My A1C is High. What Should I Do? : Integrative Primary Care: Internists

My A1C is High. What Should I Do? : Integrative Primary Care: Internists

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If you’re among the millions of Americans with Type 2 diabetes, knowing your A1C is a key step in managing your condition. This quick blood test reveals your average blood sugar level over the previous 2-3 months.

When your A1C is high, it’s a sign that it’s time to make some important dietary and lifestyle changes. If you don’t lower your A1C, you increase your risk of developing some serious complications, such as heart disease and blindness. 

At Integrative Primary Care in Katy, Texas, our primary care providers help patients in the Houston area struggling with diabetes reclaim their lives by getting their blood sugar under control. We also want to be sure you have the information you need to make healthy choices.  

We put together this post with the info you need regarding your A1C, what can happen when it’s high, and the steps you can take to lower it. Keep reading to learn what you need to know about your A1C!

What is A1C?

A1C is a blood test. It’s sometimes called other names, such as glycohemoglobin test, hemoglobin A1C, or HbA1C. This test tells you your body’s average blood sugar (glucose) level over the previous 2-3 months.

Your blood contains hemoglobin, a protein that moves oxygen and other cellular nutrients around your body. When it picks up glucose, the sugar binds to the protein, creating something called “glycated hemoglobin.” This means hemoglobin with glucose attached. 

The more glucose you have in your blood, the more blood sugar will attach to your hemoglobin. An A1C test measures the amount of glycated hemoglobin (hemoglobin with glucose attached) you have in your blood.

If you have Type 2 diabetes, knowing your A1C levels can help you make changes to your lifestyle, diet, and treatment plan before serious complications set in. It can also alert people who haven’t been diagnosed with diabetes that they’re prediabetic. 

How can I tell if my A1C is high?

Experts who study diabetes have created a range of A1C levels to help you understand where you stand. A1C results are shown in percentages. This number shows you what percent of glycated hemoglobin you have. 

For example, if you get an A1C result of 10%, this means you have 10 glycated hemoglobins out of every 100 hemoglobins in your blood. The range of A1C levels is:

• Normal: Under 5.7%
• Prediabetes: 5.7% – 6.4%
• Diabetes: 6.5% and above

The higher your percentage, the higher your blood sugar levels. A higher A1C also means a greater risk of developing serious diabetes-related conditions. 

Why is a high A1C dangerous?

Research shows a strong link between high A1C levels and very serious diabetes complications. The diabetes-related complications include:

• Coronary artery disease
• Heart attack
• Stroke
• Vision complications (glaucoma, cataracts, retinopathy, macular edema)
• Blindness
• Diabetic neuropathy (nerve damage)
• Kidney disease
• Gum disease

Again, the higher your A1C, the greater your risk of developing one of these conditions. This is why having a high A1C can be dangerous. 

How can I lower my A1C?

The good news is you can manage your blood sugar to help lower your A1C levels. By doing this, you can reduce your risk of developing diabetes-related complications. 

At Integrative Primary Care, our providers work with you to create a diabetes management plan that fits your health care needs and lifestyle. If your A1C levels are high, talk with your provider about the best ways to lower them. 

Your Integrative Primary Care provider may make adjustments to your medications to help lower your A1C. You may also need to make key lifestyle changes to protect your health. These may include:

• Changing your diet
• Tracking your meals
• Practicing healthy stress management (e.g., yoga)
• Getting and staying physically active
• Regular blood sugar testing at home

To learn more about A1C tests or for more information about Type 2 diabetes, call 832-500-7585 or book an appointment online with Integrative Primary Care today.

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HbA1c: 8

Elle Penner, MPH, RD

5 mins

What does an A1c level of 8 mean? Are there any symptoms associated with this A1c level?

An A1c level of 8 percent is considered high and means that 8% of the hemoglobin in your blood is saturated with sugar. A1c levels of 6.5 or greater are considered diabetes. 

If your A1c is high, a combination of diet and lifestyle changes and medications can help you lower your levels. The lower your A1c the less risk you have for developing some of the more serious complications of diabetes including cardiovascular disease, nerve and kidney damage, and vision loss.

An A1c of 8 may or may not have noticeable symptoms. Common symptoms of diabetes include increased thirst and hunger, frequent urination, unintentional weight loss, fatigue, and blurred vision.

