tag:blogger.com,1999:blog-78905485353930869262024-03-14T05:01:09.779-04:00Barker's Type 2 Ketosis Prone Diabetes / Atypical Diabetes T1b/ Flatbush DiabetesThe 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.Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.comBlogger51125tag:blogger.com,1999:blog-7890548535393086926.post-14270286968917635082013-02-14T00:18:00.001-05:002013-03-31T13:39:52.328-04:00Most vegetable oils are bad for you!<div dir="ltr" style="text-align: left;" trbidi="on">
<!--[if gte mso 9]><xml>
<w:WordDocument>
<w:View>Normal</w:View>
<w:Zoom>0</w:Zoom>
<w:Compatibility>
<w:BreakWrappedTables/>
<w:SnapToGridInCell/>
<w:WrapTextWithPunct/>
<w:UseAsianBreakRules/>
</w:Compatibility>
<w:BrowserLevel>MicrosoftInternetExplorer4</w:BrowserLevel>
</w:WordDocument>
</xml><![endif]--><br />
<!--[if gte mso 10]>
<style>
/* Style Definitions */
table.MsoNormalTable
{mso-style-name:"Table Normal";
mso-tstyle-rowband-size:0;
mso-tstyle-colband-size:0;
mso-style-noshow:yes;
mso-style-parent:"";
mso-padding-alt:0in 5.4pt 0in 5.4pt;
mso-para-margin:0in;
mso-para-margin-bottom:.0001pt;
mso-pagination:widow-orphan;
font-size:10.0pt;
font-family:"Times New Roman";}
</style>
<![endif]-->
<br />
<div class="MsoNormal">
<span style="font-size: large;">I've said it before but rather than saying it again, I'm going to let this article do it for me. </span></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span style="font-size: 12.0pt;">Use of dietary linoleic acid for secondary
prevention of coronary heart disease and death: evaluation of recovered data
from the Sydney Diet Heart Study and updated meta-analysis</span></div>
<h1>
<a href="http://www.bmj.com/content/346/bmj.e8707"><span style="font-size: 12.0pt;">http://www.bmj.com/content/346/bmj.e8707</span></a></h1>
<h1>
<span style="font-size: 12.0pt; font-weight: normal; mso-bidi-font-weight: bold;">It
shows that most of the vegetable oils that we have been told are healthy not
only are not but are, in fact, harmful. If you have consistently been reading
this blog then you know I addressed this with this post some while back.</span></h1>
<h1>
<span style="font-size: 12.0pt;"><a href="http://ketosisprone.blogspot.com/2011/07/thinking-about-western-technology-food.html">http://ketosisprone.blogspot.com/2011/07/thinking-about-western-technology-food.html</a></span><span style="font-size: 12.0pt; font-weight: normal; mso-bidi-font-weight: bold;"></span></h1>
<h1>
<span style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;"><span style="font-weight: normal;"><span style="font-size: 12.0pt; font-weight: normal; mso-bidi-font-weight: bold;">I
won’t gloat. I reached my differing conclusions because as a Ketosis Prone Type
2 diabetic the advice that was given to me about health was an
unmitigated disaster. This type of diabetes, makes us the knockout mice of
diabetics. We always seem to stand outside the standard dogma and, because we
do, we point at other answers that have been obscured or forgotten. This is why
I say our type of diabetes should be studied and studied, hard. Of course, till
that day comes, you’ve still got me. ; )</span></span></span></span></h1>
<h1>
<span style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;"><span style="font-weight: normal;"><span style="font-size: 12.0pt; font-weight: normal; mso-bidi-font-weight: bold;">Anyway,
I’ve no intention of reinventing the wheel. What I’ve done is gone off and
found some very good discussions of this paper that you can read at your
leisure.</span></span></span></span></h1>
<h1>
<span style="font-size: 12.0pt;"><a href="http://stan-heretic.blogspot.com/2013/02/us-study-double-mortality-after.html">http://stan-heretic.blogspot.com/2013/02/us-study-double-mortality-after.html</a></span><span style="font-size: 12.0pt; font-weight: normal; mso-bidi-font-weight: bold;"></span></h1>
<h1>
<span style="font-size: 12.0pt;"><a href="http://barrygroves.blogspot.ca/2013/02/heart-attack-risk-in-healthy-spreads.html">http://barrygroves.blogspot.ca/2013/02/heart-attack-risk-in-healthy-spreads.html</a></span><span style="font-size: 12.0pt; font-weight: normal; mso-bidi-font-weight: bold;"></span></h1>
<h1>
<span style="font-size: 12.0pt;"><a href="http://hopefulgeranium.blogspot.co.nz/2013/02/the-results-show-that-omega-6-linoleic.html">http://hopefulgeranium.blogspot.co.nz/2013/02/the-results-show-that-omega-6-linoleic.html</a></span><span style="font-size: 12.0pt; font-weight: normal; mso-bidi-font-weight: bold;"></span></h1>
<h1>
<span style="font-size: 12.0pt;"><a href="http://anthonycolpo.com/research-update-polyunsaturated-vegetable-fats-are-not-heart-healthy/">http://anthonycolpo.com/research-update-polyunsaturated-vegetable-fats-are-not-heart-healthy/</a></span><span style="font-size: large;"><span style="font-weight: normal;"> </span></span></h1>
<h1>
<span style="font-size: large;"><span style="font-weight: normal;"> </span></span></h1>
<h1>
<span style="font-size: large;"><span style="font-weight: normal;">I want to add this brief addendum. Note that the reduction i<span style="font-size: large;">n</span> cholesterol did not change the rate of mortality.</span></span> <span style="font-weight: normal;"><span style="font-size: large;">This may<span style="font-size: large;">be the first nail in the coffin of the cholesterol hypothesis.</span></span></span></h1>
<h1>
<span style="font-weight: normal;"><span style="font-size: large;"><span style="font-size: large;">Here's some more o<span style="font-size: large;">n the same topic over at the "Heretic".</span></span></span></span></h1>
<h1>
<span style="font-weight: normal;"><span style="font-size: large;"><span style="font-size: large;"><span style="font-size: large;"><a href="http://stan-heretic.blogspot.com/2013/03/more-animal-fat-less-veg-oils-longevity.html" target="_blank">http://stan-heretic.blogspot.com/2013/03/more-animal-fat-less-veg-oils-longevity.html</a> </span> </span></span></span></h1>
<h1>
<span style="font-weight: normal;"><span style="font-size: large;"><span style="font-size: large;"> </span></span></span></h1>
</div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com15tag:blogger.com,1999:blog-7890548535393086926.post-61821361929281423742013-02-11T19:02:00.000-05:002013-02-11T19:02:04.897-05:00Ethnic minorities in the U.S. have nearly twice the risk of diabetes even with low BMI's<div dir="ltr" style="text-align: left;" trbidi="on">
<!--[if gte mso 9]><xml>
<w:WordDocument>
<w:View>Normal</w:View>
<w:Zoom>0</w:Zoom>
<w:Compatibility>
<w:BreakWrappedTables/>
<w:SnapToGridInCell/>
<w:WrapTextWithPunct/>
<w:UseAsianBreakRules/>
</w:Compatibility>
<w:BrowserLevel>MicrosoftInternetExplorer4</w:BrowserLevel>
</w:WordDocument>
</xml><![endif]--><br />
<!--[if !mso]><img src="//img2.blogblog.com/img/video_object.png" style="background-color: #b2b2b2; " class="BLOGGER-object-element tr_noresize tr_placeholder" id="ieooui" data-original-id="ieooui" />
<style>
st1\:*{behavior:url(#ieooui) }
</style>
<![endif]--><!--[if gte mso 10]>
<style>
/* Style Definitions */
table.MsoNormalTable
{mso-style-name:"Table Normal";
mso-tstyle-rowband-size:0;
mso-tstyle-colband-size:0;
mso-style-noshow:yes;
mso-style-parent:"";
mso-padding-alt:0in 5.4pt 0in 5.4pt;
mso-para-margin:0in;
mso-para-margin-bottom:.0001pt;
mso-pagination:widow-orphan;
font-size:10.0pt;
font-family:"Times New Roman";}
</style>
<![endif]-->
<br />
<div class="MsoNormal">
This came across my desk from Medscape. <a href="http://www.medscape.com/viewarticle/779072?src=nl_topic">http://www.medscape.com/viewarticle/779072?src=nl_topic</a></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
Recently, the Excellence in Diabetes 2013 conference was
held in Turkey.
One of the big statements to come out of it was this: “ type 2 diabetes,
usually associated with obesity, can occur in many seemingly thin people from
ethnic minorities.”</div>
<div class="MsoNormal">
</div>
<div class="MsoNormal">
"Diabetes risk is higher in all ethnic groups than in
whites, and of course some of this is just due to body weight, but evidence is
now building that people of many races may be at increased risk of diabetes and
cancer before they are even considered conventionally overweight."</div>
<div class="MsoNormal">
<br /></div>
Meanwhile, Chittaranjan Yajnick, MD, from King Edward Memorial Diabetes
Unit, Pune, India,
also gave a talk on what makes Indians so susceptible to diabetes. "We
have seen that Indians are often diagnosed with diabetes 10 years earlier and
5- to 10-units BMI thinner than
whites," he noted.<br />
Both believe the explanation lies in "hidden" visceral fat found
inside the body, between organs, in Asians and probably other ethnic groups
too, but not in whites. This in turn affects the levels of adipokines secreted,
such as leptin and adiponectin, which can have adverse metabolic effects.<br />
<div class="MsoNormal">
The knowledge that Asians and other ethnic groups are at
much greater risk for diseases associated with obesity, such as diabetes and
many cancers, than whites, is not new, Dr. Maskarinec explained. But more
recently, researchers have begun to show that nonwhites who are not even
particularly overweight or who are of "normal" weight are at much
higher risk than whites.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
"People have talked about some kind of adaptation for
white people, who have had a greater number of years to adjust to the type of
food we are eating now," she postulated.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
What they aren’t saying is that the connection between
weight gain and diabetes isn’t as tight as they thought. Most of all
prescriptions for holding off diabetes suggest that the key is healthy eating
and exercise. This, I think, is largely due to how Americans view being
overweight, which is strongly associated with diabetes in this country. People
become fat because they over eat and don’t exercise. It is the same old
“gluttony and<span style="mso-spacerun: yes;"> </span>sloth“ line. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
This attitude has pervaded the science as well. The first
suggestion is that thin diabetics are secret fat people. Their fat is hidden
because of its visceral nature. <span style="mso-spacerun: yes;"> </span>So the
relationship still holds even if only by the slimmest of margins.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
There is one thing which does, however, come through loud
and clear.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
Ethnic minorities that come to the U.S.
and take up the standard American diet are at a very high risk of diabetes.
There is something toxic in our food/environment that isn’t as widespread in
the rest of world. It is becoming so though as we see in the rising rates of
diabetes around the world. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
People here who aren’t part of ethnic minorities tend to
discount problem but they should view this as a “canary in a coal mine”
situation. On some level, this is affecting everyone. We really need to quit
looking at fat and start looking at what in our environment forces our bodies
to put on fat.</div>
</div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com9tag:blogger.com,1999:blog-7890548535393086926.post-47023638294032050382013-02-03T00:46:00.000-05:002013-02-03T00:46:15.049-05:00Thinking about Diabesity 3<div dir="ltr" style="text-align: left;" trbidi="on">
<!--[if gte mso 9]><xml>
<w:WordDocument>
<w:View>Normal</w:View>
<w:Zoom>0</w:Zoom>
<w:Compatibility>
<w:BreakWrappedTables/>
<w:SnapToGridInCell/>
<w:WrapTextWithPunct/>
<w:UseAsianBreakRules/>
</w:Compatibility>
<w:BrowserLevel>MicrosoftInternetExplorer4</w:BrowserLevel>
</w:WordDocument>
</xml><![endif]--><br />
<!--[if !mso]><img src="//img2.blogblog.com/img/video_object.png" style="background-color: #b2b2b2; " class="BLOGGER-object-element tr_noresize tr_placeholder" id="ieooui" data-original-id="ieooui" />
<style>
st1\:*{behavior:url(#ieooui) }
</style>
<![endif]--><!--[if gte mso 10]>
<style>
/* Style Definitions */
table.MsoNormalTable
{mso-style-name:"Table Normal";
mso-tstyle-rowband-size:0;
mso-tstyle-colband-size:0;
mso-style-noshow:yes;
mso-style-parent:"";
mso-padding-alt:0in 5.4pt 0in 5.4pt;
mso-para-margin:0in;
mso-para-margin-bottom:.0001pt;
mso-pagination:widow-orphan;
font-size:10.0pt;
font-family:"Times New Roman";}
</style>
<![endif]-->
<br />
<div class="MsoNormal">
These “Thinking about “ pieces are my highly speculative way
of working out diabetes <span style="mso-spacerun: yes;"> </span>using the KPT2
perspective, right now I’m wondering about obesity and whether it really is
what we’ve been told it is.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<span class="vcard"><a href="http://asweetlife.org/author/robert/" title="Robert Scheinman">Robert
Scheinman</a></span> on <a href="http://asweetlife.org/" title="Go to A Sweet Life.">A Sweet Life</a> 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. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.<span style="mso-spacerun: yes;"> </span>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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<a href="http://ketosisprone.blogspot.com/2010/06/increased-weight-and-insulin-resistance.html">http://ketosisprone.blogspot.com/2010/06/increased-weight-and-insulin-resistance.html</a></div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
This situation continued until eventually the people
relapsed. Their blood sugars rose sharply<span style="mso-tab-count: 1;"> </span>.
