impossible but it isn’t. It very simply takes 6 months and a person can be DKA, if they continue on their same diet, which has been the accepted healthy diet.

One of the reasons for this is that muscle does not protect against high blood sugars as well as fat. The continual insult to endocrine tissues does not abate. When a person has finished a work out and carbohydrates loads, once the muscles have taken up all they can, the body will evince higher blood sugars that will continue until the next round of exercise. This is a creeping effect, continual insult but with most of the blood sugar problem generally being contained by the consistent exercise of muscle. This will keep the blood sugars down most of the time but will not ameliorate the effects of the continual inflammation of endocrine and other tissues.

Maybe, at one time this would occur but this is inflammation. Continual exercise keeps the dog from the door but never reduces the effects of inflammation that has already been introduced. It is still there and all the disruptions in signals between the organs is still present due to the continual post prandial challenges and, probably, other continual environmental challenges

The KPT2 point of view of Diabesity Pt 1

Recently, I was at a diabetes conference representing the Michigan Minority Health Coalition. There were many presentations that dealt with ways to slow or reverse the diabetes epidemic. Typically, they involved ways to get people to control what they ate and getting exercise. I was sitting with a group of researchers and they, unfortunately, asked me what I thought. I went on my usual depressing rant.

I’m not seeing any of this as being useful and the data seems to bear me out. Diabetes continues to increase across the US. We are pouring more time and resources into it with little or no effect.

One of the reasons for my negativity is that Ketosis Prone Type 2 diabetes seems to contradict most of the standard wisdom we know about diabetes.

First of we are the Type 2’s that can and do go DKA. Though people think of us as relatively rare, we are increasingly being recognized as a problem in emergency medicine as we force the costs of treatment up worldwide..

Not only do we go DKA, we also can go into remission. Taking no medications just simply using diet, some exercise and no weight loss, we can return to near normal blood sugars for years.

What is even odder about this DKA and remission is how close they occur together. Two weeks after a DKA episode, where blood sugar readings were nearly off the charts, the person can start experiencing hypos. Remember, KPT2 is classified by the ADA as a Type 1, specifically Type 1b. Yet, typically after six months, the person doesn’t even need insulin or much of anything else. As I’ve noted in previous posts, this recovery is much too fast to be attributed to beta cell regeneration. Even if you are inclined to believe that there might be super fast regeneration, I detail in past posts, how I was able to manipulate my pancreatic output in days by taking an anti-inflammatory.

It is well documented that weight is not a major factor. In fact, KPT2s who are overweight do better than those who have, so called “healthy weights”. It is obvious that the last recommendation that a doctor would make is for that person to lose weight.

What if we were the prevalent diabetes of the world. How would the rules be different? 

Stay tuned for part 2.

Recognition for KPT2D

It’s been a bit of a while since I wrote on this blog. It isn’t that I’ve lost interest but it seems as if the world has. I continually monitor for papers on it but there really isn’t much.

I have taken the view that this blog is not personal but is a way of gathering as much scientific and medical information as possible on KPD so that sufferers and their friends and family will have a source to explore and maybe gain hope or understanding.

I present this information in this light. This is from the Diabetes in Control Mastery Series. It is based on the work of researchers out of Athens, Greece. The book is about diabetic emergencies but it takes the time to illuminate KPD because of its recognition as a large component in the rising rate of DKA worldwide.

There isn’t one word here that you won’t find in this blog. It is, however, important, that we get recognition anyway we can. This sort of thing, hopefully, will bring more money and more research.

http://www.diabetesincontrol.com/diabetes-in-control-newsletters/dcms-99

Thinking about: Western technology, food and the health of people of color and world food production and trade.

I've added, what I think, is an important addition to this post. If you've read this already just skip to the bottom.

Guess whose back? Me! I've finished my latest assignment so it's back to KPD or abrupt type 2 diabetes; however you wish to look at it.

