Tag Archives: Ketosis Prone Diabetes

Ketosis versus Ketoacidosis

Courtesy of Master Isolated Images

Courtesy of Master Isolated Images

 

I hear over and over again that low carb dieting can lead to ketoacidosis.  It’s confusing to me because of the people out there who thrive on very little carbohydrates.  How do they avoid diabetic ketoacidosis?  How have I in the past?  I looked it up and learned that: (and correct me if I’m wrong)

Ketones are organic compounds that result when body fat is broken down for energy.  If you lose, say, a pound of fat you will make ketones.

Ketosis is the presence of excess ketones in the body.  It is the continuous state of fat metabolism.

Diabetic Ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism.  The most common causes are underlying infection, disruption of insulin treatment, and new onset of diabetes.

Ketones resulting from low carb dieting or from fat loss measure around 5 to 20 mg/dl while the quantity of ketones associated with DKA is quite higher.  The warning to diabetics is if one low carb diets and then has elevated blood sugars, they are perhaps more likely to reach a point of ketoacidosis sooner than if they had no trace or small amount of ketones in their system to begin with.

What I’m understanding is that low carb dieting in diabetics should only be done with very tightly managed blood sugars. 

I could be wrong.  But it seems people might confuse the two because I’ve heard people say that they wouldn’t limit carbs because they don’t want to go into DKA.  These people I’m referring to don’t have diabetes of any kind so that is where my confusion stemmed.  If you don’t have diabetes and you limit carbs for some reason, then the ketosis in the body is not going to lead you to DKA-it just means you’re a constant fat burning machine?

Any thoughts on this?

Ketosis Prone Type 2 Diabetes, Heard of it?

 knowledgeispower

I was recently surprised to hear about a diabetes which is not type 1, not type 2, not type 1.5, not gestational, and not pre-diabetes.  Years ago I heard about a boy whose type 1 diabetes was misdiagnosed.  He was on insulin just like a type 1 and he had the signs of a type 1.  Yet, he takes no insulin today and is doing well.  I automatically thought at the time, “Well, clearly he had type 2 diabetes and was misdiagnosed.”  Although in the back of my mind I was confused because his case didn’t seem like typical type 2.  So was his case just a misdiagnosis?  Maybe not.

Recently, I found a well written website about Type 2 Ketosis Prone Diabetes  by Michael Barker.  He has this type of diabetes and says it is not commonly heard of in the United States.  The big shocker however, came when he said it’s actually not an uncommon type of diabetes.

Barker estimates there to be millions of Ketosis Prone Diabetics out there and on his website writes that “There is no way to identify a KPD before a diabetic emergency occurs.”  You can bet this all struck my curiosity so I have asked him some questions which he has graciously agreed to answer.

 

Michael, What are the different names for KPD?

There are actually quite a few. The official ADA classification is Type 1b. Flatbush Diabetes comes from researchers in NYC who discovered it in Brooklyn. Atypical Type 1b is added to recognize the fact that no antibodies are detected. Researchers have recently settled on the name, “Ketosis Prone Type 2” diabetes. I occasionally see “sudden or abrupt onset type2 diabetes”, which is what I actually prefer since it better captures the real nature of this diabetes.

I’m going to go with the name you use on your website which is Ketosis Prone Diabetes (KPD).  What is KPD and how is it different from type 1 and type 2 diabetes?

Really the big difference between T1 and T2 is the amount of insulin available to maintain blood sugars. T1 is autoimmune and the beta cells are being destroyed by the body. T2 typically has beta cells but the insulin resistance is so great that there isn’t enough insulin to control blood sugars. Overtime, the beta cells are eventually lost to this high insulin and high glycemic environment.

KPD is just like T1 at the start, in fact it’s worse. The body very quickly begins shutting down insulin production even though the beta cells are largely intact. The blood sugars spiral out of control. The hyperglycemic environment shuts down more and more of the beta cell functioning until there is virtually none. Without medical intervention, the person will die. With medical intervention, by way of insulin, the blood sugars can be brought back to near normal and will stabilize. This process takes place within weeks. The person will then be, for all intents and purposes a T2 and, in some cases, will be able to maintain blood sugars with only diet and exercise. The big difference between T2 and KPD is that the KPD can and do relapse and they will essentially appear like a type 1 again.

There’s actually more to it than this because there are at least five identified types of KPD, each with different processes and, I’m sure, more will be identified.

I saw on your website that you keep your A1c within excellent range.  How do you manage your diabetes?

The biggest component of managing my blood sugars is diet. I have taken meds, including insulin. I’ve measured all the various variables and how they effect blood sugar and diet is the winner. The type of diet is very low carb. My experience with KPD’s has been that we are very carb sensitive. The chief foods in the diet are saturated fat and then protein. This, unfortunately, tends to keep me on the thin side.

How and when were you diagnosed?

I was diagnosed last year in June of 09. Mine was easy to figure out. My A1c was 10 and my FBG was around 300. I was headed south – fast!

Do you believe Halle Berry has KPD?

She’s actually a pretty classic early KPD. She was diagnosed before the major scientific articles were written on KPD. In that time, anyone who showed up with DKA, who was thin was automatically classed T1. She was put on a regimen of insulin and given a high carb diet. The diet, in itself, would have been so detrimental to her, the only way she could survive would have been on insulin.

Once she changed her diet, she was able to slowly back off insulin. This is classic, as well. KPD really came to notice because people of color, who had been diagnosed as T1 typically couldn’t afford the insulin but did not go back into hyperglycemia immediately. They lasted weeks, months and in some cases years before relapse. Those that stayed on insulin had to be withdrawn due hypos as their beta cells recovered. We are the disguised diabetics masquerading as T1. Anyone who says they can cure T1 but doesn’t mention KPD is missing it. The best case in point occurs in “30 Days Raw”.

In your opinion, are there any foods which you’d consider off limits?

Wheat, especially whole grain, should be avoided but so should Rye and Barley. These are the trifecta of bad news. They have high glycemic indexes, they tend to correlate with autoimmune disease, they have phytic acid which tends to block the absorbance of minerals. I really don’t think anybody should be eating them but a sudden onset T2 would be asking for it. The rest is pretty simple – no starch, no sugar.

Why don’t more people hear about KPD?

Let’s face it. It is largely a disease of people of color and until very recently most research and even more importantly, the training of researchers, has been done in Europe and the US. KPD has a strong association with malaria. These areas don’t typically have an environment where that is a worry. KPD is a subset of T2 even in communities of color, though I’m willing to bet this will be changing as more becomes known. Unless you separated out ethnic communities then its effect would be small, what they call an outlier. If you add this to the fact that minority voices tend to be ignored in the media then you’ve pretty much got a blackout on this issue.

How come “There is no way to identify a KPD before a diabetic emergency occurs”?

Diabetes, in the case of T2, is inferred from blood sugar tests. There is no particular mechanism that can be tested for that will tell you who will become a T2.

So really there aren’t any tests anyway. KPD is very hard because it doesn’t show progression.

A1c progression graph

This chart is the average A1c of 84 known KPD’s for 40 months after they had recovered from a DKA. There is virtually no change until it takes off. If you showed up at a doc’s with a A1c of 6.3, they would tell you to come back in 6 months and they would check it again. KPD is sudden onset and it could take off at anytime, in six months a person could easily be in the hospital.

Should this information alert those who have been diagnosed type 1 or type 2 diabetes?  Should we look for anything in particular?

Antibodies are the big key. They assumed I was a type 1 but I had no antibodies. A c-peptide that’s normal to low normal. They call this being beta positive. The last thing is that KPD takes off quickly but also subsides quickly. People typically have very high number and within 8 months have brought the numbers down to near normal even without losing weight. This is the big tip off to me. They go up fast and can be brought down fast. This leads people to talk about “diabetes reversal” with diet. I have better than normal numbers (A1c – 4.7) as long as I stay away from a “healthy diet”. Minimize the carbs, increase the saturated fats and most KPD’s don’t need much beyond Met.

What is the most difficult thing about living with KPD?

Giving up pasta, bread, brown rice and noodles, all the other starches and sweets never meant that much to me. I’ve done a complete turnaround in my diet. I wasn’t that big of a meat or fat eater, now I search for the biggest fattest cuts I can find. Hell, until I became diabetic I really didn’t know how to cook large cuts of meat. I actually haven’t changed many things beyond diet. I exercise less now than before I was diagnosed. I still like cigars and I’ve got some brandy sitting on the table next to me.

Michael, is there anything else you would like to add:

I am coming to understand that this isn’t a diabetes of loss but derangement. T1’s lose their beta cells. T2’s lose their insulin sensitivity. Abrupt diabetics don’t lose anything but the ability of their internal systems to communicate effectively with each other due to hyperglycemia. The people I’ve talked to are all over the place. For some it’s the liver putting out glucose, for others it’s counter regulatory hormones forcing up blood sugars. Insulin production shuts down under these conditions because, as I’ve come to believe, insulin has more restraints on it. Too much insulin will kill you in a day but hyperglycemia takes years. There is a failsafe in the body for insulin.

The body has many ways to raise blood sugar but actually only one to bring them down in terms of hormones. These systems are in a delicate dance but once they stop communicating the dance becomes chaos. Stopping the hyperglycemia, in most cases, simply brings back communication. This is the reason they can so quickly go back into remission. The pieces aren’t missing, they simply aren’t in sync. My little experiments on myself have allowed me to see that.

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Michael Barker, Thank you so much for answering my questions. 

It troubles me that I haven’t heard about this type of diabetes before last week and I think awareness on this issue is very important.  How many people are on this roller coaster and find they don’t fit the description for typical type 1 or 2 diabetics? 

I hope this information sparks an interest in others to learn more about this type of diabetes.  I’ll be asking some doctors about it very soon to see what they have to say.   

In addition, the US is seeing a lot of growth within ethnic minority groups and we might start to see cases like these more often.  At the very least, this sounds like something to learn more about and definitely follow up on.

Michael’s website has a lot of detailed information and links if you’re interested in reading more about his findings and observations. 

As always, thanks for reading :)

 

 

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