Weaning Type 1’s from insulin

This seems to be a burning topic that I thought I’d answered in my previous post but because of Halle Berry  and YouTube videos like “Raw for thirty days”,  I must revisit the topic.

What does it mean to “wean” anybody from insulin? It means to withdraw it from their system, take it away from them. People, none of us can live without insulin! The body isn’t accepting any substitutes, either. Those who have been “weaned” from taking insulin obviously have working beta cells which produce insulin. If they did not, it would probably be over pretty quickly.

The claim for this “weaning” then is based on the reanimation of dead beta cells through various techniques. Now what makes this plausible are the testimonies of many individuals who were diagnosed as T1 and then found themselves able, through the use of (name your technique), to become insulin independent. These people are adamant. They were DKA, might have even gone into a coma. They were thoroughly dependent upon insulin injections, for maybe years and now they don’t need it.

Unlike some, I’m not going to call them liars, I will even vouch for their experience but I want to examine this rationally.

The very first thing to note is that they were diagnosed and told they were T1 because of severe hypoglycemia, DKA, weight loss and maybe or maybe not the presence of antibodies. They were given the ADA diet of 200 to 300 grams of carbs a day, with most of the carbs coming from healthy grains and stuff like that.

They believed the diagnosis, as anyone would, but they, just like most of us experimented with their situations. The major thing that they all found was “Bernsteins’ law of small numbers”. If carbs are reduced then the insulin adjustment can be reduced as well. This simply means a change in diet.  If the carbs are going down something else must be replacing them. If you now throw in some sort of physical regimen then you’ve got something going. This is a type of “weaning” but reducing the insulin need isn’t the same as producing insulin. How does that happen? It doesn’t. You either have it or you don’t. But a person might object saying that they didn’t produce hardly any insulin before and now they don’t need it and this has gone on longer than any honeymoon on record.

The key to this is diagnosis. At the point of diagnosis, they were given the T1 designation, because there isn’t another. What if there were? Well, there is, the problem is there is no way to distinguish a T1 from a Ketosis Prone T2 Diabetic at diagnosis. It is only after months and with a c-peptide test can they be told apart. This is because, for whatever reason, a KP T2 can regenerate their beta cells once glucose levels return to normal even in the face of testing positive for antibodies.

The other key is the ADA diet. This diet is high in carbohydrates and KPD’s have  a 20% higher deficiency G6PD then even regular T2 diabetics. This is a significant disadvantage in handling carbs. High carb intake will keep them from regenerating beta cells and they will effectively stay T1. A KPD T2 is the only known diabetic that can go from a T1 status (no beta cell functioning, no insulin) to a T2 status.

Anytime there is a claim of “weaning “ a T1 from insulin, it should be viewed in this light. A person who makes that claim must know of KPD T2 and must demonstrate that the T1 they have “cured” is not, in fact, a KPD T2. Guess what, they can’t because there is no real test but time 

Magnesium

Once again, this is addressed to KPD's and also to a wider population. This is about magnesium so it's a continuation of the previous Vitamin D topic since it's needed for the proper action of Vitamin D.

Magnesium is an essential mineral that's slowly disappearing from the modern diet, as industrial agriculture and industrial food processing increasingly dominate our food choices. One of the many things it's necessary for in mammals is proper insulin sensitivity and glucose control. A loss of glucose control due to insulin resistance can eventually lead to diabetes and all its complications.

Magnesium status is associated with insulin sensitivity (2, 3), and a low magnesium intake predicts the development of type II diabetes in most studies (4, 5) but not all (6). Magnesium supplements largely prevent diabetes in a rat model* (7). Interestingly, excess blood glucose and insulin themselves seem to reduce magnesium status, possibly creating a vicious cycle.
http://wholehealthsource.blogspot.com/2010/02/magnesium-and-insulin-sensitivity.html
Stephan Guyenet

Oral Magnesium Supplementation Improves Insulin Sensitivity and Metabolic Control in Type 2 Diabetic Subjects

http://care.diabetesjournals.org/content/26/4/1147.long

Most Americans are considered to be deficient in magnesium. This is a mineral and we get it by eating plants or animals that have taken it up. The point Stephan is making is that our industrial system of agriculture isn't replacing essential minerals therefore they are falling as a percent of our diet.