I was working down in Southwest Detroit (One of the few multicultural areas there.) and I was looking at many of the people walking around and many of them were heavy. The thing about this area is that it isn't a "food desert" there are plenty of stores with many types of produce. This is also a working class area so most people do work that requires a certain amount of physical effort. Yet the story remains the same, way too much weight and with all the problems that this portends.

One of the things that helped to keep this in mind was looking at the stats on this blog while I was away. This blog in particular seemed to be getting a lot of those hits. I tried to address this issue further while I was away with this blog. Now I want to go back again and try to put this all a little more together.

In the last thirty years diabetes appears to be surging both in the US and around the world and it seems to affect people of color disproportionately.

You should look at this graph very carefully. Something happened after 1990. One of them is probably a statistical fluke having to do with the change in what is considered diabetic or the fact that the US baby boomer population is entering its mature years but you would expect for that to flatten out eventually. It hasn't.

Here's another fact to consider. Diabetes is a chronic disease that develops overtime. How long this period of time is varies. Even in the case of Abrupt onset T2, there appears to be a long lag before our type of diabetes becomes full blown. You can view that here. My point is that viewing the take off point of diabetes isn't enough. We have to look at the preceding years and what might have occurred in them, if we wish to see some turning point.

The time frame we're looking at is about 30 to 40 years and frankly there are plenty of changes that have occurred in this time that could be correlated with this sudden take off in diabetes. This is diabetes, however, and the dog that hunts best here, at least for me, is diet.

I've talked about the contamination of traditional foods before. Here. You could look at this post as an expansion of that post. My point was that due to economics the constituents of foods around the world are being replaced with cheaper products that I think are problematic.

First up: wheat. Wheat has been around for years. It was first domesticated around the Fertile Crescent and this wheat is Emmer. Later on with get Eichorn wheat and a host of other varieties. Wheat has been bred and bred through out the years for all types of qualities. It has become one of the central characters in the diseases  of civilization. Take a normal healthy society of humans and introduce them to flour and problems tend to arise. Denise Minger on her blog statistically demonstrates a strong correlation between wheat and cardiovascular disease. What should be even more worrying is that 99% of all wheat is of one kind, the dwarf wheat variety. Many people have pointed to this variety as having toxic properties especially as relates to blood sugars. Anecdotally, I've read where people have tried Eikhorn wheat and found no big jump in blood sugars.

My standard answer to any ketosis prone diabetic is to give up wheat. It really doesn't matter what their symtoms are. I say, "Give up wheat." and if they do they always feel better after a month. It makes me appear as if I know what I talking about.The truth of the matter is the giving up of wheat seems to always ease physical problems. Give it a try.

What this has to do with traditional foods is the fact that, due to global trade, a cheaply produced product is easily substituted for a more traditional product that tends to be more expensive. The more plentiful that cheap product is; the more likely it will be used as a substitute. Dwarf Wheat became the dominant variety starting in the late 70's. Unless that traditional food is tightly regulated such as Fasso wheat in Italy, it is more than likely Dwarf Wheat. More Dwarf Wheat If you look at our chart, it was just in time for our diabetes epidemic.

On to seed oils. These have been around since the start of agriculture but except for a few cases like olive oil they could not be produced in great quantity until we had the industrial techniques to do so. These are what we call vegetable oils.

Here's some nice charts.

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So what are these graphs about? This is about fats particularly polyunsaturated fats. These typically come from seeds that are processed to get the oil out of them. The fats obtained from seeds tends to be mostly Omega -6's. The body uses Omega-6's and Omega-3's as building blocks. The problem is that the body doesn't distinguish between the two. This really wasn't necessary because in nature they would generally be found in roughly a 1 to 1 ratio. Thanks to modern technology, this has changed. The consumption of seed oils has continues to climb so much so that the ratio is now guessed to be between 10:1 to 25:1. Well what of it?

