The accepted knowledge is that Diabetes destroys gradually over years. Ketosis Prone Type 2 diabetes is an acute form of type 2. This type 2 can reach fasting blood sugars of 300 or higher in months. This blog brings together all the documentation that I could find in the world and my speculation of what it means for KPD’s in specific and diabetics in general. I ask you to leave your stories about what happened to you so that we can all gain a better understanding of what we are dealing with.

Thursday, February 14, 2013

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 

 

Monday, February 11, 2013

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.

Sunday, February 3, 2013

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.


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.