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 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^st 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^st 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^st 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^st 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?

Thinking about: A1c Relapse Progression and the Insidious Nature of KPD

These are the graphs from Ketosis-Prone Type 2 Diabetes in Patients of Sub-Saharan African Origin. These graphs especially C & D  are too important not to be seen.

This is my recreation of C for clearer viewing.

Let's recap.

Ketosis Prone Diabetes is known for sudden onset without a precipitating factor. I posted this Here

The A1c at which the diabetes stayed controlled is about 6.3. This is in the previous post.  Here

Spontaneous Remission is the norm where there are no antibodies present. This is posted everywhere on this site.

What we have is a type 1 like syndrome that shows up out of seemingly nowhere then vanishes, leaving a type 2 diabetic, who can maintain blood sugars with diet and exercise.

My speculation is that the KPD syndrome is insidious. I have speculated in other posts using anecdotal evidence that this is the case but it occurs to me that there is enough here to do better.

The graph is important because what we need to wonder about is: what is a KPD before DKA?  This graph puts the regular blood sugars at about 6.3 A1c or 134. Jenny Ruhl's "Blood Sugar 101"  talks about dangerous blood sugars and, the short of it is, that blood sugars above 140 cause damage. She details other blood sugar levels that are considered safe but are bad as well. If you're new to diabetes I strongly advise you to read this site, carefully.

No one's blood sugar is steady. It goes up and down during the day and an A1c is best viewed as an average of blood sugars over a 3 month period. Actually, it's a measure of glycation of blood cells but seeing it as an average will do just fine for my purposes.

As I said, no ones blood sugars are steady and the more metabolic damage you have, the more they tend to fluctuate. Now, for whatever reason, KPD's tend to have great big fluctuations. This means that at 134 KPDs are going to spend considerable time above the dangerous 140. In fact it is so close to 140 as to almost be the same thing. KPDs have another trick that most other diabetics don't seem to have and that's remission. Rather than continue on a path of gradual rise, they can and do drop back to near normal. This would essentially reset their diabetes and they would, once again be back to a gradual rise.

What I'm saying is that the flat portion of this graph represents both the tendency to fluctuate wildly and the tendency to balance this with a fall back into remission. A KPD would get in trouble if the numbers stayed significantly above 140 but even then, if intensive insulin therapy were applied blood sugars once brought down would go back into a range where things would balance.

There is a problem here. Over time, continuous damage would be occurring. It would be small each time but the cumulative effect over decades would cause serious damage body-wide.

If we run this all back, we could start with a normal blood sugar but with a tendency to get large fluctuations from certain types of foods. Whatever the mechanism is for remission would keep pulling blood sugars down but over time they would rise as more and more damage was being done metabolically and to other body systems. The abrupt onset would occur when this remission mechanism itself broke down. Maybe it has a limited range to work in and the KPDs that go DKA have a functionally smaller range.

Okay, this is speculation. There are many ways this could be playing out, all I've done is outline one possible scenario. What isn't speculative is the nearness of normoglycemia to the line of danger and how quickly this takes off.

Once again we visit the ADA guidelines.

ADA Criteria for the diagnosis of diabetes

1. A1C 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*

OR

2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*

OR

3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT. 

It isn't said but if the FBG (fasting plasma glucose) is below 126 most medical people will not go to the other tests. Even if they did, the next test would be an A1c and a KPD would pass there as well. The OGTT (oral glucose tolerance test) would catch it but it isn't done if the first two don't give indicators.

Years of damage with an attendant rise in mortality would occur because all those numbers sit in the danger zone for KPD's and the graph shows that DKA could easily be around the corner.

If you're reading this, you're probably KPD. You should recognize that it has a strong genetic component so if you've got family members they are likely to have it or some component of it. This is where I diverge from all the diabetic advice on diet. Screw looking at or adjusting diet. You don't know what precipitates KPD. The only thing that is known is that the blood sugar numbers represented by the "prediabetes" ADA recommendations are, in fact, the launching point for a serious diabetic emergency.

I said that the OGTT would more than likely have shown diabetes but this test tends not to be performed. You can do something similar with a meter, a couple of bowls of breakfast cereal and a glass of juice. Just test someone an hour after they took their first bite of breakfast and see if their numbers are above 160. I think that would catch a lot but since we really don't know what the bad actor in the food is, wisdom dictates testing the blood sugar with all types of food. What puts the blood sugar above 160 should always be avoided because whether you're a KPD or not, damage occurs to the body above that number diabetic or not.