As noted before, the body does not distinguish much between these two fatty acids. If the body is taking in 6's when it should be taking in 3's then the building blocks for a healthy body are wrong. It sets up a situation of chronic inflammation. This is from Wikipedia.

Some medical research suggests that excessive levels of certain n−6 fatty acids, relative to certain n−3 (Omega-3) fatty acids, may increase the probability of a number of diseases.<sup>[1][2][3]</sup>

Modern Western diets typically have ratios of n−6 to n−3 in excess of 10 to 1, some as high as 30 to 1. The optimal ratio is thought to be 4 to 1 or lower.<sup>[4][5]</sup>

Excess n−6 fats interfere with the health benefits of n−3 fats, in part because they compete for the same rate-limiting enzymes. A high proportion of n−6 to n−3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, proinflammatory and proconstrictive.<sup>[6]</sup>

Chronic excessive production of n−6 eicosanoids is associated with heart attacks, thrombotic stroke, arrhythmia, arthritis, osteoporosis, inflammation, mood disorders, obesity, and cancer.

Here's a listing of the Omega 6 amounts in some of the most used seed oils.

Most of these oils are not bought by people for consumption. They, for the most part, are used in the preparation of foods because they are cheap. Just imagine if your traditional food now made with flour from Dwarf Wheat is cooked in Soy oil.

I was going to throw sugar in this overlong post but if you don't know about that then nothing I'm going to say here is going to change things. I will say this that once again cost is driving cheap substitutes like high fructose corn syrup into more and more foods.

Look back up at the graphs. Look at the times. Does it seem as if we are doing something in our diets that have led to our present problems?

Now back to the problems of people of color and this quiet but possibly toxic mix that has invaded their foods. If we once again look at a graph of the A1c's of KPD's we see a long running period of elevated A1c's.

Normal A1c's should be around 5. These hover at about 6.3 month after month before taking off. I suggest that what we're seeing is inflammation caused by dietary components that over time essentially

damage our bodies. I'm thinking that these elevated numbers are due to a low level hyperglycemia that is a reaction to chronic infection. In this case, I once again bring up the hypothalamus which is an active part of this system and is susceptible to malfunction due to high blood sugar. 

Remember, we are already prone to problems with dealing with carbohydrates, if you throw some fructose in there and cause the liver problems then you can be well on your way to DKA even with a traditional diet.

We are looking at economics possibly overwhelming good sense. Cheap food additives produced thousands of miles away are quietly replacing the traditional healthy foods. I would say simply eat whole foods but under what conditions was this food raised?You should be reading labels on anything that is manufactured but do you know what you're seeing. Did you know that the "emulsifiers" you now see on labels is more than likely a transfat?  Once again I make my usual plea. Get a meter and test the foods that you and your family eats.

This is an addendum to this post. I started thinking that the key to much of what I have said is food production and the trade in food products. A little research found me this graph.

http://maps.grida.no/go/graphic/trends-in-world-agricultural-exports

Once again I ask you to look back at the graph of the growth of diabetes. The growth of trade takes off at about 1986. Ten years later in about 1996 diabetes takes off as well and both increase rapidly from there to the present. I don't see this being explained by ideas of food palatability though there is certainly some of that there, nor do I see genetics or behavior explaining this either. Food has not got that much better tasting. Certainly genetics hasn't changed that much and I doubt we have become less industrious in the entire world in the last forty years. This last graph suggests to me that we have done something in the production of our foods that is metabolically traumatic. I well know that correlation is not causation but there seems to be something here and all I can do is nibble around the edges. This calls for a better mind than mine or more specifically some one like a Ned Kock who could possibly tease out what might be going on here.

One could say that this is simply the usual "diseases of civilization" but one has to answer the question "Why does this occur now?". 

I'm at Michigan State University, where some of the best agricultural scientists in the world do their work and though I'm not at liberty to divulge any specifics, world food production is about to seriously take off in the next 10 years. The tests that I have seen suggests we could see a doubling to quadrupling of food production. In other words, an end to famine. More food is good but what if the food isn't?

