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.

Showing posts with label Minority Health. Show all posts
Showing posts with label Minority Health. Show all posts

Sunday, February 14, 2010

The obesity epidemic or what's up with all the fat people.


Most likely, if you're reading this, you're diabetic and you're overweight. You might have tried diets and lost a little bit or a lot but you probably gained it back and have pretty much learned to live with it. This isn't all that unusual unfortunately. We are in an unprecedented epidemic of obesity with rising diabetes.

The usual prescription is for more exercise and cutting the calories. The basic prescription has at its base the biblical idea of gluttony and sloth. If you are fat, you feel shame. I'm going to row against the tide on this one with something called "common sense".

I will start with the single principle that all humans are animals and that the basic principles of being a living being applies to all living beings. The idea I wish to bring forth from here has to do with eating and this idea is this: animals eat because they are hungry and they stop eating when they are not.

Now you could bring up various animal experiments about fat mice and rats and how they will eat long after they are so fat that they can't stand and other bizarre displays but I didn't mention obesity. I only said that:animals eat because they are hungry and they stop eating when they are not. I didn't mention obesity because I don't think it's relevant to the discussion. Obesity, I have come to believe, is a symptom and not a cause.

If obesity is not a cause but a symptom, what's the cause? Hunger! Yep, hunger. I'm putting forth the proposition that we are in the midst of famine.

My youngest boy is exhibit A. He was a poor college student who went to school in his hometown so he was able to scrounge food from family and friends. His typical procedure was to arrive for dinner and then try to eat - forever. He would sit and eat until he was full and then, not knowing where his next meal was coming from, would continue to try and put food away. It was horrible to watch. He would slowly chew with a mild revulsion on his face then swallow. No matter how hard he tried, he could never seem to get beyond a few fork fulls before he had to give up.

This isn't news. Eating after you're full is very hard and the thought of doing it over and over again makes you feel green. Try it. You can't do it. But you might say that you've seen people overeat all the time. Once again, stick with the idea. I didn't say people don't overeat. I said that it is nearly impossible to eat, if you aren't hungry.

I am exhibit B. For the last thirty years, I have been a bike rider. What ever I had to do, I would try to do it on a bike. I would put somewhere between four thousand and five thousand miles a year on a bike. I ate carbs like crazy in order to do this because carbo loading was the thing to do when you were putting in a lot of physical exertion. My reputation for absolute gluttony is based on this. I was never fat but I could eat plate after plate of food. I ate until my stomach was full and then ate some more but I remained hungry. This was my life. I couldn't stop eating because I was famished.

You can't diet, if you're hungry. It will only make you hungrier. You can't excercise when you're hungry because your body cuts back on motion. You can, however, grow fat because there really isn't a connection between appetite and obesity.

I hear the experts talk about empty calories, large portions and too many snacks but rats, no matter the density or type of calories, would stop eating. Hunger is basic and at a level far below regard.

Stole this from Peter of HyperLipid




Now I'll say it again: we eat because we are hungry not out of some lascivious need. What we are seeing now is hunger, one that isn't slacked by eating. Something has gone wrong with our diet and we are now hungry at a level that causes us to eat in search of a satiation which we can't achieve.

Mike

Thursday, February 4, 2010

Western Diet Implicated in African American Diabetes

PUT THE SODA DOWN, NOW!

Okay, now that I've got your attention, I want to tell you why. Diabetes has a very large footprint in the African American community and researchers have been looking for the reason why. Here I have a novel paper that says that it is genetic and that we are the victims of the FDA food pyramid. To put it concisely, people of African descent have a problem with processing carbohydrates at a genetic level. This may very well be the cause of a good deal of the metabolic problems noted in African Americans.


Stable Patterns of Gene Expression Regulating Carbohydrate Metabolism Determined by Geographic Ancestry



Individuals of African descent in the United States suffer disproportionately from diseases with a metabolic etiology (obesity, metabolic syndrome, and diabetes), and from the pathological consequences of these disorders (hypertension and cardiovascular disease)...

...Differences in expression of several carbohydrate metabolism genes suggest both genetic and transcriptional mechanisms contribute to these patterns and may play a role in exacerbating the disproportionate levels of obesity, diabetes, and cardiovascular disease observed in Americans with African ancestry.

The KPD's I've spoken to all have lamented their problems with post prandial spikes. This specifically refers to the hour after a person has taken their first bite of a meal. This blood sugar should never go over 140. A normal blood sugar doesn't and there is a very good reason why. Research has shown this is the point where damage begins to occur throughout the body.

