Struggling to understand Type 1/Insulin/Weight loss

Justkeepswimmin

You can be type 1 at any age, although it is more frequent earlier in life. My husband become type 1 at the age of 29, and was never type 2. His diabetes was caused by chemical exposure in the miltary to something that ruined his pancreatic function, specificially the beta cells in it that tell the body when/how to creat insulin.

A fantastically not so intelligent doctor diagnosed him as type 2 diabetes, gave him pills, and sent him home for the weekend (with 800 blood sugar) By Monday he was in the hospital with DKA.

So now, his body produces absolutely ZERO insulin on it's own, which is only a slight blessing because we can moderate his insulin based on what's in his shots as opposed to what is not. He's 51 and been a diabetic for 22 years.

As for weight loss, he has lost (and gained) weight since being diagnosed with his diabetes. It takes time, and occurs much much more slowly, however some important tips.

1. As with any diet, grains are better than starchy carbs, but not only are the considered 'healthier' they will release into your blood stream slower (the sugar), so you wont spike your sugar, then take a shot to correct that spike, then get into a low (which is just as dangerous as DKA). DKA is scarry but takes a few days (usually) to occur (unless you exercize with high blood sugar then you can go into DKA). Low blood sugar is more frightening for me because my husband has a rediculous tolerance for low blood sugar and doens't notice it is low until it is very low, and it can drop fast. Of course if your sugar is low enough you can pass out, and your entire body can shut down (ie die).

2. Test, test test test (your sugar). Then accomodate what the test shows. So if your sugar is running high, but you're trying to 'snack' every 2-3 hours for a diet...eat protein only when the sugar is high, and focus on the carbs when it is lower.

3. Build yourself a buffer into MFP. Keep your goals for the week 'lower' but try to consistently be under about 100-200 calories of that goal. For example, hubby's caloric 'net' goal *was* 1700. We found that he would get lows sometimes, and then the sugar would put him over goal, and he'd be discouraged. So we decreased the ammt we wanted him to lose/week so his goal is now 1980 (still a loss for him, he's very tall) but he tries to get around 1700 in, and if he goes over due to a sugar low he doesn't worry about it. This is just a mental strategy.

4. Ask your doctor about Symlin - it's not insulin, it IS an extra shot. It's basically a way of making sure your body is processing proteins properly, since it's been discovered that some type 1 diabetics do not process proteins properly. This is important for you to be able to build musle. A great side effect is it supresses appetite. (I think the FDA was going to look into approving it for weight loss too eventually).

5. Try to keep healthy carbs on hand for lows and resort to pure sugar only in desperate situations (ie. 100% juices, and fruits for lows, and maybe some healthy crackers for only slight lows as they take longer to process than juice or fruit)

6. Pay attention to your sodium, diabetics are prone to all sorts of heart issues which are also aggravated bo sodium. This will also curb your bloating.

7. Eat a few carbs before exercize if you find you're getting low during exercize and resorting to unhealthy carbs right after your exercize to bring it up.

8. Keep a routine schedule for eating times.

Being insulin dependent does not necessarily make you type 1. Also, you can be what some call a type 1 and a 'half' (doctors say that about my husband) It does not mean you're between either condition, but more so that you have both conditions. Meaning that your body doesn't produce insulin AND your body is resistant to insulin when it is in your body. It's important that you find a great endocrinologist - most of which have nutritionists that they have in house or one they reccomend.

jamja72

Bump

badgerbadger1

You can disagree but they are facts, or so I was taught in medical school which may be wrong.

What year are you? 1st? 2nd? Get back to me when you finish your residency. I don't mean to pick on you but you are providing misinformation. Do you have any clinical experience at all? I don't know any nephrologists, endocrinologists, vascular surgeons or even residents who would agree with you.

Diabetes isn't "essentially" vascular, it's endocrine with significant metabolic, neurological, vascular and renal etc sequelae if uncared for.

Diabetes produces vascular sequelae by making the blood essentially stickier, sticking to vessel walls eventually causing them to occlude. By this and higher blood pressure, small vasculature such as renal, retinal, peripheral vasculature, and coronary vasculature are more likely to occlude resulting in the effects noted.