Chinese study on Ketosis Prone T2 Diabetes

This is for our Chinese KPD's. Here's a study presently recruiting KPD's in China. Chinese KPT2D Trial One of it's big novel features is that it's recruiting both lean and obese KPD's. This isn't one of those studies showing that KPDM exists in a given population. They quite clearly know it exists. This study is meant to try and understand it.

This is one of the things I've been waiting for. Most of the research on KPD research has been done in the US and Europe even the studies done in African have mostly been carried out by Europeans. What I've been waiting for is for the third world to start picking up the research and expanding it. This is, after all, a growing problem in their countries.

Here it is buried in both bad science and a majority culture which largely ignores it. I talk to Blacks, Hispanics and Native Americans and all of them get this big surprised face when I talk about a diabetes that is prominent in peoples of color in the US.

I am especially perturbed by the advice given them by their local medical people. These people have no idea about this and so treat it just like a regular type 2, type 1 or LADA. This is probably one of the reasons DKA's have doubled in the last thirty years in the US.



Good for you China and let's hope the rest of the world gets going too.

Caution on NSAIDS

I've pointed out a NSAID as the drug I was using to effect my 1st phase insulin response but anyone who is thinking about trying this should be aware of the risks involved. Beyond the usual issues of stomach and intestinal distress, there are other issues. You can read about many of them here.  Jenny's Blood Sugar 101

One thing that she doesn't cover is that NSAIDs are NOT recommended for those who are G6PD deficient because of the chance of hemolytic anemia. If you've been reading this blog you should know that KPD's have a very high rate of this deficiency. So I do urge caution in their use.

How I got normal blood sugars for 60 cents a week

Being that I'm still on assignment, I've decided to let you in on the experiment that I did on myself to try to understand the nature of Ketosis Prone Type 2 diabetes or as I call it Abrupt onset type 2 diabetes.


Okay, a bit of a review. Ketosis prone type 2 diabetes is an abrupt onset type 2 diabetes though highly prevalent in people of color it can and does pop up in any group. The fact is that KPDM is actually a subset of this form of diabetes. I know LADA's that have gone DKA. There is a real question in my mind whether Abrupt onset T2 (AOT2) is a type of diabetes or simply a mechanism through which diabetes is expressed.


At any rate, this is a diabetes that comes on very strong because the body simply quits producing insulin. It is therefore classified as a type 1 diabetes, T1b. It comes out of nowhere. In 6 months time a person can go from near normal blood sugars to DKA. I talk about this process in these posts. Relapse

It has also been shown to vanish just as quickly, if handled correctly. In the space of a year, a person can go from near normal blood sugars  to close to death from DKA and then back again. This not a regular diabetes and so far has failed serious classification. It is so fantastical that most people don't know it exists, even those most susceptible to it such as people of Latin, African and Asian descent.

I, however, got lucky. About six months ago, I found myself with a revived 1st phase insulin response. I wasn't content with this. I had to find out what happened and how this could be and I kept experimenting until I not only found it but was able to manipulate it. I could turn it off and on with a simple manipulation. You can read about this process through this link, This is a dialogue on diabetesforums where I talk about this experiment

Here are some of the citations that I dug up to back up what I believed to be the cause of my suddenly restored 1st phase insulin response.
Non-steroidal anti-inflammatory drugs increase insulin release from beta-cells by inhibiting atp-sensitive potassium channel

EFFECT OF NAPROXEN ON GLUCOSE METABOLISM AND TOLBUTAMIDE KINETICS AND DYNAMICS IN MATURITY ONSET DIABETICS

Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice

Use of Salsalate to Target Inflammation in the Treatment of Insulin Resistance and Type 2 Diabetes


Targeting INflammation using SALsalate for Type 2 Diabetes.

