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.

Thinking out loud about how prevalent is KPD T2?

Tip of the Iceberg
"It is our view that KPD patients (especially those with A forms of KPD) represent only the “tip of the iceberg”; below the surface is likely to be a much larger pool of patients who have early or primary -cell defects in development, expansion in the face of insulin resistance, regeneration in response to injury, or insulin secretion."
Syndromes of Ketosis-Prone Diabetes Mellitus
Ashok Balasubramanyam, Ramaswami Nalini, Christiane S. Hampe, and Mario Maldonado


"Idiopathic type 1diabetes is highly common in major cities whose populations include large numbers of African-Americans."
Idiopathic Type 1 Diabetes in Dallas, Texas -ANTONIO PI ˜NERO-PILO ˜NA, MD, PATRICK LITONJUA, MD LARISSA AVILES-SANTA, MD PHILIP RASKIN, MD


One of the things I keep trying to figure out the prevalence of KPD in the diabetic community. I'm obviously getting no help from the medical community, in this regard. Since we have not championed our cause, medicine has been allowed to shrug and let things go on as they are. All I can do is take the few hints out there and make a supposition.


In various papers I have quoted, the concensus is that 60% of new diabetic emergency admissions are Ketosis Prone T2. The rest of the cases can be attributable to poor diabetic management, T1 admissions and stress related type things, such as illness.


I must state here again the basic rule of our secret diabetes. "Ketosis Prone Type 2 Diabetes can not be distinguished from either Type 1 or Type 2." What does this mean? It means that all or most of those admittances could have been KPD. KPD is recognized due to its acute onset and then restoration of some semblance of beta cell functioning. This is to say that it has been allowed to be known only by its consequences. There is a car crash. It is noted as such but no cause exists or is considered. This is pretty much where we are now.
What we have been getting is the car crash equivalent of stating that all side crashes are KPD and the others are T1 and T2. They are being distinguished by no real criteria except result. It means nothing in terms of actual cause. Where can we go from here? I think we can go anywhere we wish.


What we can say about its prevalence, at least in terms of Blacks and Latinos, is that it represents 10% of diabetics. This is a guess made by researchers based on hospital admissions. This is the car crash equivalent of saying that the problem only exists when there are accidents. All driver error and equipment malfunctions cause accidents. If there is no accidents then those things did not occur. Basing prevalence on acute incidences, strongly under counts all things that don't reach that level of acuteness.


Where would I put the number for prevalence? Since there is no test, the best I can go from is my experience with Black diabetics. Most of the people I know, had symptoms and went to their doctors and were diagnosed as T2. These symptoms typically involved the usual thirst, excessive urination, tiredness, blurred vision and tingling in the feet. This onset could have been due to a undiagnosed T2's pancreas finally giving out or it could have been the beginnings of KPD onset.


After a bit more thought and research on this, I realized that DKA is the extreme situation of Ketosis Prone Type 2 Diabetics. Obviously, there's going to be a greater number as we move away from the extremes and more towards the mean. If I took 3 standard deviations, I might have got this up to 30% of Black and Hispanic type 2 diabetics. This would have given me at least 2 million KPD's in this country alone!


I've decided that a goodly percent were actually KPD. Most hadn't been diagnosed as even prediabetic. The fasting blood sugar isn't generally going to pick up most KPD's. One of the hallmarks of KPD is the sense that it came out of nowhere. Their fasting blood sugars, like mine, were typically near or above 300 with spikes passed 400 when diagnosed. Now, even without weight loss, their sugars are near normal, controlled mostly by diet and exercise with a little Met.


These are going to be my KPD's. They didn't reach acuteness and maybe never would have. These would be mild KPD's. What would prevalence be now? Well over 25%. This would put the overall number into the millions.


Most would argue that I've played a little fast and loose here. My point is that, we don't know. I could be wrong and I would love for somebody to do the research and prove me wrong. People should know if they have a time bomb ticking inside them.

Thinking out loud: The month of diagnosis

I spend an inordinate amount of time reading blogs and scientific literature. This gives me a great deal to think about but I find that many of these thoughts can't be moved to completion because there are too many uncertainties. Instead of keeping all this stuff fermenting in my head, I've decided to share it with others. Okay, this is a nice way of saying I'm dumping but I did say it nicely.

I would love to know this piece of information. When people go DKA, are the months that it occurs in random or do they group? I ask this because I still wonder about the Vit D link to diabetes in general and KPD in particular. Does it show a seasonal effect? I am betting that it would be during the winter months that DKA goes up. You could say that this would buttress my idea of Vit D implication but actually it doesn't. We tend to exercise a lot less in the winter months because of the danger and inconvenience. Blood sugars are often offset by exercise.

I started going bad in March basically because I wasn't out riding much. I doubt, if I lived in a warmer clime, that I would have ever found out I was diabetic until it was far too late. March, now that I think about it, would still be an interesting month. If we start at November as the time of, more or less, enforced sloth then by February a person should start to feel pretty bad from high blood sugars. This is passed the holidays, when gluttony would have pushed the glucose toxicity through the roof. The glucose toxicity would have pared back much of the pancreases functioning and the highs would be continuing and mounting. By February or March, the crap should have been hitting the fan.