This link is to "Blood Sugar 101": http://www.phlaunt.com/diabetes/14045678.php . It is run by Janet (Jenny) Ruel and any time you spend there will be profitable if you're really interested in the ins and outs of diabetes.

If you have a genetic problem handling carbohydrates and have the added problem of being Ketosis Prone this combination will eventually move you into hyperglycemia and / or DKA. The eating of carbs will force your blood sugar up which will create glucostoxicity. This is glucose poisoning. Beta cells in the pancreases of KPD's are very sensitive to this and will slowly shutdown. The more carbs ingested the worse the condition will come and god help you, if you drink soda or juice to try to slack your thirst because they are almost pure carbs and filled with High Porn Corn.

The truth is there is almost no average American meal that will not push your blood sugar beyond the 140 mark. I can't handle better than 20 grams of carbs at any setting and those carbs need to be very complex to keep me from spiking my blood sugar. Even the supposedly healthy diet is problematic here. Whole grains, potatoes, brown rice, apples, bananas, oranges and pastas are just a few things that I have to avoid.

This doesn't match what you would get from a dietitian but you have to recognize that most of the research has been done on Europeans and the minority communities have not been factored into this. Some might claim this is racism but it more neglect than anything. We, much like the LADA and MODY community, must look after ourselves here. I've got one more piece of the puzzle that I want to put out and then I can really lay this out in a logical fashion.

Mike

Wednesday, February 3, 2010

Ketosis Prone diabetes as a MODY

It has been one of my conclusions that KPD is a type of MODY which shows up unannounced and then works its wickedness undetected for years. The italics are mine.


Endocrinol Metab Clin North Am. 1999 Dec;28(4):765-85.

Monogenic diabetes mellitus in youth. The MODY syndromes.

Department of Pathology, Immunology, University of Florida College of Medicine, Gainesville, USA. winter.pathology@mail.health.ufl.edu
Maturity onset diabetes of the young is characterized by early onset diabetes inherited in an autosomal dominant pattern. Classic MODY occurs predominantly in Caucasians and presents before age 25, is nonketotic, and is generally not insulin-requiring. Less than 5% of cases of childhood diabetes in Caucasians are caused by MODY. ADM is a subtype of MODY that occurs in approximately 10% of African-Americans with youth onset diabetes. In contrast to MODY in Caucasians, ADM presents clinically as acute onset diabetes often associated with weight loss, ketosis, and even diabetic ketoacidosis. Approximately 50% of patients with ADM are obese. Therefore, based strictly on clinical grounds, at onset, ADM cannot be distinguished from type 1 diabetes. Months to years following diagnosis, a non-insulin-dependent clinical course develops in patients with ADM that is clearly different from type 1 diabetes. Mutations in five genes can cause MODY. These genes encode hepatocyte nuclear factor-4 alpha (HNF-4 alpha, MODY1), glucokinase (MODY2), hepatocyte nuclear factor-1 alpha (HNF-1 alpha, MODY3), insulin promoter factor-1 (IPF-1, MODY4), and hepatocyte nuclear factor-1 beta (HNF-1 beta, MODY5). These monogenic forms of MODY have been used as model systems to investigate the inheritance and pathophysiology of type 2 diabetes. Clinicians, should be able to diagnose MODY. Type 1 diabetes, the most common form of diabetes in Caucasians, is always insulin-requiring for control and survival, whereas patients with MODY do not usually require long-term insulin for survival. Diagnostic confusion can lead to inappropriate management and patient expectations. Primary care physicians must be alert to avoid therapeutic confusion when patients with ADM enter into the non-insulin-dependent stage. An approach to the diagnosis of childhood diabetes is offered in Table 4. The majority of youth onset diabetes remains type 1; however, the frequency of type 2 diabetes is rising in obese children and adolescents and especially in obese minority youth. The diagnosis of MODY can be made through a careful review of the patient's clinical course, severity of hyperglycemia, and family history. The identification of islet autoantibodies is confirmatory evidence of autoimmune (type 1) diabetes. Because testing for MODY mutations is expensive and is performed at a select number of research laboratories only, routine molecular genetic studies to search for the various MODY mutations should be limited to research investigations. In the future, the availability of gene chip technology may allow rapid screening of mitochondrial and MODY mutations.

Winters is one of the original investigators of KPD and has written extensively on it.