One of the first signs of diabetes is not urine protein. The first sign of diabetes is high blood sugar. Renal effects are not notable until GFR drops to nearly 5% of baseline function. Urine protein would be a LATE sign, therefore.

Diabetic ketoacidosis is not a result of high carb eating. It's due to inability to utilise insulin or lack of insulin usually in the presence of an illness such as the flu or infection.

chuckles217

What year are you? 1st? 2nd? Get back to me when you finish your residency. I don't mean to pick on you but you are providing misinformation. Do you have any clinical experience at all? I don't know any nephrologists, endocrinologists, vascular surgeons or even residents who would agree with you.

Diabetes isn't "essentially" vascular, it's endocrine with significant metabolic, neurological, vascular and renal etc sequelae if uncared for.

Diabetes produces vascular sequelae by making the blood essentially stickier, sticking to vessel walls eventually causing them to occlude. By this and higher blood pressure, small vasculature such as renal, retinal, peripheral vasculature, and coronary vasculature are more likely to occlude resulting in the effects noted.

One of the first signs of diabetes is not urine protein. The first sign of diabetes is high blood sugar. Renal effects are not notable until GFR drops to nearly 5% of baseline function. Urine protein would be a LATE sign, therefore.

Diabetic ketoacidosis is not a result of high carb eating. It's due to inability to utilise insulin or lack of insulin usually in the presence of an illness such as the flu or infection.

I have my masters in biochemistry and am a 3rd year medical student. I have done 5 years of bench research into auto-immune diseases, my particular focus was type 1 diabetes. I have numerous publications as a 2nd author under the MD/Ph.D. I worked under.

High blood sugar is the first "sign" per say of diabetes but is rarely symptomatic, so the first positive test most often to come back would be a non-fasting finger stick of >126 given that 126 glucose is the new standard for declaring diabetes. However, the 126 levels must be found on two separate occasions during fasting episodes for a definitive diagnosis. Most physicians air on the side of caution and run a urinalysis and look for microalbumin and other protein such as a dipstick protein. Dipstick protein [whole albumin] won't be positive until late into the diabetic glomerulopathy of the kidney disease, but the initial uncontrolled blood sugar drives the non-enzymatic glycosylation of the efferent tubule of the kidney's gloumerular blood flow. This in essence increases the GFR of a kidney by constricting the efferent arteriole and leads to the leakage of micro albumin and is a very early sign. It is a very sensitive test, but relatively unspecific which is why it is followed up with the specific test of the blood sugar confirmation.

And yes it is an underlying endocrine disorder varying between destruction of beta islet cells in the pancreas for type 1 or the insensitivity to insulin in type 2, but the disease process is that of vascular. Every symptom relates to a vascular component that results from hyperglycemia leading to non-enzematic glyocsylation of various substrates not limited to the basement membranes of arteries. Why are their neurological symptoms such as peripheral neuropathy and painless foot ulcers? Peripheral vascular disease obliterates the blood supply and necrosis the nerves. If further left untreated, the kidney arterioles further fibrose and those they initially increased GFR since the efferent arteriole was first affected, the afferent arteriole eventually fibroses along with the efferent leading to nodular glomerulosclerosis and ultimately nephrotic syndrome with a steady decline in GFR until chronic kidney disease (aka renal failure) results. Hence why ACE inhibitors are a must to aid in dilating the efferent arteriole and keeping the GFR up.

And as far as diabetic ketoacidosis, the glucose stays within the blood stream and has extreme trouble entering muscle and target organs. Excess carbohydrate (specifically that of high glycemic index) leads to large spikes in blood sugar which depending on the type of diabetic, has various effects. Ultimately, it drives the body to a fasting state driving the production of acetoacetic acid, beta-hydroxybuteric acid and other ketones as a last ditch fuel. This produces severe metabolic acidosis if allowed to persist for a while and then combined with the kidney pathology, titratable acids can not be secreted nearly as well further increasing the severity of the acidosis. So the underlying cause may be insulin (whether it be lack of or insensitivity) but the excess glucose load of an uncontrolled diet is proven to accelerate a person towards DKA.

badgerbadger1

So then I'm confused why you stated what you did. You are essentially agreeing with me, however by stating things like "urine protein is the first test/sign" is incorrect, it IS high blood sugar, as you said in your latest post.. Urine protein is more specific for kidney disease. Stating eating too many carbs being THE cause is incorrect, as you are apparently well aware that there are many factors involved in producing a state of DKA. Stating diabetes is a vascular disease is incorrect, as you have just now stated. Your first post does not jive with your latest one and it is misleading to the otherwise uneducated, you must concur.

I think your lab/textbook knowledge is causing you to overthink this, which is a common error. Occam's razor and the concept of KISS apply in medicine. Why would you do a test that is more expensive and less specific when it will tell you the same thing as a simple stick? It's only after the sticks come back positive that you start running more specific tests like urine protein, if and only if, you have reason to believe there may be renal involvement. It's like sending someone for a full body CT when it will not effect your treatment plan or outcome whatsoever.

When speaking to a patient, it is important to use layman's terms and ensure you are not bringing extraneous info into the picture. Urine protein has little if anything to do with the topic at hand.

I'm really not trying to slam you, that is not my intent. However years in the classroom and lab do not compare to years in the clinical environment. As a M3 I'm sure you are already clerking and are aware of this. As a clerk you probably get challenged like this daily by your attending. What you have done in the lab is great, but they are more concerned with how you APPLY it. It does not always translate. We occasionally get M4's in our unit for a 2 week optional exposure and they're way out of their league. Regardless of background. Even PGY2s can struggle and will need our guidance or will be challenged. That's how we learn. When rounding, you know that you can propose treatment or testing options, but you had better be prepared to provide a good rationale for it. Please consider my challenge more like a challenge on rounds, not as a personal attack.

chuckles217

So then I'm confused why you stated what you did. You are essentially agreeing with me, however by stating things like "urine protein is the first test/sign" is incorrect, it IS high blood sugar, as you said in your latest post.. Urine protein is more specific for kidney disease. Stating eating too many carbs being THE cause is incorrect, as you are apparently well aware that there are many factors involved in producing a state of DKA. Stating diabetes is a vascular disease is incorrect, as you have just now stated. Your first post does not jive with your latest one and it is misleading to the otherwise uneducated, you must concur.

I think your lab/textbook knowledge is causing you to overthink this, which is a common error. Occam's razor and the concept of KISS apply in medicine. Why would you do a test that is more expensive and less specific when it will tell you the same thing as a simple stick? It's only after the sticks come back positive that you start running more specific tests like urine protein, if and only if, you have reason to believe there may be renal involvement. It's like sending someone for a full body CT when it will not effect your treatment plan or outcome whatsoever.

When speaking to a patient, it is important to use layman's terms and ensure you are not bringing extraneous info into the picture. Urine protein has little if anything to do with the topic at hand.

I'm really not trying to slam you, that is not my intent. However years in the classroom and lab do not compare to years in the clinical environment. As a M3 I'm sure you are already clerking and are aware of this. As a clerk you probably get challenged like this daily by your attending. What you have done in the lab is great, but they are more concerned with how you APPLY it. It does not always translate. We occasionally get M4's in our unit for a 2 week optional exposure and they're way out of their league. Regardless of background. Even PGY2s can struggle and will need our guidance or will be challenged. That's how we learn. When rounding, you know that you can propose treatment or testing options, but you had better be prepared to provide a good rationale for it. Please consider my challenge more like a challenge on rounds, not as a personal attack.

I understand what you're getting at. I just got off rounds of IM with a nephrologist hence why I am so "full" of knowledge as the area we are in we see large majority of T2D patients with no medication/diet compliance. The whole micro albumin came directly from the attending I was under as he grilled me on that on a regular basis stating more cases of T2D are initially discovered on a urinalysis with Microalbumin than by symptomatic blood sugar levels. So I guess my error lies in declaring frequency, not chronology of symptoms.

Anyways... Tossing out all the jargon and pardon the interruption, back on topic per say?

badgerbadger1

Yep, good luck on your next rotation! I'm out for a run.

Cheers.