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
I’m using blood sugars here but what is body putting on fat in
response to?<span style="mso-spacerun: yes;"> </span>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. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
This carrying capacity runs largely between the two poles of
skeletal muscle<span style="mso-spacerun: yes;"> </span>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. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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 <span style="mso-spacerun: yes;"> </span>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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
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.</div>
</div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com22tag:blogger.com,1999:blog-7890548535393086926.post-137771662922517262012-12-31T17:04:00.000-05:002012-12-31T17:04:27.849-05:00Traditional foods ... again<div dir="ltr" style="text-align: left;" trbidi="on">
<span style="font-size: large;"><span style="font-size: small;">This popped up a few days ago and is very much in line with what I<span style="font-size: small;">'ve been saying about diet and food. <b><span style="font-size: small;"></span></b><a href="http://ketosisprone.blogspot.com/2011/07/thinking-about-western-technology-food.html" target="_blank">Here.</a></span></span></span><br />
<span style="font-size: small;"> </span><br />
<span style="font-size: small;">This is a study done in Lebanon (KPD is well-documented in the Middle East).<span style="font-size: small;"> It should be <span style="font-size: small;">noted that there was one other diet that was examined <span style="font-size: small;">but it showe<span style="font-size: small;">d <span style="font-size: small;">no association with diabetes. This diet <span style="font-size: small;">would be close to a low car<span style="font-size: small;">b diet.</span></span></span></span></span></span></span></span><br />
<br />
<br />
<span style="font-size: large;"><b>The findings of this study demonstrate direct associations of the Refined Grains &
Desserts and Fast Food patterns with T2D and an inverse association between the Traditional
Lebanese pattern and the disease among Lebanese adults. </b></span><br />
<a href="http://www.nutritionandmetabolism.com/content/9/1/111/abstract" target="_blank">Dietary patterns and odds of Type 2 diabetes in Beirut, Lebanon: a case - a case study</a><br />
<br />
<span style="font-size: small;">What should be <span style="font-size: small;">noted is that this diet maybe safe now but it too is subject to the substitu<span style="font-size: small;">tion of ingredients as well so complacency, as regards ones diet, should be guarded against.</span></span></span><br />
<br />
<br /></div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com4tag:blogger.com,1999:blog-7890548535393086926.post-89446954442747274342012-12-31T02:14:00.000-05:002012-12-31T13:10:58.624-05:00Diabesity 2<div dir="ltr" style="text-align: left;" trbidi="on">
<div dir="ltr" style="text-align: left;" trbidi="on">
<br /></div>
<b>This is my rant taking my type of diabetes as the major form in the world. I make no apologies to anyone. We are forgotten but we are important because it gives a view of diabetes that is different and necessary.</b><br />
<br />
Diabetes is ultimately caused by the failure of the immune system due to inflammations introduced by environmental toxicity. An environment is toxic if it does not support the health of an organism. This can be toxins that are viral, bacterial, physical or chemical and it may also be the case that the environment is toxic if it doesn’t supply the necessary components for health. It is also true that almost anything can be toxic above a certain threshold. This is where long term genetic adaptation comes in.<br />
<br />
Over time a successful organism will change in ways to suit that environment. It will develop the mechanisms to recognize then offset or neutralize toxins. What is important is the very systems that must cooperate are in some ways disrupted and can not complete their functions leading to more inflammation and less cooperation. We see autoimmune diseases, sensitivities and deficiencies as part of this.<br />
<br />
The net effect of this is a some what continuous suboptimal functioning which forces the body to compensate. The outcome of all this is what we call “diabetes”.
There are all kinds of toxins out there but the one I’m going to concentrate on has to do with diet.<br />
<br />
Why diet, two things: diseases of civilization and obesity.
“Diseases of civilization” have been noted for centuries and is caused when some previously unexposed culture adopts our diet. This occurred largely before we had the scientific sophistication to develop most of the chemicals that people say plague our environment today. It also precedes the wide spread manipulation of foods, both plants and animals, by industrial systems to increase yields and profits. The rise of diabetes and obesity seem to be moving hand in hand. Weight gain, no matter whatever else it is about, is about eating and eating is the port of our major exposure to the environment.<br />
<br />
I was an athlete and many of the people I’ve corresponded with were as well. A change of less workouts, for whatever reasons, but still the same eating pattern turned quickly into the abrupt onset of diabetes. How can you go quickly from athleticism to diabetes? On the face of it, this would seem impossible but it isn’t. It very simply takes 6 months and a person can be DKA, if they continue on their same diet, which has been the accepted healthy diet.<br />
<br />
One of the reasons for this is that muscle does not protect against high blood sugars as well as fat.
The continual insult to endocrine tissues does not abate. When a person has finished a work out and carbohydrates loads, once the muscles have taken up all they can, the body will evince higher blood sugars that will continue until the next round of exercise. This is a creeping effect, continual insult but with most of the blood sugar problem generally being contained by the consistent exercise of muscle. This will keep the blood sugars down most of the time but will not ameliorate the effects of the continual inflammation of endocrine and other tissues.<br />
<br />
Maybe, at one time this would occur but this is inflammation. Continual exercise keeps the dog from the door but never reduces the effects of inflammation that has already been introduced. It is still there and all the disruptions in signals between the organs is still present due to the continual post prandial challenges and, probably, other continual environmental challenges
</div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com5tag:blogger.com,1999:blog-7890548535393086926.post-88186293109951197772012-11-28T20:57:00.000-05:002012-11-28T20:57:15.922-05:00The KPT2 point of view of Diabesity Pt 1<div dir="ltr" style="text-align: left;" trbidi="on">
<!--[if gte mso 9]><xml>
<w:WordDocument>
<w:View>Normal</w:View>
<w:Zoom>0</w:Zoom>
<w:Compatibility>
<w:BreakWrappedTables/>
<w:SnapToGridInCell/>
<w:WrapTextWithPunct/>
<w:UseAsianBreakRules/>
</w:Compatibility>
<w:BrowserLevel>MicrosoftInternetExplorer4</w:BrowserLevel>
</w:WordDocument>
</xml><![endif]--><br />
<!--[if !mso]><img src="//img2.blogblog.com/img/video_object.png" style="background-color: #b2b2b2; " class="BLOGGER-object-element tr_noresize tr_placeholder" id="ieooui" data-original-id="ieooui" />
<style>
st1\:*{behavior:url(#ieooui) }
</style>
<![endif]--><!--[if gte mso 10]>
<style>
/* Style Definitions */
table.MsoNormalTable
{mso-style-name:"Table Normal";
mso-tstyle-rowband-size:0;
mso-tstyle-colband-size:0;
mso-style-noshow:yes;
mso-style-parent:"";
mso-padding-alt:0in 5.4pt 0in 5.4pt;
mso-para-margin:0in;
mso-para-margin-bottom:.0001pt;
mso-pagination:widow-orphan;
font-size:10.0pt;
font-family:"Times New Roman";}
</style>
<![endif]-->
<br />
<div class="MsoNormal">
Recently, I was at a diabetes conference representing the Michigan Minority Health Coalition. There were many
presentations that dealt with ways to slow or reverse the diabetes epidemic.
Typically, they involved ways to get people to control what they ate and
getting exercise. I was sitting with a group of researchers and they,
unfortunately, asked me what I thought. I went on my usual depressing rant.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
I’m not seeing any of this as being useful and the data
seems to bear me out. Diabetes continues to increase across the US.
We are pouring more time and resources into it with little or no effect.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
One of the reasons for my negativity is that Ketosis Prone
Type 2 diabetes seems to contradict most of the standard wisdom we know about
diabetes.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
First of we are the Type 2’s that can and do go DKA. Though
people think of us as relatively rare, we are increasingly being recognized as
a problem in emergency medicine as we force the costs of treatment up
worldwide..</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
Not only do we go DKA, we also can go into remission. Taking
no medications just simply using diet, some exercise and no weight loss, we can
return to near normal blood sugars for years.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
What is even odder about this DKA and remission is how close
they occur together. Two weeks after a DKA episode, where blood sugar readings
were nearly off the charts, the person can start experiencing hypos. Remember, KPT2
is classified by the ADA as a Type
1, specifically Type 1b. Yet, typically after six months, the person doesn’t
even need insulin or much of anything else. As I’ve noted in previous posts,
this recovery is much too fast to be attributed to beta cell regeneration. Even
if you are inclined to believe that there might be super fast regeneration, I
detail in past posts, how I was able to manipulate my pancreatic output in days
by taking an anti-inflammatory. </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
It is well documented that weight is not a major factor. In
fact, KPT2s who are overweight do better
than those who have, so called “healthy weights”. It is obvious that the last
recommendation that a doctor would make is for that person to lose weight.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
What if we were the prevalent diabetes of the world. How
would the rules be different? </div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
Stay tuned for part 2.</div>
</div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com6tag:blogger.com,1999:blog-7890548535393086926.post-23402406015246120792012-10-03T15:35:00.000-04:002012-12-31T13:35:22.602-05:00Recognition for KPT2D<div dir="ltr" style="text-align: left;" trbidi="on">
<br />
<div class="MsoNormal">
It’s been a bit of a while since I wrote on this blog. It
isn’t that I’ve lost interest but it seems as if the world has. I continually
monitor for papers on it but there really isn’t much.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
I have taken the view that this blog is not personal but is
a way of gathering as much scientific and medical information as possible on
KPD so that sufferers and their friends and family will have a source to
explore and maybe gain hope or understanding.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
I present this information in this light. This is from the
Diabetes in Control Mastery Series. It is based on the work of researchers out
of <st1:place><st1:city>Athens</st1:city>, <st1:country -region="-region">Greece</st1:country></st1:place>.
The book is about diabetic emergencies but it takes the time to illuminate KPD
because of its recognition as a large component in the rising rate of DKA
worldwide.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
There isn’t one word here that you won’t find in this blog.
It is, however, important, that we get recognition anyway we can. This sort
of thing, hopefully, will bring more money and more research.</div>
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
<a href="http://www.diabetesincontrol.com/diabetes-in-control-newsletters/dcms-99">http://www.diabetesincontrol.com/diabetes-in-control-newsletters/dcms-99</a></div>
</div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com6tag:blogger.com,1999:blog-7890548535393086926.post-10163240993303072262011-09-06T02:20:00.006-04:002011-12-21T12:35:11.861-05:00Thinking about: Western technology, food and the health of people of color and world food production and trade.<div dir="ltr" style="text-align: left;" trbidi="on">
<div class="separator" style="clear: both; text-align: center;">
</div>
<br />
<div class="MsoNormal">
<span class="apple-style-span"><span style="background-attachment: initial; background-clip: initial; background-color: whitesmoke; background-image: initial; background-origin: initial; color: black; font-family: 'Trebuchet MS', sans-serif; font-size: 13.5pt; line-height: 115%;">I've added, what I think, is an important addition to this post. If you've read this already just skip to the bottom.</span></span><span style="background-attachment: initial; background-clip: initial; background-color: whitesmoke; background-image: initial; background-origin: initial; color: black; font-family: 'Trebuchet MS', sans-serif; font-size: 13.5pt; line-height: 115%;"><br />
<br />
<span class="apple-style-span">Guess whose back? Me! I've finished my latest assignment so it's back to KPD or abrupt type 2 diabetes; however you wish to look at it.</span><br />
<br />
<span class="apple-style-span">I was working down in Southwest Detroit (One of the few multicultural areas there.) and I was looking at many of the people walking around and many of them were heavy. The thing about this area is that it isn't a "food desert" there are plenty of stores with many types of produce. This is also a working class area so most people do work that requires a certain amount of physical effort. Yet the story remains the same, way too much weight and with all the problems that this portends.</span><br />
<br />
<span class="apple-style-span">One of the things that helped to keep this in mind was looking at the stats on this blog while I was away. <a href="http://ketosisprone.blogspot.com/2010/02/western-diet-implicated-in-african.html"><span style="text-decoration: none;">This blog</span></a> in particular seemed to be getting a lot of those hits. I tried to address this issue further while I was away with <a href="http://ketosisprone.blogspot.com/2011/02/contamination-of-traditional-foods.html"><span style="text-decoration: none;">this blog</span></a>. Now I want to go back again and try to put this all a little more together.</span><br />
<br />
<span class="apple-style-span">In the last thirty years diabetes appears to be surging both in the US and around the world and it seems to affect people of color disproportionately.</span></span></div>
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgeSNMkacofpem9aygRcOHtrMaBNQeb0xJiAG7yI-vOUQ7hWgj2JQc-IgdZ76v_LWRnQ2sB-uBpVS5iIuhorR59Bxrq5Lx4gkhXiML9uzSj_p-YLgrBvMLre38vzk6EQiKDuYGbURyDbMQ/s1600/fNumber1.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="460" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgeSNMkacofpem9aygRcOHtrMaBNQeb0xJiAG7yI-vOUQ7hWgj2JQc-IgdZ76v_LWRnQ2sB-uBpVS5iIuhorR59Bxrq5Lx4gkhXiML9uzSj_p-YLgrBvMLre38vzk6EQiKDuYGbURyDbMQ/s640/fNumber1.gif" width="640" /></a></div>
<br />
<div class="separator" style="clear: both; text-align: center;">
</div>
<br />
You should look at this graph very carefully. Something happened after 1990. One of them is probably a statistical fluke having to do with the change in what is considered diabetic or the fact that the US baby boomer population is entering its mature years but you would expect for that to flatten out eventually. It hasn't.<br />
<br />
Here's another fact to consider. Diabetes is a chronic disease that develops overtime. How long this period of time is varies. Even in the case of Abrupt onset T2, there appears to be a long lag before our type of diabetes becomes full blown. You can view that <a href="http://ketosisprone.blogspot.com/p/central-graph-for-understanding-abrupt.html">here</a>. My point is that viewing the take off point of diabetes isn't enough. We have to look at the preceding years and what might have occurred in them, if we wish to see some turning point.<br />
<br />
The time frame we're looking at is about 30 to 40 years and frankly there are plenty of changes that have occurred in this time that could be correlated with this sudden take off in diabetes. This is diabetes, however, and the dog that hunts best here, at least for me, is diet.<br />
<br />
I've talked about the contamination of traditional foods before. <a href="http://ketosisprone.blogspot.com/2011/02/contamination-of-traditional-foods.html">Here</a>. You could look at this post as an expansion of that post. My point was that due to economics the constituents of foods around the world are being replaced with cheaper products that I think are problematic.<br />
<br />
First up: wheat. Wheat has been around for years. It was first domesticated around the Fertile Crescent and this wheat is Emmer. Later on with get Eichorn wheat and a host of other varieties. Wheat has been bred and bred through out the years for all types of qualities. It has become one of the central characters in the diseases of civilization. Take a normal healthy society of humans and introduce them to flour and problems tend to arise. Denise Minger on her <a href="http://rawfoodsos.com/2010/09/02/the-china-study-wheat-and-heart-disease-oh-my/">blog</a> statistically demonstrates a strong correlation between wheat and cardiovascular disease. What should be even more worrying is that 99% of all wheat is of one kind, the dwarf wheat variety. Many people have pointed to this variety as having toxic properties especially as relates to blood sugars. Anecdotally, I've read where people have tried Eikhorn wheat and found no big jump in blood sugars.<br />
<br />
My standard answer to any ketosis prone diabetic is to give up wheat. It really doesn't matter what their symtoms are. I say, "Give up wheat." and if they do they always feel better after a month. It makes me appear as if I know what I talking about.The truth of the matter is the giving up of wheat seems to always ease physical problems. Give it a try.<br />
<br />
What this has to do with traditional foods is the fact that, due to global trade, a cheaply produced product is easily substituted for a more traditional product that tends to be more expensive. The more plentiful that cheap product is; the more likely it will be used as a substitute. Dwarf Wheat became the dominant variety starting in the late 70's. Unless that traditional food is tightly regulated such as Fasso wheat in Italy, it is more than likely <a href="http://www.medpedia.com/news_analysis/68-The-Heart-Scan-Blog/entries/62642-Heroin-Oxycontin-and-a-whole-wheat-bagel">Dwarf Wheat</a>. <a href="http://www.ncbi.nlm.nih.gov/pubmed/19013359">More Dwarf Wheat</a> If you look at our chart, it was just in time for our diabetes epidemic.<br />
<br />
On to seed oils. These have been around since the start of agriculture but except for a few cases like olive oil they could not be produced in great quantity until we had the industrial techniques to do so. These are what we call vegetable oils.<br />
<br />
Here's some nice charts.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="http://images.quickblogcast.com/8/9/8/7/3/147167-137898/oilsomega6chart.png?a=17" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="624" src="http://images.quickblogcast.com/8/9/8/7/3/147167-137898/oilsomega6chart.png?a=17" width="640" /></a></div>
````````````````````````````````````````````````````````````````````````````````````````````````````````````````````````<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEifC7dW1OnSeW1GUXtHgSNPR3Kz-s1cx79EoK2uqezlD32HSZegNl8SP7FWFK5Pm3_iTR2lzR48ro0DLuZMM9-nU8sT-G7NeEr8KJoBtUSfT-GTQsSQKXJ8E2tymd8OwVv-prtXT9-YeKf9/s1600/u_s_pufa_consumption,_1909-2005.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="454" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEifC7dW1OnSeW1GUXtHgSNPR3Kz-s1cx79EoK2uqezlD32HSZegNl8SP7FWFK5Pm3_iTR2lzR48ro0DLuZMM9-nU8sT-G7NeEr8KJoBtUSfT-GTQsSQKXJ8E2tymd8OwVv-prtXT9-YeKf9/s640/u_s_pufa_consumption,_1909-2005.png" width="640" /></a></div>
So what are these graphs about? This is about fats particularly polyunsaturated fats. These typically come from seeds that are processed to get the oil out of them. The fats obtained from seeds tends to be mostly Omega -6's. The body uses Omega-6's and Omega-3's as building blocks. The problem is that the body doesn't distinguish between the two. This really wasn't necessary because in nature they would generally be found in roughly a 1 to 1 ratio. Thanks to modern technology, this has changed. The consumption of seed oils has continues to climb so much so that the ratio is now guessed to be between 10:1 to 25:1. Well what of it?<br />
<br />
As noted before, the body does not distinguish much between these two fatty acids. If the body is taking in 6's when it should be taking in 3's then the building blocks for a healthy body are wrong. It sets up a situation of chronic inflammation. This is from Wikipedia.<br />
<br />
<span class="Apple-style-span" style="font-family: sans-serif; font-size: 13px; line-height: 19px;"></span><br />
<div style="line-height: 1.5em; margin-bottom: 0.5em; margin-left: 0px; margin-right: 0px; margin-top: 0.4em;">
Some medical research suggests that excessive levels of certain <i>n</i>−6 fatty acids, relative to certain <a href="http://en.wikipedia.org/wiki/Omega-3_fatty_acid" style="background-attachment: initial; background-clip: initial; background-color: initial; background-image: none; background-origin: initial; background-position: initial initial; background-repeat: initial initial; color: #0645ad; text-decoration: none;" title="Omega-3 fatty acid"><i>n</i>−3 (Omega-3) fatty acids</a>, may increase the probability of a number of diseases.<sup class="reference" id="cite_ref-Lands2005_0-0" style="font-style: normal; font-weight: normal; line-height: 1em;"><a href="http://en.wikipedia.org/wiki/Omega-6_fatty_acid#cite_note-Lands2005-0" style="background-attachment: initial; background-clip: initial; background-color: initial; background-image: none; background-origin: initial; background-position: initial initial; background-repeat: initial initial; color: #0645ad; text-decoration: none; white-space: nowrap;">[1]</a></sup><sup class="reference" id="cite_ref-Hibbeln2006_1-0" style="font-style: normal; font-weight: normal; line-height: 1em;"><a href="http://en.wikipedia.org/wiki/Omega-6_fatty_acid#cite_note-Hibbeln2006-1" style="background-attachment: initial; background-clip: initial; background-color: initial; background-image: none; background-origin: initial; background-position: initial initial; background-repeat: initial initial; color: #0645ad; text-decoration: none; white-space: nowrap;">[2]</a></sup><sup class="reference" id="cite_ref-Okuyama2007_2-0" style="font-style: normal; font-weight: normal; line-height: 1em;"><a href="http://en.wikipedia.org/wiki/Omega-6_fatty_acid#cite_note-Okuyama2007-2" style="background-attachment: initial; background-clip: initial; background-color: initial; background-image: none; background-origin: initial; background-position: initial initial; background-repeat: initial initial; color: #0645ad; text-decoration: none; white-space: nowrap;">[3]</a></sup></div>
<div style="line-height: 1.5em; margin-bottom: 0.5em; margin-left: 0px; margin-right: 0px; margin-top: 0.4em;">
Modern Western diets typically have ratios of <i>n</i>−6 to <i>n</i>−3 in excess of 10 to 1, some as high as 30 to 1. The optimal ratio is thought to be 4 to 1 or lower.<sup class="reference" id="cite_ref-daley2004_3-0" style="font-style: normal; font-weight: normal; line-height: 1em;"><a href="http://en.wikipedia.org/wiki/Omega-6_fatty_acid#cite_note-daley2004-3" style="background-attachment: initial; background-clip: initial; background-color: initial; background-image: none; background-origin: initial; background-position: initial initial; background-repeat: initial initial; color: #0645ad; text-decoration: none; white-space: nowrap;">[4]</a></sup><sup class="reference" id="cite_ref-simopoulos2002_4-0" style="font-style: normal; font-weight: normal; line-height: 1em;"><a href="http://en.wikipedia.org/wiki/Omega-6_fatty_acid#cite_note-simopoulos2002-4" style="background-attachment: initial; background-clip: initial; background-color: initial; background-image: none; background-origin: initial; background-position: initial initial; background-repeat: initial initial; color: #0645ad; text-decoration: none; white-space: nowrap;">[5]</a></sup></div>
<div style="line-height: 1.5em; margin-bottom: 0.5em; margin-left: 0px; margin-right: 0px; margin-top: 0.4em;">
Excess <i>n</i>−6 fats interfere with the health benefits of <i>n</i>−3 fats, in part because they compete for the same rate-limiting enzymes. A high proportion of <i>n</i>−6 to <i>n</i>−3 fat in the diet shifts the physiological state in the tissues toward the pathogenesis of many diseases: prothrombotic, proinflammatory and proconstrictive.<sup class="reference" id="cite_ref-simopoulos2003_5-0" style="font-style: normal; font-weight: normal; line-height: 1em;"><a href="http://en.wikipedia.org/wiki/Omega-6_fatty_acid#cite_note-simopoulos2003-5" style="background-attachment: initial; background-clip: initial; background-color: initial; background-image: none; background-origin: initial; background-position: initial initial; background-repeat: initial initial; color: #0645ad; text-decoration: none; white-space: nowrap;">[6]</a></sup></div>
<div style="line-height: 1.5em; margin-bottom: 0.5em; margin-left: 0px; margin-right: 0px; margin-top: 0.4em;">
Chronic excessive production of <i>n</i>−6 eicosanoids is associated with heart attacks, thrombotic stroke, arrhythmia, arthritis, osteoporosis, inflammation, mood disorders, obesity, and cancer.</div>
<span class="Apple-style-span" style="font-family: sans-serif; font-size: 13px; line-height: 20px;">Here's a listing of the Omega 6 amounts in some of the most used seed oils.</span><br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhuCsZPsEvnoXYBQu11mMd1sIObYyI_sqAMXL7QJGhBK0ZaovljFgRm2b1sH1XuU8-LUEhgB4VOzRv_Xm5Rrf0FNyRW_13XrngIggkiUyLu9FT3s_PjeKkjZsqn_LZiEeNCgE95bTcRpEA/s1600/efacontentoils.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="350" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhuCsZPsEvnoXYBQu11mMd1sIObYyI_sqAMXL7QJGhBK0ZaovljFgRm2b1sH1XuU8-LUEhgB4VOzRv_Xm5Rrf0FNyRW_13XrngIggkiUyLu9FT3s_PjeKkjZsqn_LZiEeNCgE95bTcRpEA/s400/efacontentoils.png" width="400" /></a></div>
<div class="separator" style="clear: both; text-align: center;">
<br /></div>
<br />
Most of these oils are not bought by people for consumption. They, for the most part, are used in the preparation of foods because they are cheap. Just imagine if your traditional food now made with flour from Dwarf Wheat is cooked in Soy oil.<br />
<div>
<br /></div>
<div>
I was going to throw sugar in this overlong post but if you don't know about that then nothing I'm going to say here is going to change things. I will say this that once again cost is driving cheap substitutes like high fructose corn syrup into more and more foods.</div>
<div>
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="http://www.sweetsurprise.com/sites/default/files/SweetenerConsumption2010.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="302" src="http://www.sweetsurprise.com/sites/default/files/SweetenerConsumption2010.jpg" width="400" /></a></div>
<div>
<br /></div>
<div>
<br /></div>
<div>
Look back up at the graphs. Look at the times. Does it seem as if we are doing something in our diets that have led to our present problems?</div>
<div>
<br /></div>
<div>
Now back to the problems of people of color and this quiet but possibly toxic mix that has invaded their foods. If we once again look at a graph of the A1c's of KPD's we see a long running period of elevated A1c's.</div>
<div>
<br /></div>
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiDb7XQ_L3_3lD0WlgwS16NEgrxyITF-mlSwXKbeWN6WGJg-9drwmst_WeM2vfn9fZ8Gtab_HCCEhShwlaZMf_CkdNTMQFWu25WKokHvKxHI-2ftj83RTEQRtgGO_YuNzKyZ0F1X5xcch0/s1600/weight+A1c+graphs_26526_image002.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="418" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiDb7XQ_L3_3lD0WlgwS16NEgrxyITF-mlSwXKbeWN6WGJg-9drwmst_WeM2vfn9fZ8Gtab_HCCEhShwlaZMf_CkdNTMQFWu25WKokHvKxHI-2ftj83RTEQRtgGO_YuNzKyZ0F1X5xcch0/s640/weight+A1c+graphs_26526_image002.gif" width="640" /></a></div>
<div>
<br />
Normal A1c's should be around 5. These hover at about 6.3 month after month before taking off. I suggest that what we're seeing is inflammation caused by dietary components that over time essentially</div>
<div>
damage our bodies. I'm thinking that these elevated numbers are due to a low level hyperglycemia that is a reaction to chronic infection. In this case, I once again bring up the hypothalamus which is an active part of this system and is susceptible to malfunction due to high blood sugar. </div>
<div>
<br /></div>
<div>
Remember, we are already prone to problems with dealing with carbohydrates, if you throw some fructose in there and cause the liver problems then you can be well on your way to DKA even with a traditional diet.</div>
<div>
<br /></div>
<div>
We are looking at economics possibly overwhelming good sense. Cheap food additives produced thousands of miles away are quietly replacing the traditional healthy foods. I would say simply eat whole foods but under what conditions was this food raised?You should be reading labels on anything that is manufactured but do you know what you're seeing. Did you know that the "emulsifiers" you now see on labels is more than likely a transfat? Once again I make my usual plea. Get a meter and test the foods that you and your family eats.<br />
<br />
This is an addendum to this post. I started thinking that the key to much of what I have said is food production and the trade in food products. A little research found me this graph.<br />
<br />
<div class="separator" style="clear: both;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgNm7wJRs_ip9yFcnQPuShIPXcnEuWjRHMbJ7yE56bKsdYnnD0lr8MIySAGb6Mm_8GsDHpUcfO0-Wgkap1-ntGWGO5_1XVtDqf020Y6DanPsifBHop9pZMZsi18j9rYiKDfmQiL1F7vzNM/s1600/worldagriculturetrade.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="640" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgNm7wJRs_ip9yFcnQPuShIPXcnEuWjRHMbJ7yE56bKsdYnnD0lr8MIySAGb6Mm_8GsDHpUcfO0-Wgkap1-ntGWGO5_1XVtDqf020Y6DanPsifBHop9pZMZsi18j9rYiKDfmQiL1F7vzNM/s640/worldagriculturetrade.jpg" width="547" /></a></div>
<br />
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgNm7wJRs_ip9yFcnQPuShIPXcnEuWjRHMbJ7yE56bKsdYnnD0lr8MIySAGb6Mm_8GsDHpUcfO0-Wgkap1-ntGWGO5_1XVtDqf020Y6DanPsifBHop9pZMZsi18j9rYiKDfmQiL1F7vzNM/s1600/worldagriculturetrade.jpg"></a><a href="http://maps.grida.no/go/graphic/trends-in-world-agricultural-exports">http://maps.grida.no/go/graphic/trends-in-world-agricultural-exports</a><br />
<br />
<a href="http://maps.grida.no/go/graphic/trends-in-world-agricultural-exports"></a>Once again I ask you to look back at the graph of the growth of diabetes. The growth of trade takes off at about 1986. Ten years later in about 1996 diabetes takes off as well and both increase rapidly from there to the present. I don't see this being explained by ideas of food palatability though there is certainly some of that there, nor do I see genetics or behavior explaining this either. Food has not got that much better tasting. Certainly genetics hasn't changed that much and I doubt we have become less industrious in the entire world in the last forty years. This last graph suggests to me that we have done something in the production of our foods that is metabolically traumatic. I well know that correlation is not causation but there seems to be something here and all I can do is nibble around the edges. This calls for a better mind than mine or more specifically some one like a <a href="http://healthcorrelator.blogspot.com/">Ned Kock</a> who could possibly tease out what might be going on here.<br />
<div class="separator" style="clear: both;">
<br /></div>
<div class="separator" style="clear: both;">
One could say that this is simply the usual "diseases of civilization" but one has to answer the question "Why does this occur now?". </div>
<br />
I'm at Michigan State University, where some of the best agricultural scientists in the world do their work and though I'm not at liberty to divulge any specifics, world food production is about to seriously take off in the next 10 years. The tests that I have seen suggests we could see a doubling to quadrupling of food production. In other words, an end to famine. More food is good but what if the food isn't?</div>
</div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com5tag:blogger.com,1999:blog-7890548535393086926.post-50134709902642266242011-08-04T19:00:00.000-04:002012-12-02T18:15:17.922-05:00Chinese study on Ketosis Prone T2 Diabetes<div dir="ltr" style="text-align: left;" trbidi="on">
This is for our Chinese KPD's. Here's a study presently recruiting KPD's in China. <a href="http://apps.who.int/trialsearch/trial.aspx?TrialID=ChiCTR-ECC-00000063">Chinese KPT2D Trial</a> One of it's big novel features is that it's recruiting both lean and obese KPD's. This isn't one of those studies showing that KPDM exists in a given population. They quite clearly know it exists. This study is meant to try and understand it.<br />
<br />
This is one of the things I've been waiting for. Most of the research on KPD research has been done in the US and Europe even the studies done in African have mostly been carried out by Europeans. What I've been waiting for is for the third world to start picking up the research and expanding it. This is, after all, a growing problem in their countries.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
</div>
Here it is buried in both bad science and a majority culture which largely ignores it. I talk to Blacks, Hispanics and Native Americans and all of them get this big surprised face when I talk about a diabetes that is prominent in peoples of color in the US.<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
</div>
I am especially perturbed by the advice given them by their local medical people. These people have no idea about this and so treat it just like a regular type 2, type 1 or LADA. This is probably one of the reasons DKA's have doubled in the last thirty years in the US.<br />
<br />
<img alt="Graph showing Number (in Thousands) of Hospital Discharges with Diabetic Ketoacidosis as First-Listed Diagnosis, United States, 1980-2005. Links for data figures, sources, methodology and data limitations, and detailed tables follow this figure." height="460" src="http://www.cdc.gov/diabetes/statistics/dkafirst/fNumber.gif" width="640" /><br />
<br />
Good for you China and let's hope the rest of the world gets going too.</div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com22tag:blogger.com,1999:blog-7890548535393086926.post-71563106759982020282011-04-18T19:03:00.001-04:002011-04-18T21:09:00.257-04:00Caution on NSAIDS<div dir="ltr" style="text-align: left;" trbidi="on">I've pointed out a NSAID as the drug I was using to effect my 1st phase insulin response but anyone who is thinking about trying this should be aware of the risks involved. Beyond the usual issues of stomach and intestinal distress, there are other issues. You can read about many of them here. <a href="http://diabetesupdate.blogspot.com/2009/04/go-easy-on-advil-motrin-ibuprofen-etc.html">Jenny's Blood Sugar 101</a><br />
<br />
One thing that she doesn't cover is that NSAIDs are <b>NOT </b>recommended for those who are G6PD deficient because of the chance of hemolytic anemia. If you've been reading this blog you should know that KPD's have a very high rate of this deficiency. So I do urge caution in their use.</div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com18tag:blogger.com,1999:blog-7890548535393086926.post-76174206097835407352011-04-11T20:49:00.002-04:002011-04-18T18:47:26.470-04:00How I got normal blood sugars for 60 cents a week<div dir="ltr" style="text-align: left;" trbidi="on"><span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><br />
</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;">Being that I'm still on assignment, I've decided to let you in on the experiment that I did on myself to try to understand the nature of Ketosis Prone Type 2 diabetes or as I call it Abrupt onset type 2 diabetes.</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><br />
</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;">Okay, a bit of a review. Ketosis prone type 2 diabetes is an abrupt onset <b>type 2 </b>diabetes though highly prevalent in people of color it can and does pop up in any group. The fact is that KPDM is actually a subset of this form of diabetes. I know LADA's that have gone DKA. There is a real question in my mind whether Abrupt onset T2 (AOT2) is a type of diabetes or simply a mechanism through which diabetes is expressed.</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><br />
</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;">At any rate, this is a diabetes that comes on very strong because the body simply quits producing insulin. It is therefore classified as a type 1 diabetes, T1b. It comes out of nowhere. In 6 months time a person can go from near normal blood sugars to DKA. I talk about this process in these posts. </span><span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://ketosisprone.blogspot.com/search/label/relapse">Relapse</a></span><br />
<br />
It has also been shown to vanish just as quickly, if handled correctly. In the space of a year, a person can go from near normal blood sugars to close to death from DKA and then back again. This not a regular diabetes and so far has failed serious classification. It is so fantastical that most people don't know it exists, even those most susceptible to it such as people of Latin, African and Asian descent.<br />
<br />
I, however, got lucky. About six months ago, I found myself with a revived 1st phase insulin response. I wasn't content with this. I had to find out what happened and how this could be and I kept experimenting until I not only found it but was able to manipulate it. I could turn it off and on with a simple manipulation. You can read about this process through this link, <span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://www.diabetesforums.com/forum/type-2-diabetes/55941-getting-1st-phase-insulin.html">This is a dialogue on diabetesforums where I talk about this experiment</a></span><br />
<br />
Here are some of the citations that I dug up to back up what I believed to be the cause of my suddenly restored 1st phase insulin response.<br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://www.springerlink.com/content/956hm125155q7486/"> Non-steroidal anti-inflammatory drugs increase insulin release from beta-cells by inhibiting atp-sensitive potassium channel</a></span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><br />
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1401608/pdf/brjclinpharm00211-0073.pdf"> EFFECT OF NAPROXEN ON GLUCOSE METABOLISM AND TOLBUTAMIDE KINETICS AND DYNAMICS IN MATURITY ONSET DIABETICS</a></span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://www.springerlink.com/content/956hm125155q7486/" rel="nofollow" style="color: #417394; text-decoration: none;" target="_blank"></a></span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211567/">Effect of selective cyclooxygenase-2 (COX-2) inhibitor treatment on glucose-stimulated insulin secretion in C57BL/6 mice</a></span><br />
<br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1752-8062.2008.00026.x/abstract">Use of Salsalate to Target Inflammation in the Treatment of Insulin Resistance and Type 2 Diabetes</a></span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: x-small;"><br />
</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://www.tinsal-t2d.org/t2d.php?pg=0">Targeting INflammation using SALsalate for Type 2 Diabetes.</a></span><br />
<br />
<a href="http://www.theannals.com/cgi/content/abstract/44/7/1207">Potential Role of Salicylates in Type 2 Diabetes</a><br />
<br />
This got me to thinking about KPDM and its quick rise and fall which you can read here. <a href="http://ketosisprone.blogspot.com/2010/11/abrupt-type-2-diabetes-onset-and-1st.html">Here</a><br />
<br />
Now you know. It was a NSAID called Sodium Naproxen taken as needed. The net cost was about 60 cents. More when I have the time.<br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: x-small;"><br />
</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: x-small;"><br />
</span><br />
<span class="Apple-style-span" style="font-family: Verdana, Tahoma, Arial, Calibri, Geneva, sans-serif; font-size: 13px;"><a href="http://www.theannals.com/cgi/content/abstract/44/7/1207" rel="nofollow" style="color: #417394; text-decoration: none;" target="_blank"></a><br />
</span></div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com4tag:blogger.com,1999:blog-7890548535393086926.post-5729598739741641912011-04-07T17:32:00.003-04:002012-12-02T19:15:32.057-05:00Roux-en-Y gastric bypass<div dir="ltr" style="text-align: left;" trbidi="on">
<br />
<div style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px; padding-bottom: 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px;">
I, in no way, endorse this procedure but it does have some bearing on Abrupt T2. It was orignally thought that much of the gains from this surgery was due to the limiting of / and types of food that people could eat once this surgery was performed. The citation below, however, shows that, in this case, there are far ranging effects on the hypothalamus that suddenly take effect. These effects proceed weight loss and involve the whole series of hormones that influence metabolism.</div>
<div style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px; padding-bottom: 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px;">
<br style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px;" /></div>
<div style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px; padding-bottom: 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px;">
My point for Abrupt T2 is that this shows that the hypothalamus is a higher order mechanism that can certainly effect, if not control, the whole insulin cycle. Once again, there is no change in the underlying beta cell structure. The change isn't there but higher up. </div>
<div style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px; padding-bottom: 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px;">
<br style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px;" /></div>
<div style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px; padding-bottom: 0px; padding-left: 0px; padding-right: 0px; padding-top: 0px;">
<a _mce_href="http://journals.lww.com/annalsofsurgery/Abstract/2004/08000/The_Early_Effect_of_the_Roux_en_Y_Gastric_Bypass.7.aspx" href="http://journals.lww.com/annalsofsurgery/Abstract/2004/08000/The_Early_Effect_of_the_Roux_en_Y_Gastric_Bypass.7.aspx" rel="nofollow" style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 16px;" target="_blank">http://journals.lww.com/annalsofsurgery/Abstract/2004/08000/The_Early_Effect_of_the_Roux_en_Y_Gastric_Bypass.7.aspx</a></div>
</div><script type="text/javascript">
var _gaq = _gaq || [];
_gaq.push(['_setAccount', 'UA-36759429-1']);
_gaq.push(['_setDomainName', 'blogspot.com']);
_gaq.push(['_setAllowLinker', true]);
_gaq.push(['_trackPageview']);
(function() {
var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true;
ga.src = ('https:' == document.location.protocol ? 'https://' : 'http://') + 'stats.g.doubleclick.net/dc.js';
var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s);
})();
</script>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com6tag:blogger.com,1999:blog-7890548535393086926.post-32805544067043961452011-04-07T16:55:00.001-04:002011-04-08T16:51:40.656-04:00Facebook Page for Abrupt Onset Type 2 Diabetes<div dir="ltr" style="text-align: left;" trbidi="on">People have suggested that I put up a Facebook page so that people can easily comment and add information.<br />
<br />
Okay, I've done this and I'll be adding more in the future. Hopefully, while I'm off on this project, this will keep the dialogue going.<br />
<br />
<a href="http://www.facebook.com/home.php?sk=group_112805178790934&ap=1">Abrupt Onset Type 2 Diabetes</a><br />
<br />
<span class="Apple-style-span" style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 14px;"><span class="Apple-style-span" style="font-size: x-small;">Obviously, I just got this set up before I went off on my latest assignment. I really didn't know what it was going to be but now I think I'm getting it. I don't have time to seriously go through scientific papers at this moment. I still am thinking about things and interesting citations still come across my desk. What I plan to use facebook for are these clues about Abrupt Onset that keep arising. </span></span><br />
<span class="Apple-style-span" style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 14px;"><span class="Apple-style-span" style="font-size: x-small;"><br />
</span></span><br />
<span class="Apple-style-span" style="font-family: 'lucida grande', tahoma, verdana, arial, sans-serif; line-height: 14px;"><span class="Apple-style-span" style="font-size: x-small;">This will give me a chance to talk about and hopefully get feed back on ideas that you might find interesting.</span></span><br />
<br />
</div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com1tag:blogger.com,1999:blog-7890548535393086926.post-56163088451362354032011-04-07T16:42:00.001-04:002011-04-25T19:50:40.085-04:00Who gets KPD T2? Everybody!<div dir="ltr" style="text-align: left;" trbidi="on"><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;">I've decided to keep updating this with citations as they come in.<o:p></o:p></span><br />
<span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><br />
</span><br />
<span style="color: black; font-family: Arial, sans-serif;"><a href="http://www.medicthai.com/admin/news_detail.php?id=5093"><b>Thai</b></a></span><br />
<span class="Apple-style-span" style="font-family: Arial, sans-serif;"><a href="http://www.google.com/url?sa=t&source=web&cd=19&ved=0CDQQFjAIOAo&url=http%3A%2F%2Fwww.bhartihospital.com%2FResearch%2520For%2520Website%2Fketosis%2520prone%2520T2DM.doc&rct=j&q=%22Ketosis-Prone%20T2DM%22&ei=6pyvTKe9GZagnAfWs-H7BQ&usg=AFQjCNHr2i_4xpDx0O-c0epGH0QsJkt5WQ"><b>Indian</b></a></span><br />
<span class="Apple-style-span" style="font-family: Arial, sans-serif; font-size: 9.16667px; line-height: normal;"><b><br />
</b></span><br />
<span class="Apple-style-span" style="font-family: Arial, sans-serif; font-size: 9.16667px; line-height: normal;"><b><span class="Apple-style-span" style="font-size: small;"><a href="http://aace.metapress.com/content/r0159512563p65u2/">Peruvian</a></span></b></span><br />
<div style="font-family: 'Times New Roman'; line-height: normal; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><b><span class="Apple-style-span" style="font-size: small;"><br />
</span><span class="Apple-style-span" style="font-size: small;"> </span></b></span></div><div style="font-family: 'Times New Roman'; line-height: normal; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><a href="http://www.banglajol.info/index.php/IMCJ/article/viewFile/2942/2443"><b><span class="Apple-style-span" style="font-size: small;">Bangladeshi</span></b></a></span></div><div style="font-family: 'Times New Roman'; line-height: normal; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><b><span class="Apple-style-span" style="font-size: small;"><br />
</span><span class="Apple-style-span" style="font-size: small;"> </span></b></span></div><div style="font-family: 'Times New Roman'; line-height: normal; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><a href="http://journals.indexcopernicus.com/abstracted.php?icid=900021"><b><span class="Apple-style-span" style="font-size: small;">Turkish</span></b></a></span></div></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><br />
</div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><b><span style="color: black; font-family: Arial, sans-serif;">Hispanics</span></b><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"> have higher rate of KPD<br />
<a href="http://care.diabetesjournals.org/content/26/8/2485.1.full.pdf"><span style="color: blue;">http://care.diabetesjournals.org/content/26/8/2485.1.full.pdf</span></a><o:p></o:p></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><br />
</div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black; font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: xx-small;">Adult-Onset Atypical (Type 1) Diabetes: Additional Insights And Differences With Type 1a Diabetes In A </span><b>European Mediterranean </b><span class="Apple-style-span" style="font-size: xx-small;">Population. </span><a href="http://www.ncbi.nlm.nih.gov/pubmed/15111529" style="font-size: 8pt;"><span style="color: blue;">Http://Www.Ncbi.Nlm.Nih.Gov/Pubmed/15111529</span></a><span class="Apple-style-span" style="font-size: xx-small;"><o:p></o:p></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black; font-family: Arial, sans-serif;"><br />
<span class="Apple-style-span" style="font-size: xx-small;"> Severe diabetes in remission: a Singapore's perspective - </span><b>Malay<br />
</b><a href="http://www.ncbi.nlm.nih.gov/pubmed/11817290?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pub" style="font-size: 8pt;"><span style="color: blue; text-decoration: none;">http://www.ncbi.nlm.nih.gov/pubmed/11817290?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pub</span></a><span class="Apple-style-span" style="font-size: xx-small;"><o:p></o:p></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><br />
</div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black; font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: xx-small;">Clinical characteristics of </span><b>Korean</b><span class="Apple-style-span" style="font-size: xx-small;"> patients with new-onset diabetes presenting with diabetic ketoacidosis.</span></span><span style="color: blue; font-family: Arial, sans-serif; font-size: 8pt;"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19477546"><span style="color: blue;">http://www.ncbi.nlm.nih.gov/pubmed/19477546</span></a></span><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><br style="mso-special-character: line-break;" /> <br style="mso-special-character: line-break;" /> </span><span lang="EN-GB" style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><o:p></o:p></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span lang="EN-GB" style="color: black; font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: xx-small;">Ketosis-onset diabetes in </span><b>Tunisian</b><span class="Apple-style-span" style="font-size: xx-small;"> adults: immunological markers and β-cell function <o:p></o:p></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: blue; font-family: Arial, sans-serif; font-size: 8pt;"><a href="http://www.emro.who.int/publications/emhj/1601/article12.htm"><span style="color: blue;">http://www.emro.who.int/publications/emhj/1601/article12.htm</span></a><o:p></o:p></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><br />
</div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black; font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: xx-small;">High Frequency of Type 1B (Idiopathic) Diabetes in </span><b>North Indian</b><span class="Apple-style-span" style="font-size: xx-small;"> Children With Recent-Onset Diabetes</span></span><span style="color: blue; font-family: Arial, sans-serif; font-size: 8pt;"><a href="http://care.diabetesjournals.org/content/26/9/2697.1.full"><span style="color: blue;">http://care.diabetesjournals.org/content/26/9/2697.1.full</span></a></span><span style="color: black; font-family: Arial, sans-serif; font-size: 8pt;"><br />
</span><span style="color: blue; font-family: Arial, sans-serif; font-size: 8pt;"><br />
</span><span style="color: black; font-family: Arial, sans-serif; text-transform: uppercase;"><span class="Apple-style-span" style="font-size: xx-small;">[HETEROGENEITY OF TYPE 1 DIABETES MELLITUS] - </span><b>Brazilian</b></span><b><span style="color: blue; font-family: Arial, sans-serif; font-size: 8pt; text-transform: uppercase;"><o:p></o:p></span></b></div><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif; line-height: 18px;"><span class="Apple-style-span" style="color: blue; font-family: Arial, sans-serif; font-size: 10.8333px; line-height: 18px;"><span style="color: blue;"><a href="http://www.ncbi.nlm.nih.gov.proxy1.cl.msu.edu/pubmed/18438531">http://www.ncbi.nlm.nih.gov.proxy1.cl.msu.edu/pubmed/18438531</a></span></span></span><br />
<span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif; line-height: 18px;">A Subtype of Markedly Abrupt Onset With Absolute Insulin Deficiency in Idiopathic Type 1 Diabetes in </span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif; line-height: 18px;"><b>Japanese</b></span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif; line-height: 18px;"> Children</span><br />
<div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span style="color: blue;"><a href="http://care.diabetesjournals.org/content/25/12/2353.2.full"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">http://care.diabetesjournals.org/content/25/12/2353.2.full</span></a></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><a href="http://care.diabetesjournals.org/content/25/12/2353.2.full"></a></span><span class="Apple-style-span" style="color: blue;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
<b> South Asian</b> version of flatbush diabetes mellitus- A case report and review article<br />
</span><span style="color: blue;"><a href="http://www.acadjourn.org/IJMMS/abstracts/abstracts/abstracts2009/Sept/Khan%20and%20%20Akram.htm"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">http://www.acadjourn.org/IJMMS/abstracts/abstracts/abstracts2009/Sept/Khan%20and%20%20Akram.htm</span></a></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><a href="http://www.acadjourn.org/IJMMS/abstracts/abstracts/abstracts2009/Sept/Khan%20and%20%20Akram.htm"></a></span><span class="Apple-style-span" style="color: blue;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
Ketoacidosis in <b>Apache Indians</b> with non-insulin-dependent diabetes mellitus<br />
</span><span style="color: blue;"><a href="http://www.ncbi.nlm.nih.gov/pubmed/9382666"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">http://www.ncbi.nlm.nih.gov/pubmed/9382666</span></a></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><a href="http://www.ncbi.nlm.nih.gov/pubmed/9382666"></a></span><span class="Apple-style-span" style="color: blue;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
Cetoacidosis diabética:una complicación frecuente de la diabetes tipo 2 en <b>hispanoamericanos</b><br />
</span><span style="color: blue;"><a href="http://www.sediabetes.org/resources/revista/00011519archivoarticulo.pdf"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">http://www.sediabetes.org/resources/revista/00011519archivoarticulo.pdf</span></a></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><a href="http://www.sediabetes.org/resources/revista/00011519archivoarticulo.pdf"></a></span><span class="Apple-style-span" style="color: blue;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
The Occurrence of Diabetic Ketoacidosis in Type 2 Diabetic <b>Chinese</b> Adults<br />
</span><span style="color: blue;"><a href="http://www.tsim.org.tw/journal/jour10-6/P10_230.PDF"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">http://www.tsim.org.tw/journal/jour10-6/P10_230.PDF</span></a></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><a href="http://www.tsim.org.tw/journal/jour10-6/P10_230.PDF"></a></span><span class="Apple-style-span" style="color: blue;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
Characteristics of <b>Caucasian</b> type 2 diabetic patients during ketoacidosis and at follow-up<br />
</span><span style="color: blue;"><a href="http://www.ncbi.nlm.nih.gov/pubmed/10842773"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">http://www.ncbi.nlm.nih.gov/pubmed/10842773</span></a></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><a href="http://www.ncbi.nlm.nih.gov/pubmed/10842773"></a></span><span class="Apple-style-span" style="color: blue;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></span><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
The prevalence of ketosis-prone type 2 diabetes is not known, but observational studies suggest that this type of diabetes accounts for a substantial number of patients with diabetic ketoacidosis. In the United States, the prevalence has been estimated to be between 20% and 50% in African-American and Hispanic patients with new diagnoses of diabetic ketoacidosis . In addition to ethnicity, clinical features predictive of future near-normoglycemic remission are obesity and a family history of type 2 diabetes. Among 154 consecutive African-American patients admitted to the hospital with diabetic ketoacidosis, we observed that obesity was present in 29% and that the prevalence of obesity was higher among those with newly diagnosed diabetes (56%). More than 80% of patients have a family history of type 2 diabetes. The mean body mass index at presentation in African-American patients with ketosis-prone type 2 diabetes has ranged between 28 kg/m2 to 37 kg/m2 . A high rate of obesity is also reported in Hispanic and Chinese persons and in sub-Saharan black African immigrants to Europe. Obesity in persons with diabetic ketoacidosis from minority ethnic groups is more common than in white persons, in whom the rate of obesity is less than 20%. <o:p></o:p></span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
Balasubramanyan and colleagues reviewed the clinical profiles of 141 adults admitted to the hospital with diabetic ketoacidosis. At presentation, 39% of patients were considered to have type 1 diabetes, 53% were considered to have type 2 diabetes, and 8% were not classified.Twenty-eight percent of patients had newly diagnosed diabetes, 93% of whom were reassessed at least 2 years after their initial episode of diabetic ketoacidosis and were considered to have type 2 diabetes. More recently, Pin˜ero-Pilon˜a and Raskin reported that the incidence of this type of diabetes among persons with new-onset diabetes with diabetic ketoacidosis was approximately 60%. In agreement with the U.S. experience, African studies have reported that 42% to 64% of patients with diabetic ketoacidosis initially treated with insulin therapy do not have classic type 1 diabetes and may experience prolonged remission. The prevalence of ketosis-prone type 2 diabetes seems to be lower in Asian and white persons and may represent fewer than 10% of cases of diabetic ketoacidosis.</span></span></div><div class="MsoNormal" style="line-height: 11.5pt; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
<br />
</span><b><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">Narrative Review: Ketosis-Prone Type 2 Diabetes Mellitus<br />
</span><a href="http://www.annals.org/content/144/5/350.abstract"><span style="color: blue;"><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">http://www.annals.org/content/144/5/350.abstract</span></span></a><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span></b><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
The extent of the prevalence of this syndrome really isn't known. As far as I know, there is no ready test for KPD T2. What we have is hospital admittance records for DKA. The numbers quoted for Mexican and African Americans is about 60% of all the DKA cases. What this means in terms of the general Mexican and African American population is in question but you have to recognize that for every case where it is bad enough to cause hospitalization there has to be many multiples of it in existence.<o:p></o:p></span></span></div><br />
<span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span><br />
<span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;"><br />
</span><br />
<div><span class="Apple-style-span" style="font-family: Arial, Helvetica, sans-serif;">Mike</span></div></div></div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com4tag:blogger.com,1999:blog-7890548535393086926.post-66979437672639254202011-02-06T18:35:00.000-05:002011-02-06T18:35:07.752-05:00Contamination of traditional foods<div dir="ltr" style="text-align: left;" trbidi="on">I'm still off on assignment but this subject came up and I thought that it would be good to drop a brief note on it.<br />
<br />
We tend to think that if we stick to traditional foods that we can expect to be safe from problems with blood sugar. What needs to be recognized is that traditional foods were typically raised by the consumer or the farmer was near to the consumer. Preparations were carried out by the person eating the food.<br />
<br />
The modern world is different, however. You might very well be eating a traditional diet but what are its constituents? Is that wheat the traditional wheat which was used in the preparation of that bread? How was it prepared? This is important. Traditional preparation will do nothing to offset problems of diet, if the underlying food is problematic.<br />
<br />
If you look at our "diabetes epidemic", you will note how much it has taken off in peoples of color across the world in the last few decades. I suspect that some of the reason has to do with newer varieties being substituted for old traditional foods. I know I keep harping on this but the only way to truly know is to test your blood. Don't be complacent. The world isn't very dietarily safe for you or me.</div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com0tag:blogger.com,1999:blog-7890548535393086926.post-20347208534053472572010-12-28T01:32:00.000-05:002010-12-28T01:32:09.697-05:00Please make the fightI have to go back to work, and I wish to say this before I sign off. I wrote this blog because I saw unnecessary suffering, I come from a family that died young because of this accursed diabetes. The peoples who have read this blog span the world and know that we are in the grips of something horrible that has not been given name or face in the world. I see you from all corners of the globe. This is a real thing. The science is there but the recognition is not. People are dying and suffering due to this. I can't do this alone. Others must step forth and push this agenda.<br />
<br />
I come from slaves in the US. We suffered lynchings and burnings because we believed that there was something right that had to be pursued. I was brought up to make the fight for justice and this is was this blog has been for me. It is dedicated to my family who died young from heart attacks, strokes and cancer. It is based on the belief that this did not have to happen and that it can be stopped, if I would make the fight.<br />
<br />
In this blog, I have not only brought forth the information about this diabetes but also put myself on the line by actively experimenting on myself to show that this is a special type of diabetes. I can't do it alone. You, out there, have to push this issue in China, Indonesia, Brazil, Turkey, Africa. It is up to us to make this known and get proper care for our brothers and sisters.<br />
<br />
I've made the fight. Please, make the fight as well. Nothing will get better without our efforts. No more funerals, no more amputations without the understanding of what we face. This is what I ask. This is what making the fight is about. The information is here. What is needed is the will to push it and challenge all the thoughts on diabetes that endangers us.<br />
<br />
Take this information and, please, make the fight.<br />
<br />
Mike BarkerMichael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com1tag:blogger.com,1999:blog-7890548535393086926.post-90659151692212831702010-12-19T17:00:00.001-05:002010-12-19T20:47:17.032-05:00Thinking about the nature of Abrupt Onset Type 2 diabetes<div class="MsoNormal"></div><div class="MsoNormal"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"></span></div><div class="MsoNormal"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: 12px; line-height: 15px;"><br />
</span></span></div><div class="MsoNormal"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: 11.6667px; line-height: 15px;"><br />
</span></span></div><div class="MsoNormal"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: 11.6667px; line-height: 15px;"></span></span></div><div class="MsoNormal"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">This is still a continuation of the “Abrupt onset t2 series”. You can read those <a href="http://ketosisprone.blogspot.com/2010/11/abrupt-type-2-diabetes-onset-and-1st_18.html">Here.</a> 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.</span></span></span></div><br />
<span class="Apple-style-span" style="font-family: Arial, sans-serif;"> </span><br />
<div class="MsoNormal" style="line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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</span><span style="color: black; font-family: Arial, sans-serif; line-height: 115%;"><span class="Apple-style-span" style="font-size: xx-small;">.</span></span></span></span></div><div class="MsoNormal" style="line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; line-height: 115%;"><span class="Apple-style-span" style="font-size: xx-small;"><br />
</span></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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. <o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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. <o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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.<o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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<sup>st</sup> 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.<o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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.<o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
<span class="apple-style-span">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<sup>st</sup> 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<sup>st</sup> phase.<o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><span class="apple-style-span"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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.<o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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. <o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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. <b style="mso-bidi-font-weight: normal;"><a href="http://www.ncbi.nlm.nih.gov/pubmed/20963574">Pancreatic neuronal melanocortin-4 receptor modulates serum insulin levels independent of leptin receptor </a> <o:p></o:p></b></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><b style="mso-bidi-font-weight: normal;"><br />
</b></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">This talks of a hormone secreted by the hypothalamus which is part of blood sugar control but is suppressed by hyperglycemia. <b style="mso-bidi-font-weight: normal;"><a href="http://www.ncbi.nlm.nih.gov.proxy1.cl.msu.edu/pubmed/19489767">Role of orexin in the regulation of glucose homeostasis</a><o:p></o:p></b></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">This one shows the effects of hyperglycemia on the hypothalamus and suggest that these effects are reversible. <b style="mso-bidi-font-weight: normal;"><a href="http://ajpregu.physiology.org.proxy1.cl.msu.edu/content/293/2/R592.full.pdf+html">Hyperglycemia impairs glucose and insulin regulation of nitric oxide</a><o:p></o:p></b></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">Here’s a paper detailing the relationship of the hypothalamus to the production of glucose by the liver. <b style="mso-bidi-font-weight: normal;"><a href="http://physiologyonline.physiology.org/content/24/3/159.full">CNS Regulation of Glucose Homeostasis</a> <o:p></o:p></b></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">This paper, though ostensibly about brain cholesterol, does talk about the curative effect of insulin on the hypothalamus. <b style="mso-bidi-font-weight: normal;"><a href="http://www.ncbi.nlm.nih.gov/pubmed/21109190">Diabetes and insulin in regulation of brain cholesterol metabolism.</a><o:p></o:p></b></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">A well known fact of diabetes is that the loss of 1<sup>st</sup> 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. <o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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.<o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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.<o:p></o:p></span></span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;"><br />
</span></span></span></div><div class="MsoNormal"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="Apple-style-span" style="font-size: 14px; line-height: 15px;"><br />
</span></span></div><div class="MsoNormal" style="font-size: 11px; line-height: 12px;"><span class="Apple-style-span" style="font-family: Arial, sans-serif;"><span class="apple-style-span"><span style="color: black; font-family: Arial, sans-serif; font-size: 10pt; line-height: 115%;">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?<o:p></o:p></span></span></span></div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com2tag:blogger.com,1999:blog-7890548535393086926.post-69448243844030965872010-11-18T17:05:00.004-05:002011-04-11T20:45:29.274-04:00Abrupt Type 2 Diabetes Onset and 1st Phase Insulin Response - pt 2<div dir="ltr" style="text-align: left;" trbidi="on"><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;"><a href="http://ketosisprone.blogspot.com/2010/12/thinking-about-nature-of-abrupt-onset.html">Part 3</a>This is a further discussion on the previous post. </span><span style="font-size: 13.5pt;"><a href="http://ketosisprone.blogspot.com/2010/11/abrupt-type-2-diabetes-onset-and-1st.html">Here</a>.</span><span style="color: black; font-size: 13.5pt;"> I was my own lab rat and I managed to turn off and on my 1st phase insulin response. It's nice to get good numbers but this isn't what this was about. For one thing, the nature of diabetes is such that no short term answer is adequate. I monkeyed around for a couple of months and managed to find a method that allowed me to manipulate some of my insulin response. I locked down everything: little or no exercise, no supplements, no change in diet, no medications. What you have to wonder about is the sustainability of what I'm doing and I've serious questions about that.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">What’s kept me at it was that, for the first time, I got a glimpse of this diabetes and how its behavior fits with all that I've read. It clearly pointed out a few issues which I wish to discuss.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><b style="mso-bidi-font-weight: normal;"><span style="color: black; font-size: 13.5pt;">Prediabetes is diabetes<o:p></o:p></span></b></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span class="apple-style-span"><span style="color: #333333; font-family: Verdana, sans-serif; font-size: 5pt;">I</span><span style="color: #333333; font-family: Verdana, sans-serif;"><span class="Apple-style-span" style="font-size: x-small;">n 1997 and 2003, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus recognized an intermediate group of individuals whose glucose levels, although not meeting criteria for diabetes, are nevertheless too high to be considered normal. This group was defined as having impaired fasting glucose (IFG) (FPG levels of 100 mg/dL [5.6 mmol/L] to 125 mg/dL [6.9 mmol/L]) or impaired glucose tolerance (IGT) (2-h OGTT values of 140 mg/dL [7.8 mmol/L] to 199 mg/dL [11.0 mmol/L]).</span></span></span><span style="color: black; font-size: 13.5pt;"><o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">It takes me only <b style="mso-bidi-font-weight: normal;"><u>one</u></b> hyperglycemic event to lose my 1<sup>st</sup> phase. I really want to emphasize this. One big postprandial excursion (after meal blood sugar rise over 170) was all it took to set my blood sugar’s 40 pts higher. As </span><a href="http://healthcorrelator.blogspot.com/"><span style="font-size: 13.5pt;">Ned</span></a><span style="color: black; font-size: 13.5pt;">, my statistical guru, might say, “I’m a small data set”. But I am a data set and, as far as I know, the only one around because of the paucity of research on KPD. You should read this with that limitation in mind.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">This could be because I’ve already got a broken metabolism. It is entirely possible that it might take a significant amount of times to move into mild diabetes. I want to talk about the discreet steps that my blood sugars take for a moment. I find myself with the same numbers. One step puts me at 115, the other 135 and another at around 170. After 170 though, all bets seem to be off. This 170 is near the take off point for KPD’s that was talked about in a previous post. <a href="http://ketosisprone.blogspot.com/2010/09/a1c-relapse-progression.html">Here</a> It could be that there are a series of stopping points from normal blood sugars to bad blood sugars. The increment may only be 5 pts for each 500 postprandial excursions. No matter what the amount of times or the increments of increase in blood sugars, the important thing to notice is the outcome is controlled by repeated hyperglycemia. This hyperglycemia, I assume, feeds off itself. The higher it goes, the higher it will continue to go.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">Because I can see my 1<sup>st</sup> phase insulin response more clearly, I know what disrupts it. 170 is considered by the ADA as prediabetes. It isn’t. My 1<sup>st</sup> phase is gone at that point. Indeed, as I’ve come to consider, the reaching of that point means that my 1<sup>st</sup> phase has failed. Part of my pancreatic function is now missing. This is diabetes. There is nothing “pre” about it.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><b style="mso-bidi-font-weight: normal;"><span style="color: black; font-size: 13.5pt;">Healthy Foods are bad for you</span></b><span style="color: black; font-size: 13.5pt;">.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">Remember, our issues are no matter to the ADA. The rules that they apply and promulgate have almost nothing to do with us. This means that you have to forget about the dietary rules that are being put out there for diabetics. Maybe they work for some of them but they don’t work for us and we should be very careful about following them. I tried to address this in a previous post. <a href="http://ketosisprone.blogspot.com/2010/09/thinking-about-weight-maybe-one-size.html">Here</a> <o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">I can <b style="mso-bidi-font-weight: normal;">not </b>keep a 1<sup>st</sup> phase insulin response by eating so called “healthy foods”. For me, there can be no such thing as a healthy grain because they stop my first phase much the same as sugar. How about “healthy fruit”? I can handle some berries but the larger fruits are a no no. In order to sustain this first phase, I have to largely consist on fats, which are saturated, and protein. Almost all my carbs come from green vegetables.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">There is an increasing epidemic of diabetes around the world. Well meaning people are moving across the globe preaching about “healthy diets”. Unfortunately, they aren’t for anyone subject to acute onset type 2 diabetes. This is why I have said that a meter is your best friend. Diabetes educators will tell you what you should eat, even though, most have never heard of any type of acute onset type 2 diabetes, most would probably even dispute that such a thing occurs. You can’t take their advice on diet. You shouldn’t even take my advice on diet. <b style="mso-bidi-font-weight: normal;">Take your meter’s advice on diet.<o:p></o:p></b></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">With a low carb diet and this simple medication, I am effecting a change of nearly a percentage point in A1c at a cost of about 20 cents a week. No drug company can make such a claim and, as far as I know, there is no diabetic regimen that can match this. My intuition is that this will only truly work on us. We are prone to a <b style="mso-bidi-font-weight: normal;">malfunctioning but an essentially intact insulin system</b>. I couldn’t get these results, if this were not true. This is, as far as I’m concerned, the missing piece of the puzzle. <o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">If you look at the literature it assumes that we have lost beta cells much like regular type 2’s and that we would be subject to the same progressive failure as they are. My experiences tell me this idea is a fallacy. I went through fasting blood sugars of nearly 300, for god knows how long, and no meds were able to bring back my numbers to truly normal, save insulin. Suddenly, I’ve been able to produce normal numbers in a way that should be easily replicable. Upon further reflection, it could be said that I’ve lost a good deal of beta cell function due to probably years of high blood sugars and that all I’ve done is successfully bring fully on line whatever function was left.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">Even if this isn’t a workable regimen, it should at least get things pointed in the right direction and hopefully get us the type of patient management that we have been so far lacking.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-size: 13.5pt;">I am still experimenting with my 1<sup>st</sup> phase and in the months and weeks ahead I hope to communicate to you my experiences and intuitions about what is happening. In the meantime, think about my experience with hyperglycemia and its immediate effects on beta cell functioning and be very careful about what you eat. <a href="http://ketosisprone.blogspot.com/2010/12/thinking-about-nature-of-abrupt-onset.html">Part 3</a><o:p></o:p></span></div></div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com2tag:blogger.com,1999:blog-7890548535393086926.post-46721974329335386642010-11-13T17:22:00.001-05:002012-12-02T19:19:32.506-05:00Abrupt Type 2 Diabetes Onset and 1st Phase Insulin ResponseI've titled this "Abrupt Type 2 Diabetes Onset" because I'm am coming to believe that very different types of diabetics have this and that it involves, not the beta cells themselves, but a mechanism or loop that the beta cells are in that has failed.<br />
<br />
How I've come to this conclusion is personal. By sheer luck, I fell across a method of reactivating my 1st phase insulin response. You basically have two responses that come from your pancreas, basal and 1st phase. The basal is the constant but low flow of insulin that occurs all the time in your body. The 1st phase is a modifier of this basic level of insulin to account for changes in the amount of blood sugar that occurs with things like eating, exercise and stress. I use to think of it as a big wave of insulin that suddenly flowed in to your blood stream to counter act potentially high blood sugars caused by something like eating a fast acting carbohydrate. It can and will do this but mostly it's active like a computerized glucose monitoring system counter acting small spikes in the system due to the actions of other things going on in the body.<br />
<br />
It should be noted that I'm talking about spikes not drops in blood sugar. Drops aren't the problem usually. (There is reactive hypoglycemia but I view it more as part of a failed mechanism.) Your body is set up to strongly defend against hypoglycemia. This can kill you in a day while hyperglycemia make take years. There are a series of systems and hormones that interact to assure that the body has enough glucose. The one which is counter to those is insulin.<br />
<br />
At any rate, I've found a way to get that first phase back and conversely, I've found how to lose this 1st phase. In the last month, I've gotten to the point where I have been able to more or less switch it off and on and notice when it is working. I've even dropped all medications. My typical blood sugar profile kept me at about 110 with spikes of 40 to 50 points higher after meals. This is even with eating a largely low carb diet. Now my typical profile keeps me in the 90's with spikes never above 130 and generally about 20 points above my basal rate. It should be noted this is without insulin, exercise or supplements. (I'm trying to keep down the confounding variables. <a href="http://healthcorrelator.blogspot.com/">Ned Kock</a> is big on this!)<br />
<br />
One thing this has shown me is that the beta cells are there. They aren't dying off or sick. I'll have a 1st phase for a few days, make an adjustment and then I won't have a 1st phase. I'm thinking that this is very much an abrupt type 2 onset thing.<br />
<br />
Type 2 is traditionally thought of as slow onset with continually rising blood sugars over many years. With us, insulin failure occurs quickly but on the converse side insulin recovery occurs quickly as well. I've read where various methods were used to assess beta cell function or mass and it was found to be intact.<br />
<br />
I produce insulin but not a 1st phase so my constant dribble of insulin is not enough to keep down my blood sugars without additional insulin. Guess where my blood sugar average is usually, without medications? 134. This is about an A1c of 6.3 which is pretty standard for a Ketosis Prone type 2 diabetic. This A1c and its implications were discussed in a few posts back. <a href="http://ketosisprone.blogspot.com/2010/09/a1c-relapse-progression.html">Here.</a><br />
<br />
All this and more lead me to believe that this isn't a problem of beta cells desensitizing but of a failure of a control loop that the beta cells respond to by releasing 1st phase insulin. By saying "control loop", I am talking about a circuit. Think of it as a lightbulb and switch. If this switch is controlled by a sensor for certain amount of darkness then when it gets too dark, the switch is activated and the light comes on. There might be a sensor for lack of movement in area where the light is. If no motion is detected, the switch is deactivated and the light goes off. There is nothing wrong with the light, it's fine. Its behavior, however, is being controlled through the sensors that activate or deactivate the switch.<br />
<br />
What my intuition is telling me, that at least in those with "abrupt type 2 diabetes onset", the circuit isn't working and what breaks it down are hyperglycemic episodes which effect one or more components which are part of the loop that operates in the 1st phase circuit. These components could be anywhere. They could function as an aggregate or there could be just one component which is effected by hyperglycemia. What seems clear is that the message isn't getting through.<br />
<br />
I bring up hyperglycemia because all I have to do to shut down the 1st phase is to initiate a high glycemic environment which is too high for my 1st phase to cover, typically for me, this is a tub of popcorn at my local cinema. (If you're going to do something bad, you should at least enjoy it.) My blood sugars will stay below 160 then they will soar above 200 and stay there for 4 or five hours. After that, no more 1st phase and higher blood sugars till I make the adjustment.<br />
<br />
You are probably wonder what this adjustment is. I should say it is relatively safe but there are potential side effects and frankly I don't want people starting to take stuff with little or no understanding what they're undertaking. I'm going to keep this under wraps for a while.<br />
<br />
What I'd love to know is what chemicals or hormones or whatever breaks down in a high glucose environment? Some where, at least for us, that is where the answer lies I believe. <a href="http://ketosisprone.blogspot.com/2010/11/abrupt-type-2-diabetes-onset-and-1st_18.html">Part 2</a>
<script type="text/javascript">
var _gaq = _gaq || [];
_gaq.push(['_setAccount', 'UA-36759429-1']);
_gaq.push(['_setDomainName', 'blogspot.com']);
_gaq.push(['_setAllowLinker', true]);
_gaq.push(['_trackPageview']);
(function() {
var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true;
ga.src = ('https:' == document.location.protocol ? 'https://' : 'http://') + 'stats.g.doubleclick.net/dc.js';
var s = document.getElementsByTagName('script')[0]; s.parentNode.insertBefore(ga, s);
})();
</script>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com4tag:blogger.com,1999:blog-7890548535393086926.post-69349559656945131282010-10-21T22:50:00.004-04:002013-01-02T15:42:42.176-05:00Downloadable Scientific Ketosis Prone Type 2 Diabetes powerpoint presentation<div dir="ltr" style="text-align: left;" trbidi="on">
<br />
<span style="font-family: 'Times New Roman'; font-weight: bold;">Guillermo E. </span><span style="font-family: 'Times New Roman'; font-weight: bold;">Umpierrez</span><span style="font-family: 'Times New Roman'; font-weight: bold;">, Dawn Smiley, and </span><span style="font-family: 'Times New Roman'; font-weight: bold;">Abbas</span><span style="font-family: 'Times New Roman'; font-weight: bold;"> E. </span><span style="font-family: 'Times New Roman'; font-weight: bold;">Kitabchi</span><br />
<br />
There is no news for you KPD fans in this presentation. This was done in 2006. This blog has a lot more current information and speculation on that information. This, however, represents the best thoughts of the current researchers at that time and these people have undisputed credentials. Whether people have heard of Ketosis Prone Type 2 diabetes or disbelieve its existence becomes moot because of this document. Here you have a complete presentation telling all about it. I post this in that light. You can simply download it and give it to family and friends.<br />
<br />
<span style="font-family: 'Times New Roman';">I found this presentation on the web and these are some of the chief writers and researchers of Ketosis Prone Type 2 diabetes. It seems to be a presentation in China and might be a bit dated but it is very thorough.</span><br />
<span style="font-family: 'Times New Roman';"><br />
</span><br />
<span style="font-family: 'Times New Roman';">I spend a good bit of time introducing people to this subject and so I started to develop a presentation on it. Low and behold, this pops up!</span><br />
<span style="font-family: 'Times New Roman';"><br />
</span><br />
<span style="font-family: 'Times New Roman';">You no longer have to go through the long discussions. This power point will do nicely. This would be a good thing to pass around, post or show to your diabetes educators. Who knows, it might make a difference.</span><br />
<br />
<span style="font-family: 'Times New Roman';"><a href="http://ketosisprone.blogspot.com/p/blog-page_1355.html" target="_blank">Ketosis Prone Type 2 Scientific Presentation </a> </span><br />
<span style="font-family: 'Times New Roman';"><br />
</span><br />
<span style="font-family: 'Times New Roman';">PS If some one can translate the characters in this document, chime in.</span></div>
Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com1tag:blogger.com,1999:blog-7890548535393086926.post-82555110481213383562010-10-04T01:37:00.004-04:002011-08-04T23:54:52.163-04:00A1c, glycation problems and DKA<div dir="ltr" style="text-align: left;" trbidi="on"><div class="MsoNormal"><span style="font-family: Arial, sans-serif; font-size: 9pt; line-height: 115%;">This might be a bit of a mess but I wanted to get this information out and I figure I can clean it up a bit later.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="font-family: Arial, sans-serif; font-size: 9pt;">You might have noted that I keep adding on to the ethnic KPD list. You might have also noticed the strong representation of people of color in this list. It is tempting to think that there is some aspect of melanin involved in KPD but I seriously doubt it. <span style="color: black;">I tend to see color as an indicator of certain things. The first thing it indicates is global location. Fairer people tend to live in more temperate climes. Darker skinned people tend to be located in more tropical regions.<o:p></o:p></span></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span class="Apple-style-span" style="font-family: Arial, sans-serif; font-size: 11.6667px;">What is it about those regions. One thing is parasites and malaria. It is known that genetic tests tend to show that people with protection against malaria also seem to have higher rates of kpd. I won’t go into the genetics but typically the same genes tend to be cited and they all tend to give an advantage in handling malaria. Here’s a listing of G6PD deficiency.</span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><img src="http://www.cchi.com.hk/specialtopic/case1/table2a.gif" /></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><table border="1" cellpadding="0" cellspacing="0" class="MsoNormalTable" style="mso-cellspacing: 0in; mso-padding-alt: 3.75pt 3.75pt 3.75pt 3.75pt; mso-yfti-tbllook: 1184;"><tbody>
<tr style="mso-yfti-firstrow: yes; mso-yfti-irow: 0;"> <td colspan="5" style="border: none; padding: 3.75pt 3.75pt 3.75pt 3.75pt;"><div align="center" class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in; text-align: center;"><span style="font-family: 'Times New Roman', serif; font-size: 12pt;">Table 1. Common Hemoglobinopathies: Populations Affected, Prevalence, and Outcomes<o:p></o:p></span></div></td> </tr>
<tr style="mso-yfti-irow: 1;"> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt; width: 20.0%;" width="20%"><div align="center" class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in; text-align: center;"><b><span style="font-family: Arial, sans-serif; font-size: 12pt;">Hemoglobin (Hb) Variant<o:p></o:p></span></b></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt; width: 20.0%;" width="20%"><div align="center" class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in; text-align: center;"><b><span style="font-family: Arial, sans-serif; font-size: 12pt;">Populations Affected<o:p></o:p></span></b></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt; width: 20.0%;" width="20%"><div align="center" class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in; text-align: center;"><b><span style="font-family: Arial, sans-serif; font-size: 12pt;">Prevalence<o:p></o:p></span></b></div><div align="center" class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in; text-align: center;"><b><span style="font-family: Arial, sans-serif; font-size: 12pt;">(in the United States unless otherwise noted)<o:p></o:p></span></b></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt; width: 20.0%;" width="20%"><div align="center" class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in; text-align: center;"><b><span style="font-family: Arial, sans-serif; font-size: 12pt;">Outcome with One Abnormal Gene and One Normal Gene (Heterozygous State)<o:p></o:p></span></b></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt; width: 20.0%;" width="20%"><div align="center" class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in; text-align: center;"><b><span style="font-family: Arial, sans-serif; font-size: 12pt;">Outcome with Two Abnormal Genes (Homozygous State)<o:p></o:p></span></b></div></td> </tr>
<tr style="mso-yfti-irow: 2;"> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Hemoglobin S (HbS)<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">African Americans<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Hispanic Americans/Latinos<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Also found in East India, the Mediterranean, and the Middle East<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">About one in 12 African Americans has sickle cell<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">trait <a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/#s1"><sup><span style="color: #003399;">1</span></sup></a><o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">About one in 100 Hispanic Americans/Latinos has sickle cell<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">trait <a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/#s2"><sup><span style="color: #003399;">2</span></sup></a><o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Sickle cell anemia occurs in one of every 500 African American births <a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/#s1"><sup><span style="color: #003399;">1</span></sup></a><o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Sickle cell anemia occurs in one of every 1,000 to 1,400 Hispanic American/Latino births <a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/#s1"><sup><span style="color: #003399;">1</span></sup></a><o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Sickle cell trait (also called HbAS): usually asymptomatic<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Sickle cell anemia (also called HbSS disease): sickled red blood cells that interfere with circulation and decrease life span of red blood cells; can result in hemolytic, splenic sequestration, and aplastic crises and multiple complications<o:p></o:p></span></div></td> </tr>
<tr style="mso-yfti-irow: 3;"> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Hemoglobin C (HbC)<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">African Americans<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">People of West African descent<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">About 2.3 percent of African Americans have HbC trait <a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/#s3"><sup><span style="color: #003399;">3</span></sup></a><o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">HbC trait (also called HbAC): asymptomatic<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">HbC disease (also called HbCC disease): mild hemolytic anemia, mild to moderate enlargement of the spleen<o:p></o:p></span></div></td> </tr>
<tr style="mso-yfti-irow: 4;"> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Hemoglobin E (HbE)<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Asian Americans, especially those of Southeast Asian descent<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Common in Cambodia, Indonesia, Laos, Malaysia, Thailand, and Vietnam. Also seen in southern China, India, the Philippines, and Turkey<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Prevalence of HbE may be 30 percent in Southeast<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Asia <a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/#s3"><sup><span style="color: #003399;">3</span></sup></a><o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">HbE trait (also called HbAE): asymptomatic<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">HbE disease (also called HbEE disease): mild hemolytic anemia, microcytosis, and mild enlargement of the spleen<o:p></o:p></span></div></td> </tr>
<tr style="mso-yfti-irow: 5;"> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Hemoglobin SC (HbSC)<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">African Americans and people of West African descent<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Also found in East India, the Mediterranean, and the Middle East<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><br />
</div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">N/A<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">HbSC disease (also called sickle-hemoglobin C disease): mild hemolytic anemia and moderate enlargement of the spleen; may have blocking of blood vessels as in sickle cell anemia but milder symptoms<o:p></o:p></span></div></td> </tr>
<tr style="mso-yfti-irow: 6; mso-yfti-lastrow: yes;"> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Hemoglobin F (HbF) elevated<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Occurs in patients with hereditary persistence of fetal hemoglobin, sickle cell anemia, severe anemias, leukemia, and other conditions<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">About 1.5 percent have more than 2 percent HbF but some groups may have concentrations as high as 12 percent <a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/#s3"><sup><span style="color: #003399;">3</span></sup></a><o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">N/A<o:p></o:p></span></div></td> <td style="padding: 3.75pt 3.75pt 3.75pt 3.75pt;" valign="top"><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="font-family: Arial, sans-serif; font-size: 12pt;">Those with elevated HbF and sickle cell anemia may have a milder form of sickle cell anemia<o:p></o:p></span></div></td> </tr>
</tbody></table><div class="MsoNormal" style="line-height: 9.95pt; margin-bottom: .0001pt; margin-bottom: 0in;"><a href="http://www.blogger.com/post-edit.g?blogID=7890548535393086926&postID=8255511048121338356" name="s1"></a><a href="http://www.blogger.com/post-edit.g?blogID=7890548535393086926&postID=8218783436747173605"><sup><span style="color: blue; font-family: Arial, sans-serif; font-size: 7pt;">1</span></sup></a><span style="color: black; font-family: Arial, sans-serif; font-size: 7pt;"> National Heart, Lung, and Blood Institute, NIH. Sickle cell anemia. Available at: <a href="http://www.nhlbi.nih.gov/health/dci/Diseases/Sca/SCA_All.html"><span style="color: #003399;">www.nhlbi.nih.gov/health/dci/Diseases/Sca/SCA_All.html</span></a>. Posted May 2007. Accessed June 27, 2007.</span><span style="font-family: 'Times New Roman', serif; font-size: 7pt;"><o:p></o:p></span></div><div class="MsoNormal" style="line-height: 9.95pt; margin-bottom: .0001pt; margin-bottom: 0in;"><a href="http://www.blogger.com/post-edit.g?blogID=7890548535393086926&postID=8255511048121338356" name="s2"></a><a href="http://www.blogger.com/post-edit.g?blogID=7890548535393086926&postID=8218783436747173605"><sup><span style="color: blue; font-family: Arial, sans-serif; font-size: 7pt;">2</span></sup></a><span style="color: black; font-family: Arial, sans-serif; font-size: 7pt;"> National Human Genome Research Institute, NIH. Learning about sickle cell disease. Available at: <a href="http://www.genome.gov/10001219"><span style="color: #003399;">www.genome.gov/10001219</span></a>. Posted February 2007. Accessed July 3, 2007.<o:p></o:p></span></div><div class="MsoNormal" style="line-height: 9.95pt; margin-bottom: .0001pt; margin-bottom: 0in;"><a href="http://www.blogger.com/post-edit.g?blogID=7890548535393086926&postID=8255511048121338356" name="s3"></a><a href="http://www.blogger.com/post-edit.g?blogID=7890548535393086926&postID=8218783436747173605"><sup><span style="color: blue; font-family: Arial, sans-serif; font-size: 7pt;">3</span></sup></a><span style="color: black; font-family: Arial, sans-serif; font-size: 7pt;"> Bry L, Chen PC, Sacks DB. Effects of hemoglobin variants and chemically modified derivatives on assays for glycohemoglobin. </span><i><span style="color: black; font-family: Arial, sans-serif; font-size: 7pt;">Clinical Chemistry</span></i><span style="color: black; font-family: Arial, sans-serif; font-size: 7pt;">. 2001;47(2):153–163.<o:p></o:p></span></div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><br />
</div><div class="MsoNormal" style="line-height: normal; margin-bottom: .0001pt; margin-bottom: 0in;"><span style="color: black; font-family: Arial, sans-serif; font-size: 6pt;"><a href="http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/"><span style="color: blue;">http://diabetes.niddk.nih.gov/dm/pubs/hemovari-A1C/</span></a></span><span style="color: black; font-family: 'Times New Roman', serif; font-size: 13.5pt;"><o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-family: Arial, sans-serif; font-size: 9pt;">Unless you are totally blind, you will recognize that all this information matches up with who gets KPD. It also matches up with Malaria.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-family: Arial, sans-serif; font-size: 9pt;">Now the reason for bringing this up is about the tendency of these issues to affect the A1c. They can cause an over estimation of A1c but most typically they will cause and under reading for A1c. This is because the A1c is a measure of glycation. (basically carmelized blood cells)This measure, however, assumes that the average blood cell will be around for 90 days. What if the cell has a shorter life as it tends to have with these two issues? The number for glycation is going to be lower simply because the blood cell hasn’t been around long enough to get glycated as much. The A1c will appear to be lower. <o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-family: Arial, sans-serif; font-size: 9pt;">I have already written about the ADA, diabetes and the danger to KPD’s. This needs to be tossed in. We are in serious trouble with the ADA guidelines since they sit right at the point of DKA for us but what if the test is off? We shouldn’t be anywhere near an A1c of 6.3 for safety sake. The A1c number could be 5.8 but, in truth, we could be at 6.5, which is trouble.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-family: Arial, sans-serif; font-size: 9pt;">Here is what that trouble means. It means a continual rise in DKA admissions to hospitals with all the attendant costs. As has been noted before, there isn’t any real way to separate out KPD’s from Type 2’s but the suspicion is that greater than 50% of new onset DKA admissions are KPD’s and for all we know a good many of the Type 2’s are KPD, as well.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div align="center" style="margin-bottom: .0001pt; margin: 0in; text-align: center;"><span style="color: black; font-size: 13.5pt;">DKA’s Admissions per year</span></div><div align="center" style="margin-bottom: .0001pt; margin: 0in; text-align: center;"><span style="color: black; font-size: 13.5pt;"><br />
</span></div><div align="center" style="margin-bottom: .0001pt; margin: 0in; text-align: center;"><span style="color: black; font-size: 13.5pt;"><img alt="Graph showing Number (in Thousands) of Hospital Discharges with Diabetic Ketoacidosis as First-Listed Diagnosis, United States, 1980-2005. Links for data figures, sources, methodology and data limitations, and detailed tables follow this figure." src="http://www.cdc.gov/diabetes/statistics/dkafirst/fNumber.gif" /></span></div><div class="MsoNormal"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><span style="color: black; font-family: Arial, sans-serif; font-size: 9pt;">This graph shows a doubling of admissions in the last 25 years, basically 60,000 more than 25 years ago and it is rising. KPD’s are probably a little better than half this number. If you add the blood glycation problem with the ADA recommendations you can see how this might be the case.<o:p></o:p></span></div><div class="MsoNormal"><br />
</div><div class="MsoNormal"><span style="font-family: Arial, sans-serif; font-size: 9pt; line-height: 115%;">Things aren’t getting any better for us and they won't get better anytime soon because they are now going to make the A1c the diagnostic tool for diabetes. For us, this is a really really bad idea.<o:p></o:p></span></div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div><div style="margin-bottom: .0001pt; margin: 0in;"><br />
</div></div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com4tag:blogger.com,1999:blog-7890548535393086926.post-57449392558866267322010-09-19T20:45:00.007-04:002011-04-11T20:17:48.118-04:00Thinking about: A1c Relapse Progression and the Insidious Nature of KPD<div dir="ltr" style="text-align: left;" trbidi="on"><div class="separator" style="clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: left;">These are the graphs from <b>Ketosis-Prone Type 2 Diabetes in Patients of Sub-Saharan African Origin. </b>These graphs especially C & D are too important not to be seen.</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTI4EPJUIzrAdgco20rfpAfs4YLjjH1Hg0RkY4Qn9bV9uWe7smrYVorVBGD6Iyu6mtLTxSllgBKCo2xTc6rPTWLzFkALvkjf0bGoFZPvN3nzX9jP7N81EsffvrmaeG2M5kX4SGekBBxIE/s1600/F4.medium.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="488" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgTI4EPJUIzrAdgco20rfpAfs4YLjjH1Hg0RkY4Qn9bV9uWe7smrYVorVBGD6Iyu6mtLTxSllgBKCo2xTc6rPTWLzFkALvkjf0bGoFZPvN3nzX9jP7N81EsffvrmaeG2M5kX4SGekBBxIE/s640/F4.medium.gif" width="640" /></a></div><div class="separator" style="clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div class="separator" style="clear: both; text-align: center;">This is my recreation of C for clearer viewing.</div><div class="separator" style="clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjjW6UDaKqvqlWIUowE2ZXHL8ONvROzzhSAhKFtnp4uGi2YMAvui78c9xDeSWVYj5drjwzUqqJ0keTgJ0nqpl3NVq1HAm4faj52BsKfGPyseP3yJKKN3bObSk0r5UxS2MjgJPXJEeLiP20/s1600/weight+A1c+graphs_26526_image002.gif" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="262" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjjW6UDaKqvqlWIUowE2ZXHL8ONvROzzhSAhKFtnp4uGi2YMAvui78c9xDeSWVYj5drjwzUqqJ0keTgJ0nqpl3NVq1HAm4faj52BsKfGPyseP3yJKKN3bObSk0r5UxS2MjgJPXJEeLiP20/s400/weight+A1c+graphs_26526_image002.gif" width="400" /></a></div><div class="separator" style="clear: both; text-align: center;"><br />
</div><div class="separator" style="clear: both; text-align: left;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Let's recap.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Ketosis Prone Diabetes is known for sudden onset without a precipitating factor. I posted this <a href="http://ketosisprone.blogspot.com/2010/02/four-types-of-ketosis-prone-type-2.html">Here</a></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">The A1c at which the diabetes stayed controlled is about 6.3. This is in the previous post. <a href="http://ketosisprone.blogspot.com/2010/08/a1c-tipping-point.html">Here</a></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Spontaneous Remission is the norm where there are no antibodies present. This is posted everywhere on this site.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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. <a href="http://www.phlaunt.com/diabetes/14045678.php"><span class="Apple-style-span" style="color: black;">Jenny Ruhl's "Blood Sugar 101"</span></a> <span class="Apple-style-span" style="color: black;"> 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.</span></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><span class="Apple-style-span" style="color: black;"><br />
</span></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Once again we visit the ADA guidelines.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">ADA Criteria for the diagnosis of diabetes</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.*</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">OR</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">OR</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT. </div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">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.</div><br />
<div><span class="Apple-style-span" style="color: black;"><br />
</span></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div></div>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com4tag:blogger.com,1999:blog-7890548535393086926.post-5131527129144822972010-09-09T16:46:00.002-04:002010-09-22T12:12:56.851-04:00Thinking about: Eating. Maybe one size does not fit allThough most of the testing of KPD's tends to involve obese participants, it should be noted that many KPD's are not only not obese, they are lean. Typically, when I look at papers where the participants aren't chosen, the lean members comprise a quarter to a third. Even in childhood DKA episodes, the obese number about fifty percent.<br />
<br />
What does this tell us about KPD's and weight? I keep hearing and seeing ads telling parents to make sure their children are active and eating right. This is the answer to childhood obesity, exercise and diet. Okay, I am a fan of both sloth and gluttony, I tend to be good at them, but I have to admit there's nothing wrong with having children out there physically engaging the world without a candy bar in their mouths.<br />
<br />
KPD is showing us something, however. What do you say to a person who is a thin diabetic? You obviously can't ask him or her to go on a diet nor would you put them on exercise schedule to help burn calories. We don't give the same advice to the thin KPD simply because it doesn't make obvious sense. They are thin. We give it to the heavy ones because they are fat. It's still the same condition with the same underlying causes. It gets expressed differently but the numbers between fat and thin are pretty much the same. I'm saying this because, I believe we have to look deeper than this. There is something going here and the range of body types it effects doesn't seem to point at behavior.<br />
<br />
The people of sub-Saharan Africa have a much bigger problem with Ketosis Prone Diabetes but this tends to be more in urban environments. There hasn't been a study but I would hazard a guess that you could draw a trendline representing length of urbanization of KPDs and their families and find quite a correlation.<br />
<br />
Another thing to note is it tends to cluster in people of color, not that whites don't get it, they do, but the prevalence is far higher in people of color. Now I'm pretty sure you don't want to say that all these people of color are lazy and eat too much. Besides, how could that be true if a good many of them are thin?<br />
<br />
I believe that most of this is a response to diet. It is, after all, about metabolism. Its higher rate of prevalence in urban areas suggests that it has something to do with the moving from traditional diets to more modern diets. It would be logical to point out that there are many things that go with urbanization that could just as readily be pointed as a cause. This is true but I would say that this exists worldwide in varied modern environments so I would have to ask: how many things could this be? To tell the truth, I don't know nor does anybody else. What I do know is purely anecdotal and the KPD's I've talked to have had to change their diets significantly to hold their blood sugars down with diet and exercise, those on insulin, generally, have not.<br />
<br />
This difference in insulin using KPD's and non-insulin using KPD's suggest that some element of diet is effecting blood sugars. Think of it as some sort of intolerance. What is it? I really can't know. I list a bunch of blogs I follow that are all about nutrition because I'm trying to find out.<br />
<br />
I ate a very healthy diet before I was diagnosed but now I find I can't eat that same diet without a significant rise in blood sugar. Would I say that, simply because I can't eat it, no one should? No. What I will say is that KPD is different and pretending that it isn't does not work. We can not assume what is healthy. We must verify.<br />
<br />
I've just read the usual recommendations of the ADA and others about what is healthy to eat but does it include KPD? I think not. If these foods are fine there is really only one way to know and that's to test the blood sugar. I see all these recommendations about what to eat but, one size does not fit all and this is especially true of KPD. What should be recommended is that all families get a meter and test what their food is actually doing to them. If there is a significant intolerance, blood sugar will exceed 140. If this was the recommendation of the USDA there would be far fewer DKA events in this country. It would also provide important data about what is safe and what is not about a whole range of products.<br />
<br />
To repeat, there is something in the KPD diet, that may not effect others but which is probably poisonous to KPDs. We can't identify who is KPD but if people were checking their blood sugars and correlating it with what they ate, the KPDs that are out there, who aren't diagnosed, could see this truck comingMichael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com8tag:blogger.com,1999:blog-7890548535393086926.post-32131988430460627002010-08-27T16:52:00.004-04:002010-09-19T18:55:29.292-04:00The A1c tipping pointWhilst looking for correlations on some other things, I fell across this important information that didn't make an impression on me then but it certainly does now. I guess it shows that it's a good practice to go back with the new ideas that you've gained and look at the data again.<br />
<br />
Even though, by my estimates, there are millions of Ketosis Prone Diabetics out there, we remain the "mystery meat" of diabetics. There is very little research about its genesis. There is no way to identify a KPD before a diabetic emergency occurs. In fact, as far as I know, very few people are diagnosed as KPD even after they have had an extreme glycemic event and recovered. We don't even know what the numbers are for KPD. I tend to believe that an A1c greater than 10 with spikes above 300 is a good indicator, especially if the fasting blood sugar was less than 140 in the previous year. That thinking and two bucks might get you a cup of coffee.<br />
<br />
We aren't high on anybody's list of things to do. So, I think it's important to glean what facts I can from whatever data is out there to help people deal with KPD. This brings up this little fact. It has to do with the tipping point or when does KPD go from being just a type of diabetes to something that can be deadly.<br />
<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><b>Ketosis-Prone Type 2 Diabetes in Patients of </b><b>Sub-Saharan African Origin</b></div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Clinical Pathophysiology and Natural History of -Cell Dysfunction and Insulin Resistance</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><br />
</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Franck Mauvais-Jarvis,1 Eugene Sobngwi,1 Raphae¨ l Porcher,2 Jean-Pierre Riveline,3</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Jean-Philippe Kevorkian,4 Christian Vaisse,5 Guillaume Charpentier,3 Pierre-Jean Guillausseau,4</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">Patrick Vexiau,1 and Jean-Francois Gautier1</div><div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><a href="http://diabetes.diabetesjournals.org/content/53/3/645.full.pdf">http://diabetes.diabetesjournals.org/content/53/3/645.full.pdf</a></div><br />
<br />
This is a study that tracks KPD's over ten years and compares them to regular Type 2's and Ketosis Prone Type 1's. This study is out of Paris done on emigrants who come mostly from Sub-Saharan Africa. I have talked or corresponded with people who question the relevance of this research to them because they aren't remotely African or descended from Africans. As I said before, this syndrome has been documented almost every. The research is very spare and I've had to cobble data from all over the world. I suggest that beggars can't be choosy. My position is that <b>anything</b> that says <b>anything</b> about KPD is relevant to all KPD's irrespective of color or origin.<br />
<br />
<br />
ADA Criteria for the diagnosis of diabetes<br />
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.*<br />
OR<br />
2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.*<br />
OR<br />
3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT.<br />
<br />
<br />
<div class="MsoNormal"><b><span style="font-family: Futura-ExtraBold, sans-serif; font-size: 10pt; line-height: 115%;">Standards of Medical Care in Diabetes—2010</span></b><span style="font-size: 10pt; line-height: 115%;"><o:p></o:p></span></div><br />
<a href="http://care.diabetesjournals.org/content/33/Supplement_1/S11.full.pdf+html">http://care.diabetesjournals.org/content/33/Supplement_1/S11.full.pdf+html</a><br />
<br />
<br />
That being said, let's get on with it. Above I have copied the ADA guidelines for diabetes diagnosis. It's important to keep these numbers in mind. It is especially important because, as I've said, most docs have no idea about how this works so you need to look out after your needs or those you know.<br />
<br />
Buried in the KPD paper is a graph that describes the path that relapse takes in KPD's. Though it describes relapse, I am looking at it as just the course which KPD's take before their blood sugars go awry. What is my evidence for this. Well, there is one thing but I'll get to that later. Of course, A KPD, by definition, has already been diagnosed so it very definitely pertains to those.<br />
<br />
What they found was that the course before relapse could be predicted by A1c over a years time. I tried to get this but it wouldn't copy. You can find it on page 650. Here's what they had to say.<br />
<br />
<br />
<u>The median duration between the development of hyperglycemia (HbA1c 6.3%) and the onset of a ketotic relapse was 12 months (95% CI, 6–21, Kaplan-Meier). During this period, the insulin secretory reserve, measured before the onset of hyperglycemia and during readmission for relapse, dramatically deteriorated ( C-peptide, 2.88 0.21 vs. 0.19 0.08 ng/ml; P 0.05). There was no precipitating illness other than hyperglycemia. The increase in HbA1c 6.3% was associated with an increased risk of ketotic relapse with an HR of 38 (95% CI, 5–286; P 0.0004). Thus, hyperglycemia preceded and was strongly associated with</u><br />
<u>the subsequent development of an insulin-deficient, ketotic relapse.</u><br />
<br />
<br />
The chart is pretty clear. It tracks the A1c for 40 months. The A1c stays steady at around 6.3% and at about 12 months before relapse takes a slight jog up. At 6 months, it takes another jog up to about 6.6 %. From this point on, the curve becomes steep.<br />
<br />
What you can see is that below 6.3% blood sugars remained steady. Above that number events go bad very quickly. The 6.3% averages out to a blood sugar of 134. The first jog up appears to be about 6.5%, which averages to daily blood sugar of 140. This 140 is not a random number. It is thought to be the point at which blood sugars become damaging and bring on long term complications.<br />
<br />
My thought on this as occurring before the first episode is from some reading, which I can't find, that said it was frequent, that previous to diagnosis, a KPD would have a normal or near normal blood sugars 6 months before. This graph shows something similar. We have no idea what causes this catastrophe but the fact that its beginnings sit at this critical juncture seems to suggest that something gets broken here. What you have to recognize is that this is for people who've already broke down then gone into remission, so whatever got broken got fixed once the blood sugars were brought down.<br />
<br />
Now look at the ADA guidelines. They've tightened them up but look how close they are to the KPD danger point. This guideline is really for T2's. Would you give this as a guideline for KPD's knowing that they can crash very quickly? If you are a KPD should you feel safe with these guidelines?<br />
<br />
If you showed up at a doc with these numbers, the ADA recommends that the physician should inform you that you're prediabetic and that maybe you should start making adjustments with diet and exercise. You would be asked to return in 6 months for a checkup to see how things were going. This wouldn't be a problem for a Type 2 because onset isn't abrupt and acute but for a KPD these numbers should be sending off all types of alarms because in 6 months you could very well be hospitalized or at worse, dead.<br />
<br />
Until there is a diagnostic test for KPD, we will continue to windup in emergency. For those who already know what they are; keep and eye on your blood sugars because, unlike a T2, whose numbers trend steadily, you can go off the rails very quickly.<br />
<br />
<br />
<br />
<br />
<b><br />
</b>Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com2tag:blogger.com,1999:blog-7890548535393086926.post-55111243221838127412010-08-24T19:55:00.001-04:002010-09-01T15:08:48.460-04:00Increased weight and insulin resistance revisitedThis relates to a baffling previous post.<b><a href="http://ketosisprone.blogspot.com/2010/06/increased-weight-and-insulin-resistance.html">Here</a></b> This was puzzling because it involved KPD diabetics gaining weight after a DKA event and becoming normoglycemic. I've discussed remission in KPD's before and though the mechanism isn't well understood, it is known to be common enough to be considered a part of the KPD syndrome. No, what upset the apple cart here was that thin KPD's did not do as well as the ones who gained weight. This seems counter to all the advice about weight loss that is given to diabetics. Almost the first thing a doctor will say to a patient is to lose weight. If a KPD followed this advice their blood sugars would rise and lowering blood sugars is central tenet of all things diabetic. What the heck is going on here?<br />
<br />
I am now going to put forth an idea that popped into my head after reading a post by Ned Kock over at Health Correlator. <b><a href="http://healthcorrelator.blogspot.com/2010/08/growth-hormone-insulin-resistance-body.html">Here</a> What</b><b> got my attention were people who were heavy but were more insulin sensitive then their control group. </b>What was even better: once they received medication they began to lose weight but became more insulin resistant with a rise in blood sugar.<br />
<br />
Insulin Resistance is very much at the heart of obesity and thinness as far as I can see but it is also one of the central aspects of Ketosis Prone Type 2 diabetes. <span class="Apple-style-span" style="color: #333333; font-family: Arial, Tahoma, Helvetica, FreeSans, sans-serif; font-size: small; line-height: 30px;"><a href="http://ramblingsofacarnivore.blogspot.com/"><span class="Apple-style-span" style="color: black;">Pal Jabekk</span></a> </span>speaks of the fact that insulin resistance is a body wide behavior. I agree given insulin's importance in energy metabolism obviously everything has critical involvement with it. This doesn't, however, mean that insulin is used at the same rate through out the body all the time. At any given moment, there will always be some systems that are more or less resistant.<br />
<br />
This brings me back to the puzzle of KPD weight gain while at the same time reaching near normal blood sugars. First of all KPD's are infamous in the fact that weight is not an issue. Just as many KPD's are thin as obese. Some have separated this along the lines of those who lack sufficient insulin so that they become thin and those who have plenty so they become fat.<br />
<br />
When the DKA or severe ketosis event occurs KPD's, who recover, are shown to have a low normal reading of C-peptides. The cut off that has been cited is .9. In six months, it is common for this to go back into the normal range and higher. It is also known that KPD's recover near normal blood sugars even though their measurable IR isn't reduced one jot. It should be noted, as well, that the best blood sugars tend to go to the heavier KPD's and not the thin ones.<br />
<br />
Given that the IR is still high, the C-pep is normal or above and the blood sugars have normalized, we have to assume that there is relatively enough insulin present. What is the difference between thin and obese?<br />
<br />
Now the leap of faith. It has to be relative insulin sensitivity issues. We can see with a thin person that insulin is putting relatively more energy in other systems besides fat. What those systems are we really don't know. What we can tell, however, is those systems on the whole are more sensitive to insulin than fat. Likewise, if the person is putting on weight then their adipose is relatively more sensitive to insulin than other body systems.<br />
<br />
Now my thinking about the KPD's gaining weight with better A1c's. I believe fat works better for glucose storage then muscle or other systems. You can look at obesity as the body's way to reacting to high amounts of glucose. This is why I believe there are so many heavy people. Obviously, the body is sending glucose everywhere but the fat cells seem to get more. If we make this about controlling blood sugar then the fat cells become like the catch basin for the extra glucose in the system.<br />
<br />
A thin KPD is relatively more insulin resistant in the fat cells, and this is why I say fat works better, sending glucose to other systems with fat lower down on the list doesn't normalize blood sugars as well as those who can send it to fat. So thin KPD's are typically not going to have blood sugars as good as heavier KPD's. This would also say that thin KPD's are more at risk of relapse to DKA then heavier KPD's. I would also add that this probably isn't how normal people work but we have broken metabolisms. Our livers are pretty much blind to insulin.Michael Barkerhttp://www.blogger.com/profile/04768809529849718860noreply@blogger.com3