Now if that weren't bad enough, we also have the problem of malabsorption.  This means that our bodies are being blocked from taking up these nutrients even when they are present. The chief villain here are grains with the gold star for bad news and all around trouble maker going to wheat. Not only do they drive up blood sugar but they all contain Phytic Acid. This chemical binds to minerals and keeps them from being absorbed into the body. We've been told about the rich nutrients in grains but what we haven't been told is that it hardly makes a difference if the grains block the absorption of these nutrients. This is about magnesium but there are a whole bunch of essential metals that are blocked by this particular chemical. Our buddy, wheat, is particularly good at this. You may as well get this straight, almost every problem I will talk about will implicate wheat as a villain in some way. Wheat and wheat products should be avoided whether you are diabetic or not.

The recommended minimum dosage of magnesium is 350 mg. Here's a list of foods which are magnesium rich. http://www.whfoods.com/genpage.php?tname=nutrient&dbid=75 I would caution you about seeds and beans though. Beans have phytic acid and seeds tend to harbor Omega 6. They won't get you there anyway. Take the supplement on this one. Magnesium Oxide gets absorbed the worst but it's cheap so something is better than nothing.

Caution. Magnesium tends to have a laxative effect so if things start to loosen up, you should go down in dosage until the problem goes away.

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.

Fessing up to diabetes miracle cures.

The previous post posits the idea that Ketosis Prone Diabetes might be at the center of a breakthrough in curing diabetes. This would be a good thing since, it's my guess that we are also at the center of a whole bunch of "miracle cures" for diabetes.

Why am I pointing to KPD's as the bad guys here? I mean don't we pet animals? Aren't we nice to children? Yeah, all the above but I didn't say we aren't nice, I said that we are the bad guys. You just have to look at what we are and it all becomes clear. We are the essence of mystery, magic, tragedy, conquest and redemption. In other words, we are Hollywood, big time.

The first thing is our air of mystery. We are so mysterious that we don't even know about ourselves. Imagine a superhero with secret powers who doesn't know it because he has to know the secret word or situation to invoke his powers. Well, he doesn't know about his secret power because no one has ever told him such a power exists and the secret word or situation are kind of locked up in never never land. So he goes about his ordinary life doing ordinary things without a hint of the secret locked inside of him.

Okay, so we've got mystery here. Now we go for the magic. The KPD wanders through life until for some reason, maybe it was a pizza party or a triple double banana chocolate split, the magic happens. The blood sugar goes through the roof. A nurse asks him in Emergency, "How long have you been a diabetic?" Diabetic? He answers, "Ten seconds". Anyway, out of nowhere, magically, the KPD becomes a diabetic. He doesn't get to be the guy who has to give up the donuts. He gets the death sentence. He's a Type 1! A week ago he was just Joe Schmoo, now he's on death row.

This is, at least, the greater publics perception of being T1: bland foods, needles and then your body parts start getting hacked off. They don't know some of the party beast T1's we know but before we were anointed with the "Big D", we pretty much had the same view.

Life's over. It's just a matter of time. There's the brave fight in intensive care and he battles his way through only to find himself, stabbing his fingers daily, sticking needles in his body and chasing wild blood sugars around as he tries to keep up with the ADA rule of eating 300 g of carbs a day.

Then it happens, some how some where, he hears of a cure. It involves eating meat, or protein, or raw vegetables, could be anything. The point is that he starts working this new system and his need for insulin goes down and continues to go down till eventually he doesn't need to take insulin. His A1c is normal. His FBG's are fantastic and the Lipid profile is to die for. The diabetes is cured!

There you have it, all the Hollywood drama you could want and with a happy ending. I mean it's all there. Type 1 takes the cure and within 30 days, he's off insulin and living a normal life.