Potential Role of Salicylates in Type 2 Diabetes

This got me to thinking about KPDM and its quick rise and fall which you can read here. Here

Now you know. It was a NSAID called Sodium Naproxen taken as needed. The net cost was about 60 cents. More when I have the time.

Roux-en-Y gastric bypass

I, in no way, endorse this procedure but it does have some bearing on Abrupt T2. It was orignally thought that much of the gains from this surgery was due to the limiting of / and types of food that people could eat once this surgery was performed. The citation below, however, shows that, in this case, there are far ranging effects on the hypothalamus that suddenly take effect. These effects proceed weight loss and involve the whole series of hormones that influence metabolism.

My point for Abrupt T2 is that this shows that the hypothalamus is a higher order mechanism that can certainly effect, if not control, the whole insulin cycle. Once again, there is no change in the underlying beta cell structure. The change isn't there but higher up. 

http://journals.lww.com/annalsofsurgery/Abstract/2004/08000/The_Early_Effect_of_the_Roux_en_Y_Gastric_Bypass.7.aspx

Facebook Page for Abrupt Onset Type 2 Diabetes

People have suggested that I put up a Facebook page so that people can easily comment and add information.

Okay, I've done this and I'll be adding more in the future. Hopefully, while I'm off on this project, this will keep the dialogue going.

Abrupt Onset Type 2 Diabetes

Obviously, I just got this set up before I went off on my latest assignment. I really didn't know what it was going to be but now I think I'm getting it. I don't have time to seriously go through scientific papers at this moment. I still am thinking about things and interesting citations still come across my desk. What I plan to use facebook for are these clues about Abrupt Onset that keep arising. 


This will give me a chance to talk about and hopefully get feed back on ideas that you might find interesting.

Who gets KPD T2? Everybody!

I've decided to keep updating this with citations as they come in.


Thai
Indian


Peruvian

Bangladeshi

Turkish

Hispanics have higher rate of KPD
http://care.diabetesjournals.org/content/26/8/2485.1.full.pdf

Adult-Onset Atypical (Type 1) Diabetes: Additional Insights And Differences With Type 1a Diabetes In A European Mediterranean Population. Http://Www.Ncbi.Nlm.Nih.Gov/Pubmed/15111529

Severe diabetes in remission: a Singapore's perspective - Malay
http://www.ncbi.nlm.nih.gov/pubmed/11817290?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pub

Clinical characteristics of Korean patients with new-onset diabetes presenting with diabetic ketoacidosis.http://www.ncbi.nlm.nih.gov/pubmed/19477546

Ketosis-onset diabetes in Tunisian adults: immunological markers and β-cell function 

http://www.emro.who.int/publications/emhj/1601/article12.htm

High Frequency of Type 1B (Idiopathic) Diabetes in North Indian Children With Recent-Onset Diabeteshttp://care.diabetesjournals.org/content/26/9/2697.1.full

[HETEROGENEITY OF TYPE 1 DIABETES MELLITUS] - Brazilian

http://www.ncbi.nlm.nih.gov.proxy1.cl.msu.edu/pubmed/18438531
A Subtype of Markedly Abrupt Onset With Absolute Insulin Deficiency in Idiopathic Type 1 Diabetes in Japanese Children

http://care.diabetesjournals.org/content/25/12/2353.2.full

South Asian version of flatbush diabetes mellitus- A case report and review article
http://www.acadjourn.org/IJMMS/abstracts/abstracts/abstracts2009/Sept/Khan%20and%20%20Akram.htm

Ketoacidosis in Apache Indians with non-insulin-dependent diabetes mellitus
http://www.ncbi.nlm.nih.gov/pubmed/9382666

Cetoacidosis diabética:una complicación frecuente de la diabetes tipo 2 en hispanoamericanos
http://www.sediabetes.org/resources/revista/00011519archivoarticulo.pdf

The Occurrence of Diabetic Ketoacidosis in Type 2 Diabetic Chinese Adults
http://www.tsim.org.tw/journal/jour10-6/P10_230.PDF

Characteristics of Caucasian type 2 diabetic patients during ketoacidosis and at follow-up
http://www.ncbi.nlm.nih.gov/pubmed/10842773

The prevalence of ketosis-prone type 2 diabetes is not known, but observational studies suggest that this type of diabetes accounts for a substantial number of patients with diabetic ketoacidosis. In the United States, the prevalence has been estimated to be between 20% and 50% in African-American and Hispanic patients with new diagnoses of diabetic ketoacidosis . In addition to ethnicity, clinical features predictive of future near-normoglycemic remission are obesity and a family history of type 2 diabetes. Among 154 consecutive African-American patients admitted to the hospital with diabetic ketoacidosis, we observed that obesity was present in 29% and that the prevalence of obesity was higher among those with newly diagnosed diabetes (56%). More than 80% of patients have a family history of type 2 diabetes. The mean body mass index at presentation in African-American patients with ketosis-prone type 2 diabetes has ranged between 28 kg/m2 to 37 kg/m2 . A high rate of obesity is also reported in Hispanic and Chinese persons and in sub-Saharan black African immigrants to Europe. Obesity in persons with diabetic ketoacidosis from minority ethnic groups is more common than in white persons, in whom the rate of obesity is less than 20%.

Balasubramanyan and colleagues reviewed the clinical profiles of 141 adults admitted to the hospital with diabetic ketoacidosis. At presentation, 39% of patients were considered to have type 1 diabetes, 53% were considered to have type 2 diabetes, and 8% were not classified.Twenty-eight percent of patients had newly diagnosed diabetes, 93% of whom were reassessed at least 2 years after their initial episode of diabetic ketoacidosis and were considered to have type 2 diabetes. More recently, Pin˜ero-Pilon˜a and Raskin  reported that the incidence of this type of diabetes among persons with new-onset diabetes with diabetic ketoacidosis was approximately 60%. In agreement with the U.S. experience, African studies have reported that 42% to 64% of patients with diabetic ketoacidosis initially treated with insulin therapy do not have classic type 1 diabetes and may experience prolonged remission. The prevalence of ketosis-prone type 2 diabetes seems to be lower in Asian and white persons and may represent fewer than 10% of cases of diabetic ketoacidosis.

Narrative Review: Ketosis-Prone Type 2 Diabetes Mellitus
http://www.annals.org/content/144/5/350.abstract

The extent of the prevalence of this syndrome really isn't known. As far as I know, there is no ready test for KPD T2. What we have is hospital admittance records for DKA. The numbers quoted for Mexican and African Americans is about 60% of all the DKA cases. What this means in terms of the general Mexican and African American population is in question but you have to recognize that for every case where it is bad enough to cause hospitalization there has to be many multiples of it in existence.

Mike

Contamination of traditional foods

I'm still off on assignment but this subject came up and I thought that it would be good to drop a brief note on it.

We tend to think that if we stick to traditional foods that we can expect to be safe from problems with blood sugar. What needs to be recognized is that traditional foods were typically raised by the consumer or the farmer was near to the consumer. Preparations were carried out by the person eating the food.

The modern world is different, however. You might very well be eating a traditional diet but what are its constituents? Is that wheat the traditional wheat which was used in the preparation of that bread? How was it prepared? This is important. Traditional preparation will do nothing to offset problems of diet, if the underlying food is problematic.

If you look at our "diabetes epidemic", you will note how much it has taken off in peoples of color across the world in the last few decades. I suspect that some of the reason has to do with newer varieties being substituted for old traditional foods. I know I keep harping on this but the only way to truly know is to test your blood. Don't be complacent. The world isn't very dietarily safe for you or me.

Please make the fight

I have to go back to work, and I wish to say this before I sign off. I wrote this blog because I saw unnecessary suffering, I come from a family  that  died  young because of this accursed diabetes. The peoples who have read this blog span the world and know that we are in the grips of something horrible that has not been given name or face in the world. I see you from all corners of the globe. This is a real thing. The science is there but the recognition is not. People are dying and suffering due to this. I can't do this alone. Others must step forth and push this agenda.

I come from slaves in the US. We suffered lynchings and burnings because we believed that there was something right that had to be pursued. I was brought up to make the fight for justice and this is was this blog has been for me. It is dedicated to my family who died young from heart attacks, strokes and cancer. It is based on the belief that this did not have to happen and that it can be stopped, if I would make the fight.

In this blog, I have not only brought forth the information about this diabetes but also put myself on the line by actively experimenting on myself to show that this is a special type of diabetes. I can't do it alone. You, out there, have to push this issue in China, Indonesia, Brazil, Turkey, Africa. It is up to us to make this known and get proper care for our brothers and sisters.

I've made the fight. Please, make the fight as well. Nothing will get better without our efforts. No more funerals, no more amputations without the understanding of what we face. This is what I ask. This is what making the fight is about. The information is here. What is needed is the will to push it and challenge all the thoughts on diabetes that endangers us.

Take this information and, please, make the fight.

Mike Barker

Thinking about the nature of Abrupt Onset Type 2 diabetes

This is still a continuation of the “Abrupt onset t2 series”. You can read those Here. This is one of my “thinking about” pieces and this means a lot of speculation. I have to do this because the research is so spare for this. We do have the research on “ketosis Prone Type 2” diabetes but this syndrome is a lot bigger than that. Most people don’t reach ketoacidosis, I didn’t, even though I was definitely headed that way.

We are talking here about a severe metabolic derangement that comes on swiftly. This is different than just heading towards DKA. It is the parts of our metabolic system losing the ability to act in concert. Glugagon from the alpha cells causes the liver to produce glucose to respond to falling blood sugars. How long and when this happens will produce various effects depending on what the beta cells are doing with insulin. We would get a range of effects here. If insulin is high, blood sugar might rise only slightly, if at all. If insulin is high but glucagon is low, reactive hypoglycemia would occur. These systems are meant to match each other, when we have diabetes, they don't.

The term “metabolic derangement” is used because we aren’t talking about systems that have deteriorated due to autoimmune attack or toxicity. I’m talking of systems that are operational, meaning they’re functional capacity is not diminished. What is lost is the correct timing of the systems behavior.

Why would I make this statement given all the research on type 2 diabetes? One word, “speed”. Glucose toxicity or Glucose desensitization are long drawn out processes that are thought to take years to take effect. Sudden onset t2 is abrupt. It takes less than 6 months to go from near normal to fulminant and about the same time to return to near normal.  

The experiments that I’ve been performing on myself have been occurring in the space of a few weeks. This isn’t enough time for cellular failure or regeneration in any body system. This suggests that the underlying systems of blood sugar metabolism are intact but that the triggers that allow the timely interactions that give us normal blood sugars aren’t functioning correctly.

Now I’ll even go further out on a limb. The body has many more systems to prevent hypoglycemia than hyperglycemia. The obvious reason is that hypos can kill you in a day: hyperglycemia may take years. Given this, my guess, is that there is a failsafe set into the operation of insulin, in particular, the 1<sup>st</sup> phase of insulin. This first phase is essentially a dump of a large amount of insulin to offset blood sugar spikes from pushing blood sugar over the magic 140 barrier.

Now, as a thought experiment, think of a drug injected into a person that suppresses some signal that's essential for the alpha cells, liver and beta cells to cooperate to maintain blood sugars. Probably the first thing you would see would be spikes and reactive hypos. The spikes would be due to both glucagon and the liver. The liver would be putting out glycogen while glucagon suppressed insulin: this would be hyperglycemia. If the glucagon and liver stop then suddenly the person would go low, reactive hypoglycemia. This might go on for awhile but eventually something in the body would have to react to the lows and essentially shutdown part of the insulin production. I say "have to" because too much insulin will kill you very quickly and continuous hypos have been shown to increase mortality.

There has to be some sort of failsafe in the body to prevent this. Cutting off all insulin would be deadly as well but the beta cells have two phases; one is slow and steady and the other puts out large amounts of insulin in a short time. It would have to suppress the first phase. What we do know about type 2 is that early stages typically involve reactive hypos then the loss of 1<sup>st</sup> phase insulin. The later phase involves the steady rising flow of insulin to keep bringing blood sugars back in line. This is an interesting supposition but what I’ve shown is that hyperglycemia suppresses my 1<sup>st</sup> phase.

Here we go to a little control system theory. I am an Operations and Maintenance guy for industrial wastewater processes. (By the way, I’ll be going off to a project for a couple of months. This means and end to experimentation for awhile and it will slow down, if not stop, my blogging till I get done. This is another reason to try to get this post out.) I work with systems that sense conditions then send commands to various systems to keep the process in balance. Typically, systems will be nested in larger systems. Troubleshooting such systems will involve me looking at a system which isn’t functioning and testing it to see if it’s okay. If that system is fine then I move up to higher control systems to see how they are affecting the system that isn’t functioning.

What this has to do with hypoglycemia and hyperglycemia is that, if, as I’ve come to believe, the insulin system is intact, then the problem is higher up. My experiments tell me it must be involved in glucose metabolism, susceptible to the med I’ve been using, affected by hyperglycemia and interestingly enough by insulin. Why insulin? All the papers that I’ve read on KPD say that insulin performs better than any med in bringing people back to near normal blood sugars.

My candidate for this system is the hypothalamus. Here’s a paper which talks about the importance of the hypothalamus is the secretion of insulin from the beta cells. Pancreatic neuronal melanocortin-4 receptor modulates serum insulin levels independent of leptin receptor  

This talks of a hormone secreted by the hypothalamus which is part of blood sugar control but is suppressed by hyperglycemia. Role of orexin in the regulation of glucose homeostasis

This one shows the effects of hyperglycemia on the hypothalamus and suggest that these effects are reversible. Hyperglycemia impairs glucose and insulin regulation of nitric oxide

Here’s a paper detailing the relationship of the hypothalamus to the production of glucose by the liver. CNS Regulation of Glucose Homeostasis

This paper, though ostensibly about brain cholesterol, does talk about the curative effect of insulin on the hypothalamus. Diabetes and insulin in regulation of brain cholesterol metabolism.

A well known fact of diabetes is that the loss of 1<sup>st</sup> phase insulin is an early occurrence. What occurs because of this is hyperglycemia since a basal can’t catch up with the initial spike from food. A person will endure hours of blood sugars above 140. Now, I’m willing to go to the idea of beta cell toxicity due to continuously high blood sugars. I’m thinking that what we have is a mix.

This may explain the fact that, at least, half of KPD’s do not come back to remission. The damage done over time may well have reduced the amount of beta cells that are available for insulin secretion. This might explain the sudden onset as well. We have two processes, one which suppresses beta functioning, while the other is the dying off of cells due to hyperglycemia. A tipping point is going to be reached at a certain point.

What does all this mean in terms of dealing with this type of diabetes? The first thing always will be the fact that this isn’t a good set-up for carbohydrate metabolism. This is a deranged metabolism. A metabolism that has virtually no control over the liver will have serious problems with eating carbs. It doesn’t take much to spike me or many of the people I know with this. Glucose is already being added to the blood. Basal insulin is being secreted to try to match this. If you throw a significant source of glucose on top of this then you are going to be hyperglycemic. Diet, you see, is a must.

What we really need is more research and we won’t get that until we begin to get the word out on this. I’m doing my part, are you?