18Jan

Type 2 Diabetes – Do Toning Shoes Really Help Lower Blood Sugar Levels?

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Lower blood sugar levels for Type 2 diabetics because you wear a certain style of shoes, it almost sounds too good to be true. It seems like such an easy way to get your blood sugar levels in control. Just slip on a pair of Reebok EasyTones, and you get so much exercise out of just walking your blood sugars float down to normal and your thighs and butt tighten, too. But do they really work?

Toning shoes are shoes with a curved insole designed to imitate the experience of balance on a wobble board at the gym or walking on a sandy beach. They definitely cause twitching muscles in the ankles, calves, thighs, and buttocks.

The jury is still out on whether toning shoes really tone muscles. The American Council on Exercise has commissioned a team of scientists at the University of Wisconsin to put Skecher’s ShapeUps, Reebok EasyTones, and Masai Barefoot Technology to the test. The request was made after advertising claims by Reebok seemed to promise more benefits than the shoes can deliver, at least in terms of tightening muscles.

Anytime you get muscles moving, however, especially muscles in the buttocks, glucose will be burned and insulin sensitivity will increase. This doesn’t mean:

using the shoes will burn more calories overall
wearing these shoes will help your cardiovascular fitness

It just means that they will probably help your insulin sensitivity and give you lower blood sugar levels than exercise in ordinary running shoes.

Most Type 2 diabetics, of course, don’t need special running shoes. They need to try running! If your doctor approves, even a few seconds of running, rather than walking, can have noticeable or even dramatic effects on your blood sugar levels, far more than any medication.

Among the most common medical problems experienced by people with diabetes, Type 1 or Type 2, are problems related to feet. The feet, or human feet anyway, were meant to walk on grass and dirt, not on flat hardened surfaces such as concrete. One of the problems with walking or running on concrete over long periods of time, is that joints of the feet may break down!

Here are a few tips to help keep your feet healthy:

1. Look at the condition of your feet and toes each and every day.
2. Get up and move… regular body movement will help your overall circulation and muscle tone.
3. Choose footwear carefully.
4. Check your sock drawer… pitch the nylon ones or any socks that help keep in the perspiration. And the socks with holes cause irritation to the skin.
5. If you need to sit for long periods… wiggle your toes.
6. Wash you feet daily… keep them dry and clean.
7. Your skin is the first and best armor to protect your feet… keep it moisturized daily
8. Make sure your doctor checks your feet at each visit.

Smoking causes poor circulation and puts Type 2 diabetics at a higher risk of complications if and when you injure your feet. Smoking affects your circulation.

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11Jan

Type 2 Diabetes – The Weight Loss And Blood Sugar Connection!

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Are you obese and suffering from Type 2 diabetes? Do you ever wonder why your doctor keeps on nagging you about trimming your belly fat and getting rid of your excess weight? Do you know the benefits of losing weight in Type 2 diabetes? If you are still puzzled about what effective, healthy weight loss can do, the best thing for you to do is to continue reading this article.

A study published in the February 2002 issue of The New England Journal of Medicine estimates that approximately 8 percent of American adults are suffering from the direct and indirect consequences of having Type 2 diabetes. In another study published by the Journal of the American College of Nutrition in 2003, it is clearly stated obesity is the major cause for the development of diabetes mellitus 2 or Type 2 diabetes, and the excessive intake of energy in the form of calories in obese people is the number one contributor to the poor control of blood sugar in this disease.

What is the mechanism behind diabetes and excess fat accumulation?

In a study published by the European Review for Medical and Pharmacological Science in 2002, it has been shown the increase in weight causes the development of hyperinsulinemia or elevated blood insulin, the hormone responsible for the transport of energy-producing glucose or sugar into the cells. However, even with this increased blood insulin, the individual cells still can’t utilize these raw energy materials because of the development of insulin resistance, or the inability of individual cells to respond to insulin stimulation, leading to excess sugar levels in the blood. Furthermore, this obesity-induced resistance to insulin pushes individual cells to increase their fat accumulation which further increases the fat tissue bulk within your body.

Obesity is now a well-recognized major factor in the progression of insulin resistance in Type 2’s. In fact, in the study published by the European Review for Medical and Pharmacological Science, it has a large impact on the worsening of diabetes and its other complications such as cardiovascular disease.

Being obese is one of the greatest obstacles to the proper management of Type 2 diabetes. So, if you are one of those people suffering from the consequences of diabetes, getting rid of your excess weight can be one of the best decisions you have ever made. Changing your lifestyle by increasing your physical activities and making your diet healthier are your best bets for effective weight loss.

Remember this: Having a good weight management program is one of the most important tools for the management of your Type 2 diabetes. To start with lower your blood sugar levels by choosing healthy foods, you will then lose weight. And by losing weight your blood sugar levels will continue to fall… and you will continue to lose weight.

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15Dec

Type 2 Diabetes – How Likely Is a Diabetic to Fall Into a Coma?

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Okay, the question about the likelihood of falling into a coma must cross every diabetics mind. The good news is, you are not very likely to fall into a coma. The bad news is, there is a realistic possibility of such an occurrence coming about.

Unfortunately, the blood sugar of a diabetic is not as normalized as that of a non-diabetic person, so there is the possibility of hypoglycemia or hyperglycemia taking effect. In subsequent paragraphs, we’ll talk about a few symptoms that will give you advance warning as to whether a coma may be in your near future.

Since diabetic comas can be fatal, this information is worth paying attention to.

What is a diabetic coma? It is a reversible form of unconsciousness found in people with diabetes. It is classed as a medical emergency brought on by hypoglycemia or hyperglycemia.

1. Hypoglycemia is a state in which your blood sugar is too low. When it gets beyond a certain threshold, you lose consciousness and cannot be reawakened without medical treatment. Falling into a diabetic coma can actually kill you, especially if your blood sugar is critically low. Essentially, your cells need nourishment that they aren’t receiving, so they can’t function. Imagine eating plenty of food, but still essentially starving.

Some of the symptoms of hypoglycemia include:

  • being confused
  • having a racing heartbeat
  • being irritable, hostile or aggressive
  • nauseousness
  • hunger
  • sweating
  • fatigue, and
  • nervousness, possibly to the point of shaking

These symptoms need to be dealt with by eating something sweet, or by following the plan your doctor gives you for dealing with such a situation.

2. Hyperglycemia is when you have too much sugar in your blood. When you have too much sugar in there, your body becomes dehydrated and can’t function properly. That is why the number one symptom of high blood sugar is having way more thirst than you ought to. Since what goes in must come out, this thirst leads to an above average frequency of urination. Hyperglycemia also leads to:

  • fatigue
  • feeling nauseous and even vomiting
  • being short of breath with no apparent reason for it
  • having an elevated heart rate for no apparent reason
  • a pain in your stomach, and
  • a breath odor that smells like fruit

If you begin to feel any of the above symptoms, test your blood sugar immediately. If it’s not where it ought to be (based on your personal insight and your doctor’s decisions), follow your treatment plan. This might involve injecting some insulin, or eating something sweet, or a host of other things you might need to do. Basically, you have a very low chance of falling into a diabetic coma if you keep your doctor knowledgeable about what’s going on, then follow the instruction he or she gives you.

If you just trust your health to chance, however, chance will do with you whatever it likes and a diabetic coma could occur.

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07Dec

Type 2 Diabetes – Can’t Hypoglycemics Just Eat Lots of Sugar?

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If you or somebody you know suffers from hypoglycemia, you know that boiled down, it’s basically just not having enough sugar in your blood to run things properly. Really, being hypoglycemic is one of the least threatening side effects of diabetes, Type 1 or Type 2, because all you have to do is monitor your blood sugar levels, and eat some (but only a little) sweet things when it begins to drift downwards.

Hypoglycemia, also known as low blood sugar, occurs when your blood glucose falls below normal levels. So this begs the question that if your blood sugar is too low, can’t you just eat a lot of sugar and reset things? The sad fact is, very few things in life are ever that simple. And there are actually two reasons for this, which we’ll get into now.

First off, hypoglycemia is a condition in which sugar drifts too low because of metabolic reasons. Your diet may be no different from millions of other people in the world who look completely the same as you. Members of your own family may eat exactly as you do, and have perfectly normal blood sugar. Sometimes in life, you are just dealt a bad hand, and you have to play it to the best of your ability. In the case of hypoglycemia, you have to grin and bear the fact that your blood sugar is going to drop faster and less predictably than other people’s. However, all hope isn’t lost at all.

The second reason why you can’t just eat lots and lots of sugar is because sugar isn’t stored that way. It can be stored as fat, but only before it reaches your blood stream. Once it’s in your blood, sugar becomes a wrecking crew tearing through your system causing damage that you might not see in the short term, but that can have dire consequences in the long term. If you ate large amounts of sugar, you wouldn’t be “socking it away” for a later time… you would just be causing yourself damage, and increasing your short term need for insulin. This need would basically negate your attempts to fix the problem, which would put you back at square one.

How to beat hypoglycemia: As frustrating as it is, your only hope to beat hypoglycemia or low blood sugar, is to moderate your sugar intake, and to keep up to date (sometimes down to the hour) with your blood sugar levels. Eating low GI foods in moderate quantities (such as a small meal every 2 hours or so), is the best anyone has been able to find for keeping hypoglycemic blood sugar levels stable and healthy. Whatever you do, don’t OD on sugar!

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02Dec

Type 2 Diabetes – Maybe Hypoglycemia Does Not Always Apply to Diabetes!

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If you have ever found yourself in a situation where you’ve been starving, hypoglycemia is most likely more familiar to you than you would like. However, you can actually develop this problem even if you eat meals on a regular basis.

For some people, their overabundance of insulin can trigger their blood to absorb their sugar rapidly, and still want for more. Unfortunately, just as it is possible to have too much of a good thing, it is just as easy to have too little of it. This is a bizarre sort of seesaw, as your blood sugar and your insulin levels should ideally be in a state of perfect balance.

The bad news is, this is often not the case. Sometimes your body just does not quite respond as you would expect (or like), it to. The good news is that short-term hypoglycemia has no lasting effects on your brain or your body. Unfortunately, in many people’s cases the tendency is genetic, and needs to be kept from being harmful through carefully moderating their diets. But of course, there is the additional bad news in that long-term hypoglycemia can:

  • impair your mental faculties
  • reduce your ability to control your body, and
  • even cause you to lose consciousness and slip into a type of coma

Your body needs to use all of the sugar it gets, after all, and not using it well causes problems.

Hypoglycemia can also be a warning sign of an illness that is based in one of your internal organs. There are ample occasions in which hypoglycemia acts as a sort of signal that a worse ailment is present.

For instance, the over-production of insulin that we talked about earlier is officially known as hyperinsulinism.

You may also have an insulin-secreting pancreatic tumor, or an adrenal insufficiency. You may even have hypopituitarism, in which the pituitary gland may not be producing enough of one or more of its hormones to maintain your body’s internal balance.

While it may not be the worst thing that can happen inside your body, hypoglycemia is a fairly serious issue to have. Consider that it is essentially your body shutting down, just because it lacks the sugar it needs. Consider that the manifestations of this ailment are fairly large and frequent. The hypoglycemic person tends to be:

  • shaky
  • anxious and
  • nervous

They also tend to have heart palpitations, and heart problems such as tachycardia and palpitations, as well as feeling cold, clammy and having pallor.

A person having andrenergic manifestations can also feel warmer than might seem reasonable, as well as having a:

  • headache
  • nausea
  • intense hunger, and
  • the simultaneous “pins and needles” feeling that people report

Once you know how to spot hypoglycemia, you’ll know to just deal with it yourself and move on with your life.

It is possible to have low blood sugar levels without having diabetes. After your doctor checks your records and suspects more than Type 2 diabetes, he will order blood tests to measure your blood sugar and insulin levels, plus any other chemicals that play a part in your body’s energy use.

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23Nov

Pre-Diabetes – The Early Warning Signs of Type 2 Diabetes!

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Months, years, and even decades before developing full-fledged Type 2 diabetes, many people develop a condition termed pre-diabetes. They have blood sugar levels that are too high to qualify as normal, but not quite high enough to require diabetes treatment. The reason many people with these conditions go undiagnosed, however, is that their doctors almost always rely on blood tests taken while the patient is fasting.

When fasting blood sugar readings range between 100 to 125 mg/dL (5.5 to 7 mmol/L) doctors put the patient on watch for future diabetic developments. These readings mean that for some reason, too much sugar is floating around in your bloodstream. It may be because your body:

  • doesn’t make enough insulin
  • you eat more food for fuel than you can handle
  • for some reason your insulin isn’t working right, or
  • a combination of all these factors

The problem with relying on fasting sugar levels, however, is that sometimes they don’t detect an important part of the pre-diabetic condition known as impaired phase 1 secretion.

The insulin-producing beta cells of the pancreas don’t churn out insulin at the same rate all the time. They spend all their energy making pro-insulin, which they “unzip” to get sugar levels down when they are highest, which is about 90 to 120 minutes after eating, when sugars are digested from food.

Pre-diabetics often have an “unzipping” defect. The beta cells are so burdened by toxic free radicals they just can’t get their work done fast enough to keep blood sugar levels in check after meals. They can, however, release enough insulin to get fasting sugar levels back down to normal or nearly normal the next morning. Only after a period of years, as most of the beta cells die off, do fasting blood sugar levels get so high that the doctor then makes a diagnosis of Type 2 diabetes.

Don’t rely on fasting readings alone. If you blood sugar levels go up to 140 to 199 mg/dL (7.8 to 11 mmol/L) after you eat, this is also a sign that you have pre-diabetes. An occasional blood test that isn’t taken while you are fasting can give you an early warning years sooner, giving you precious time to control and even reverse your pre-diabetes.

You may be asking… what’s the big deal? Why should you worry? You haven’t been diagnosed with Type 2 diabetes… yet! Pre-diabetes, diabetes and obesity are associated with an increased risk of developing many other health problems. People don’t wake up one day to discover they’ve suddenly developed Type 2 diabetes. The progression from normal to pre-diabetic and then to Type 2 diabetic typically occurs over many years.

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11Nov

Decreasing the Risk of Diabetic Retinopathy in a Type 2 Diabetes Study: Part 4

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Mexican pharmacy

Case management may also have played a role in attendance at sessions when the photographs were taken and the immediate feedback that nonmydriatic photography can give to the health care team and thus facilitate the follow-up of patients with documented retinopathy. Whether it is the support associated with case management and the resultant adherence to nonglycemic targets such as hypertension that led to the improved retinal status, independent of improved glycemic control, cannot be addressed by this study. However, perhaps because case management clearly improves glucose control in a Medi-Cal–type population and is associated with decreased risk of new-onset retinopathy, comprehensive case management may be justified in similar health care settings.

Limitations of this study include the fact that it was not of sufficient duration to address whether case management may have also prevented progression of previously recognized retinopathy, which may have required more time or larger numbers to see an effect. Another limitation is the fact that we only used a single field for evaluation of the retina rather than the seven fields used in other studies of retinopathy, although in previous reports, this technique for diabetic retinopathy screening has been shown to be effective. In this way, minimal retinopathy may have been missed in the periphery at baseline and at the follow-up study. However, since both baseline and follow-up retinal fields were identical, it is most likely that our findings reflect a clinically meaningful decrease in the development of retinopathy over the 2-year time span that was tested. Furthermore, seven-field photography was not practical in this case management setting. Although all participants were urged to visit an ophthalmologist, those subjects with evidence of any retinopathy on the photograph were personally followed by the case management team to facilitate the consultation.

Although other studies show that improved glycemic control decreases the risk of retinopathy, this study is the first to show that even a relatively short duration of improved control (?2 years) instituted before the onset of clinically identifiable retinopathy can decrease the risk of developing new retinopathy. This study also underscores the risk of retinal disease in type 2 diabetes in that progression of retinopathy occurred within a relatively short time when glycemic control was not achieved. Further studies are necessary to determine whether early intervention to achieve glycemic control in established diabetes has a greater effect to reduce diabetic retinopathy than its introduction at a later stage of the disease.

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11Nov

Decreasing the Risk of Diabetic Retinopathy in a Type 2 Diabetes Study: Part 3

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This report is the first evidence that intensive case management reduces risk of new-onset retinopathy in people with established type 2 diabetes. The U.K. Prospective Diabetes Study first demonstrated the effects of improved glycemic control on retinopathy in type 2 diabetes, but the subjects who participated in that landmark study were all newly diagnosed, whereas the patients without retinopathy in this study had a mean duration of diabetes of 7.5 years by the time the case management intervention was begun. Although the number of subjects with established retinopathy in this study was not sufficient to draw conclusions about progression of retinopathy compared with those who had none at baseline, the response observed in the latter suggests that early intervention with case management is an effective approach to reducing the burden of retinopathy in patients with type 2 diabetes. This conclusion is reinforced by the finding that even when case management is maintained for a short duration (mean <2 years), it is sufficient to diminish the risk of retinopathy.

The mechanisms for the effect of case management on reduction in the development of new-onset retinopathy may be related to any of the different facets of the case management process, although the major factor is likely to be improved glycemic control. Although A1C concentrations were not consistently evaluated at the time the follow-up photographs were taken, in the main trial the case management group showed a persistent improvement in the A1C that was greater than in the standard care group (6), suggesting that the decreased risk of retinopathy is likely due to improvement in glycemia. This study, therefore, confirms the necessity of providing adequate education and follow-up support, as delivered in this trial that utilized case management and frequent intervention, in order to achieve and maintain an A1C improvement over and above the standard care given to this county clinic Medi-Cal population.

However, other elements of the case management approach may well have contributed to the reduction in development of new-onset retinopathy. With adequate surveillance and support, glycemia improves, but, as demonstrated in our primary report, this improvement was associated with significant decreases from baseline to end of study in diastolic blood pressure, LDL cholesterol, and total cholesterol and an increase in HDL cholesterol in the intervention group. Thus, case management not only resulted in improvement of glycemic control but also had an effect on diminishing the risk of microvascular disease, as measured by retinopathy.

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09Nov

Decreasing the Risk of Diabetic Retinopathy in a Type 2 Diabetes Study: Part 2

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One photograph was taken of each eye with a Canon CR4-45° nonmydriatic camera. Photographs were taken in a dark room to facilitate dilatation of the pupils and improve the quality of the photographs. Additionally, at the Los Angeles site, pupils were dilated before taking the photos. The retinal field photographed was identical at both sites and consisted of the area nasal to the disc and temporal to the macula and the superior and inferior arcades. All photographs were labeled with only the patient’s identification number and were sent for reading in Santa Barbara. Polaroid prints from the Canon camera were examined and graded by an experienced endocrinologist (L.J.) who, before this study, had readings verified by an ophthalmologist until agreement was virtually 100%. An overall grading was assigned for each eye at each examination using the Wisconsin Epidemiologic Study of Diabetic Retinopathy II/III–modified diabetic retinopathy levels, which used a modification of the Airlie House Criteria. This scale has nine levels per eye, ranging from no retinopathy to total vitreous hemorrhage. The scale was used as follows: no retinopathy (grade 10), very-mild nonproliferative diabetic retinopathy (NPDR) (grade 20), mild NPDR (grade 35), moderate NPDR (grade 43), severe NPDR (grade 53), mild proliferative diabetic retinopathy (PDR) (grade 61), moderate PDR (grade 65), high-risk PDR (grade 71), and advanced PDR and/or fundus partially obscured by disease (grade 85). Photograph quality was deemed adequate for accurate assignment of retinopathy grade in all of the graded photographs included for analysis. The primary outcome measures are the development of retinopathy of any degree in subjects without retinopathy at baseline and the progression of retinopathy in subjects with nonproliferative retinopathy at baseline.

Statistical analyses were performed using SAS statistical software for Windows version 9.1 (SAS Institute, Cary, NC). Continuous data were compared between groups with an unpaired t test, and categorical data were compared with a ?2 test. Odds ratio (OR) for progression of retinopathy in each group was estimated using the PROC GENMOD procedure while accounting for duration of follow-up and controlling for confounders. A repeated statement was used to specify within-subject effect. The first-order Taylor expansion approximation was used to estimate the variance of difference in the ORs between the two groups. Logistic regression with the development of any degree of retinopathy as the binary outcome variable was used to control for covariates in the subset of subjects who had no retinopathy in the baseline photograph.

There were 200 subjects (56 male and 144 female subjects) from the two centers who were included in the retinal photographic studies. Subjects randomized to the intervention (n = 102) and control (n = 98) groups were of similar age and diabetes duration, had similar A1C concentrations, had similar follow-up periods during this study, and had similar drop-out rates.