I love a good story but let's look under the hood here. Most KPD's are very sudden onset, most of them don't show diabetic FBG's six months before winding up in ER. If they are thin, like me, they are going to be diagnosed as T1 and standard practice for DKA is a insulin regimen. If they continue eating the "healthy food pyramid", which is low fat and high carb, they will continue to have to take insulin. Once the problem of diet is solved. They will have both more energy and lower blood sugars and as a consequence will lose weight and be more active. TADA! The miracle of a diabetic cure.

Of course, the real trick is knowing the secret word. Ketosis Prone Type 2 Diabetes.

Mike

Ketosis Prone T2 Diabetes, the key to finding a diabetes cure?

A interesting piece of information fell across my path today and I'd like to share it.

Some Cells in Pancreas Can Spontaneously Change Into Insulin-Producing Cells, Diabetes Researchers Show

You can find this here. 

This paper purports to look at possible cures for Type 1 diabetes but what was done seems very close to what happens to a KPD during sudden onset of DKA.

Researcher engineered mice to respond to a toxin that would destroy 99% of their beta cells inducing a sudden onset of DKA because these mice had essentially no beta cells left.What they found is that the pancreas would, without any further manipulations, grow new beta cells by using the alpha cells. If the mice were kept on insulin this process would continue until the pancreas would once again return to full functioning and the mice would no longer have diabetes.

Does this sound like anyone you know: sudden onset DKA, intensive insulin therapy and a return to near normal glycemic levels independent of insulin?

This gets better. Because of this blog, I have come in contact with quite a few KPD's, and (I might have mentioned this some where else in this blog) I've noted that many KPD's return to having very normal type numbers, hardly ever going over 100. What has seemed to be the case is that the ones who had DKA seemed to have better numbers than those who caught the process early, like me. 

The researchers found that the destruction of beta cells had to exceed 95% to get the significant rebound back to glycemic normalcy.

People, we might have caught the break we have been looking for. Researchers are looking at this experiment as a significant breakthrough in the understanding of diabetes but this was done in mice. Typically, mice studies, if they ever prove out, take years before the lessons learned result in any type of treatment. Here we might very well have the process that they are looking at as the key to solving diabetes.

Vitamin D and why

This concerns much more than KPD's. What if I told you I could reduce your risk of colon cancer by 60%  and your chance of heart attack by 30%? What if I threw into the mix, just for the heck of it, reductions in insulin resistance, improved beta cell function and defense against osteoporosis? I bet you would start to like me even though you know that whatever I'm going to tell you will probably involve 40 miles of bad road. What if I told you that you didn't have to do anything but take a pill, once a day? Guess what, it's all true and the little genie that's going to pull this off "Vitamin D". Hey, I can feel the love already.

First you need to look at this chart. Vitamin D incidence prevention 


What you see are some of the problems that Vitamin D is involved in.You also see the level that's needed in your body to get these effects. The level needed is 60. Now the bad part, if you are like most people you are probably around 25. Here's the problem, you get Vit D from the sun and most of us don't get enough good sunlight to get a healthy dosage. The fact is that is we live in a temperate zone on the planet, the angle of the sun striking our skin does not allow us to get enough Vit D. If you're dark skinned, you are seriously screwed.

I live in Michigan and it is known that if you live above Atlanta, Georgia there is no way to get enough sunshine in the winter months. Fair skin helps here. Sunlight hitting fair skin rapidly creates Vit D. Fair skin is a necessity in the north or south temperate regions. This is because the colder temps force people to cover up to preserve body temperature. This means the sun has less surface on which Vit D can be created. Being pale is an advantage here. Being dark, however, means that you will almost never get the needed Vit D, if you live in a cold climate.

This isn't a problem. You can go out and buy Vitamin D at your local drug store and make sure it's Vitamin D3 and not D2. Get the 2000 IU version, take two little pills a day and you should at least get up to 30 or 40. If you're, like me, dark skinned then taking 4 pills a day would get you up to 70 or 80. Who knows, this could change your luck.

Mike

PS If you continue to eat wheat, you might need a lot more since wheat, for whatever reason, tends to be antagonistic to Vitamin D.

Reduced plasma half-life of radio-labelled 25-hydroxyvitamin D3 in subjects receiving a high-fibre diet.

http://www.ncbi.nlm.nih.gov/pubmed/6299329?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum