Diabetes Talking

Question:

Mick Brown writes:

<< Is this idea totally off the wall? I couldn’t get my PCP to listen long enough to hear me out, I don’t remember what my CDE said exactly but IIRC it was something unresponsive along the lines that DM T2s don’t go into DKA, and the endo said to see a neurologist. Food that tastes like car deodorizers is unpleasant, but the neuroglycopenic symptoms are the killers: loss of short term memory, inability to bring words to mind, numbness–especially face mouth and tongue and arms, difficulty voiding my bladder, trembly feelings, and clumsiness such as tripping and running into doorframes. Mick, I don’t know the composition of your diet, but if it is extremely low in carbohydrates, you are likely experiencing benign dietary ketosis – a thing ketogenic dieters strive for, as it places their bodies in fat-burning mode. Home testing kits are not as good as those at the doctor’s office. I rarely show ketones in my urine, but wiill show a trace at the doctor’s office … and that is precisely where I want to me. I agree with your conclusion that you are likely feeling hypo-y at relatively high readings because for a time your glucose readings were not optimal. As long-term control improves, you should be able to drop lower and lower without feeling hypo-y. Susie

Response:

– Hide quoted text — Show quoted text – This is mostly consistent with ideopathic postprandial syndrome symptoms (basically hypo symptoms with normal bGs) which I found in a compuserve diabetes/hypoglycemia section file. My speculation is that I’m Insulin Resistant enough that my cells are feeling starved and causing fat burning etc. and hyperinsulinemic so my bGs fall very rapidly to near normal levels after meals. I’m often reading near 100 (5.5) 1 hr PP at present. Correct me if I’m wrong but I don’t think insulin resistance works that. From my understanding the reason T1’s go into DKA is because they have no endogenous insulin, nada, none.  T2’s may be insulin resistant but they (most anyway) do have insulin running around in their body.  That prevents the T2 from going into DKA but the resistance causes high BGs but a T2 still has enough insulin to prevent DKA.  There is a better scientific explanation to it, I just don’t have it.

This isn’t a full answer regarding IR & DKA, it mostly reports my interpretation of what I’ve read about DKA & HONK. AFAIK there are three main types of acidosis "related" to DM. Diabetic KetoAcidosis, HyperOsmolar NonKetotic Acidosis, and Lactic Acidosis. All usually involve dehydration as a factor. DKA and HONK are much more common than Lactic acidosis IIRC. DKA is characterised by dehydration, excessive urination, high bGs, high levels of Ketones in blood and urine, nausea. HONK has similar simptoms except for the ketones. The Http://www.glucophage.com/ppi.htm page has the list of rather vague symptoms of LA. In HONK your blood gets so sugary that it starts drawing water from surounding tissues. DKA and HONK are often precipitated by illness or infections. A tiny quibble: T1’s at Dx often have some, albeit insufficient, insulin production… that’s why so many have a honeymoon period after they get the bG levels down after diagnosis. Someone recently posted his story of Dx with DKA or severe ketosis starting on insulin and then moving onto glyburide, and I believe Bernstein mentions that some T1s maintain some beta cell function for sometimes a year or two after Dx. In any case you’re right a T2 generally produces many times the insulin of a just Dx T1. and T2s who are acidotic are more likely HONK than DKA. Anyway, what I’ve read indicates that DKA requires a dehydrating problem plus insulin insufficiency or very high insulin resistance (IR can make a relative insulin insufficiency). Basically it requires extreme polyuria or severe diarrhea or inability to ingest fluids. T2s who are vomiting or have dysentery or have dehydration may well go into DKA. As I understand the DKA (extract the ketone part for HONK) it works as follows: * Something causes bGs to go above some magic number, polyuria starts   with attending dehydration. * Dehydration increases glucose concentration in the blood. * Increased glucose concentrations create a type of insulin resistance   IIRC this is called glucose toxicity. * Increased insulin resistance makes marginally sufficient amounts of   insulin inefective at transporting glucose into cells. * Low cellular glucose turns on ketogenesis. * ketones in the blood cause increased urinary secretions. * ketone in the blood cause increased urinary secretion of sodium. * Increased bGs causes increased urinary output. * decreased sodium in the blood causes decreased blood volume, increased   glucose concentrations… * increased blood glucose concentrations decrease effectiveness of   circulating insulin… * and so on. So it is a circular process where each step increases the factors that decrease blood volume and electrolytes and increase insulin resistance (via glucose toxicity). Sounds incredibly nasty. So at least the glucose toxicity kind of insulin resistance is involved in pre Dx T1s and any T2 who is DKA. T1s and T2s do differ in the amounts of insulin production, and it may partly explain why most T2s do not get excessively ketotic, but some T2s do go into DKA so insulin production might not be the whole story for the T2s. I’ve looked for information on this, but public sites don’t seem to have the level of detail about this that I’d need to answer the question… and I don’t have accesss to a medical library at present. — Mick Brown Please visit the Pro Internet Forum http://www.delphi.com/pro_internet My address is unmangled, I report spam and get the senders’ accounts yanked I registered at http://www.SafeEPS.com Email Preference Service   and said *NO* *SPAM* at all for me.

Response:

This is mostly consistent with ideopathic postprandial syndrome symptoms (basically hypo symptoms with normal bGs) which I found in a compuserve diabetes/hypoglycemia section file. My speculation is that I’m Insulin Resistant enough that my cells are feeling starved and causing fat burning etc. and hyperinsulinemic so my bGs fall very rapidly to near normal levels after meals. I’m often reading near 100 (5.5) 1 hr PP at present.

Correct me if I’m wrong but I don’t think insulin resistance works that.  From my understanding the reason T1’s go into DKA is because they have no endogenous insulin, nada, none.  T2’s may be insulin resistant but they (most anyway) do have insulin running around in their body.  That prevents the T2 from going into DKA but the resistance causes high BGs but a T2 still has enough insulin to prevent DKA.  There is a better scientific explanation to it, I just don’t have it. Beanie, Type I (Humalog and Ultralente)

Response:

Mick, you Type 2’s almost never go into DKA, from what I’ve read, but you could very well go into ketosis if you’re eating a diet that’s low in carbohydrates.  The whole principle of the Atkins diet is to induce a state of ketosis, where you’re burning fat for energy, but not eating many carbohydrates at all.  Lots of people who do Atkins have the experience you describe.  Could that be causing it?

DKA is rare in DM T2… but my aunt has been DKA once or twice. But I’m not worried about DKA considering I’m reasonably well hydrated and not hyperglycemic. I see I forgot some essential information: I’m eating about 280-320g carbs in about 45-50% cho 25% protein 25-30% fats proportions. This should not produce low carb type of ketosis. If I were doing a very low carb diet I wouldn’t be surprised. My bGs are currently mostly euglycemic or nearly so without any meds. but I’m having hypoglycemic/neuroglycopenic and starvation (ketones) symptoms despite intake of about 2700 calories. An earlier post gave some details about an ER trip due to an oddball "hypoglycemic" event when I was I couldn’t stand for about an hour despite bGs measured between 84 (4.7) and 133 (7.4) I suspect I may have gone as low as 70 (3.9) but was too disoriented to stand let alone measure at the presumed bG nadir. This is mostly consistent with ideopathic postprandial syndrome symptoms (basically hypo symptoms with normal bGs) which I found in a compuserve diabetes/hypoglycemia section file. My speculation is that I’m Insulin Resistant enough that my cells are feeling starved and causing fat burning etc. and hyperinsulinemic so my bGs fall very rapidly to near normal levels after meals. I’m often reading near 100 (5.5) 1 hr PP at present. Last year I had several 175 fasting lab readings and I was Dx about 10 years ago with a 200 fasting lab reading. — Mick Brown Please visit the Pro Internet Forum http://www.delphi.com/pro_internet My address is unmangled, I report spam and get the senders’ accounts yanked I registered at http://www.SafeEPS.com Email Preference Service   and said *NO* *SPAM* at all for me.

Response:

Mick, you Type 2’s almost never go into DKA, from what I’ve read, but you could very well go into ketosis if you’re eating a diet that’s low in carbohydrates.  The whole principle of the Atkins diet is to induce a state of ketosis, where you’re burning fat for energy, but not eating many carbohydrates at all.  Lots of people who do Atkins have the experience you describe.  Could that be causing it? Wendy

Response:

I’m 46 Type 2 watching what I eat & physical activity Dx 3/89. (I don’t much care for the words diet or exercise, reminds me of making weight for HS wrestling). Anyway since December 1997 I’ve been having weeks of several days where I’ll smell acetone, burnt food, or my mouth will taste like I’ve been chewing on car air fresheners. Last summer the smell usually meant I had a high bG as in a 2+ urine test. This was during a period when my medicaid had lapsed. In the months since getting medicaid back and formal treatment, these episodes are fewer, and are associated with bGs less than 95 mg/dl 5.3 mmol/l or ingesting less than 2500 calories. In my testing with bayer ketodiastix I’ve never had a positive reading for ketones in urine testing. but I have had MODERATE ketones notes on lab urinalysis reports. They said I was slightly hyponatremic (low sodium) which might possibly support prolonged mild ketosis. However I did take one ketone test the other day where it did turn maroon but the strip instructions say read at 15 seconds and the color change took about a minute. I’m beginning to think that these symptoms:   ketone smells at good readings (80-100)   while maintaining good bG (<120 fasting < 110 average 2hr PP)   generally feel hypoglycemic w/ neuroglycopenic symptoms at < 95 (5.3) may mean that I’m very insulin resistant and rather hyperinsulinemic. The reasoning is that ketones are produced in starvation. If the insulin resistance is high the cells may feel underfed at normal glucose levels. Type 2s are generally insulin resistant. My uncle responds well to rezulin an insulin sensitizer so I’m likely to have a similar resistance problem. And hyperinsulinemic since my bGs fall rapidly to near my basal levels between 30 minutes and an hour PP. My body temperature also goes down as my bGs goes lower possibly indicating lower glucose oxidation rates. Is this idea totally off the wall? I couldn’t get my PCP to listen long enough to hear me out, I don’t remember what my CDE said exactly but IIRC it was something unresponsive along the lines that DM T2s don’t go into DKA, and the endo said to see a neurologist. Food that tastes like car deodorizers is unpleasant, but the neuroglycopenic symptoms are the killers: loss of short term memory, inability to bring words to mind, numbness–especially face mouth and tongue and arms, difficulty voiding my bladder, trembly feelings, and clumsiness such as tripping and running into doorframes. — Mick Brown Please visit the Pro Internet Forum http://www.delphi.com/pro_internet My address is unmangled, I report spam and get the senders’ accounts yanked I registered at http://www.SafeEPS.com Email Preference Service   and said *NO* *SPAM* at all for me.

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