The progression or development of retinopathy was noted in both the intervention and control group, and the difference in the ORs for progression between the two groups (?0.65) was not statistically significant (P = 0.226). Subjects without evidence of retinal disease at baseline were evaluated separately. As with the total sample, the intervention and control groups were similar, with the exception of follow-up time. However, among 82 subjects who remained in the study through at least a second photograph and could therefore be used to assess the development of retinopathy, the follow-up was similar in the intervention (22.0 months) and the control groups (24.6 months, P = 0.136, data not shown). Those in the intervention group who had no evidence of retinopathy at baseline (Airlie House score = 10 in each eye) were less likely to develop diabetic retinal changes during a mean of 23.1 months of follow-up (5/48) than were those in the control group (10/34, ?2 = 4.805, df = 1, P = 0.028). This difference remained significant in a logistic regression model that controlled for age at diagnosis, duration of diabetes at baseline, duration of follow-up, A1C, ethnicity, and sex (OR 5.35 [95% CI 1.14–2.12], P = 0.034). In a stepwise logistic model, only randomization group, baseline A1C concentration, and age were significant predictors of developing retinopathy (data not shown).

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08Nov

Decreasing the Risk of Diabetic Retinopathy in a Type 2 Diabetes Study: Part 1

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Between 1 July 1995 and 30 June 1999, a randomized, controlled study of subjects aged ?18 years who had type 2 diabetes of at least 1-year duration was conducted in southern California. Detailed information about the methods used in this study was presented in an earlier publication and will be briefly summarized here. Subjects with type 2 diabetes, as defined by the American Diabetes Association, were recruited at clinical sites in Santa Barbara, Los Angeles, and San Diego counties, three California counties serving predominantly ethnic minority, low-income Medicaid (called Medi-Cal in California) populations. Although specific income data were not collected as part of this study, overall 93.9% of the Medi-Cal–eligible population is classified as medically indigent or needy or is eligible for public assistance. Two of these sites, in Santa Barbara and Los Angeles counties, had access to fundus cameras and participated in the retinal photograph component of the study, and the data provided in this manuscript are limited to those two sites. Signed, witnessed, informed consent was obtained from all prospective participants using forms approved by local institutional review boards.

As previously described, the main trial recruited participants with HbA1c (A1C) levels >7.5%. At the two participating sites, 121 subjects were randomized to the intervention group and 119 to the control group. Intensive diabetes case management was provided to the intervention group in addition to the standard care that was received by both groups from a primary physician not connected with the trial. In the intervention group, subjects were seen or contacted by the case management staff at varying intervals according to the need (at least monthly) to lower A1C. In the control group, blood for A1C determination was collected at 6-month intervals, and contact between study staff and participants was generally limited to that needed to assure collection of A1C samples or to obtain retinal photographs. All subjects, in both the intervention and control groups, were referred for retinal photographs at baseline and then at least yearly. Two hundred subjects (98 control and 102 intervention subjects) had at least one photograph and 149 (70 control and 79 intervention subjects) had least two sets of retinal photographs that could be analyzed in this study. For subjects with more than two sets of photographs, only the first and last were used in this analysis. Only the main study had sufficient power to see differences in metabolic variables. Thus, for this small ancillary study of retinopathy, which utilized only two of three original participating centers, follow-up analyses of A1C, blood pressure, and lipids were not planned. Photographs were obtained at a separate case management visit, and, after baseline, photographs were not necessarily scheduled to coincide with the laboratory tests or physical examinations.

The study staff at each site, consisting of registered nurses and registered dietitians working in close collaboration with an endocrinologist, provided diabetes case management to the intervention group only. Evidence-based practice guidelines and algorithms for oral medicines and insulin initiation and adjustment were used in a collaborative practice model with the primary care provider. Treatment goals and targets for therapy were uniform across sites, with flexibility to utilize individualized treatment algorithms and strategies at each site. Interactions between the participant and study staff occurred in person at the clinic site and via telephone between visits as needed. The need for ancillary medical evaluations and/or services such as ophthalmologic examinations was monitored, with subsequent follow-up to ensure receipt of services, results retrieval, and communication of results to the primary care provider.

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