Factors that could contribute to an A1c level of 8: 

 A variety of factors can contribute to high A1c levels. Some of these include:  

• Diets that are low in fiber and high in refined carbohydrates and added sugar

• Being overweight or obese

• A sedentary lifestyle 

• Age (A1c tends to increase gradually as you get older)

• Race (people of Black, Hispanic/Latino, American Indian, Asian American, or Pacific Islander descent are at greater risk for prediabetes/ diabetes. )

• Stress

• Certain medications, including glucocorticoids

• Family history of pre-diabetes or diabetes

• Adherence to your prediabetes/ diabetes management plan

• Pregnancy

• Chronic disease/ inflammation 

Several things can also falsely increase or decrease your A1c result. Let your doctor know if any of these apply to you to determine if you need additional testing: 

• Severe anemia

• Liver disease or kidney failure

• Certain medicines, including opioids and some HIV medications

• Blood loss or blood transfusions

• Early or late pregnancy

• A less common type of hemoglobin found in people of African, Mediterranean, or Southeast Asian descent, as well as people with blood disorders like sickle cell anemia or thalassemia

What to do if your A1c level is 8?

If your A1c level is 8, a combination of diet and lifestyle changes, and medications can help you lower your levels. The goal for most adults with diabetes is an A1c below 7%, but the lower the better.

Making changes to your diet and adopting healthier habits can help lower your A1c levels. To lower your A1c:

• Be active every day. Aim to move your body for 30-60 minutes 5 days per week. 

• At every meal, fill half of your plate with non-starchy veggies, and incorporate a source of lean protein and plant-based fat to assist with blood sugar control. 

• Limit refined carbohydrates and added sugar; instead choose whole-grain carbs like whole wheat bread and pasta, quinoa, farro, and oats. 

• Lose weight if you are overweight or obese.

• Manage stress levels and get adequate sleep, as this can help balance hormone levels that can impact blood sugar.

• Follow your diabetes treatment plan if you have been diagnosed with diabetes.

Medications used to improve A1c results

Medications, along with healthy diet and lifestyle changes, can help to lower elevated A1c levels into a safer range. If necessary, your doctor and/or dietitian will work with you to determine which ones are right for you. Some common diabetes medications include: 

• Insulin: Typically given by injection or through a pump to increase glucose (sugar) uptake by cells and thus decrease blood sugar

• Sulfonylureas: Increase insulin production by stimulating insulin-producing beta cells in the pancreas

• Alpha-glucosidase inhibitors: Help your body break down starches and sugars found in food, lowering your blood sugar levels. 

• Biguanides: Reduce the amount of sugar your liver produces, as well as how much sugar your intestines absorb and makes your body more sensitive to insulin. The most common biguanide is metformin. 

• Dopamine agonist: These medications work by affecting the way the brain processes dopamine, an important neurotransmitter (chemical messenger). By increasing the activity of dopamine receptors, dopamine agonists increase insulin sensitivity, allowing cells to use blood glucose more effectively and lower blood sugar.

• DPP-4 inhibitors: Help the body continue to make insulin, which lowers blood sugar

• GLP-1 receptor agonists: Increase growth of insulin-producing beta-cells in the pancreas, slow stomach emptying, and decrease appetite and how much glucagon (which raises blood sugar) your body uses

• Meglitinides: Similar to sulfonylureas (but by a different mechanism) meglitinides stimulate the pancreas to release insulin in response to a meal. This increase in insulin production helps lower blood sugar.

• SGLT 2 inhibitors: Prevent the kidneys from holding on to glucose and increasing its excretion in urine

• Thiazolidinediones: Decrease glucose in your liver and also help your fat cells better utilize insulin

Modern strategy of hypoglycemic therapy in type 2 diabetes mellitus: the role and place of combination therapy | Nedosugova L.

V.

The spread of type 2 diabetes mellitus (T2DM) in the world exceeds all theoretical forecasts. If 15 years ago, WHO experts assumed that by 2025 the number of patients with diabetes in the world would be 380 million people [1], then, according to the International Diabetes Association (IDF), in 2011 the number of patients with diabetes has already reached 366 million, and , according to WHO experts, by 2030 the number of patients with T2DM will be 552 million people [2]. Life expectancy in patients with T2DM is on average 5 years shorter than in the general population, and this is primarily due to the rapid progression of atherosclerosis, which leads to cardiovascular mortality in T2DM patients 4–5 times more often [3]. Overall, more people with diabetes die from atherosclerosis-related diseases than from all other causes combined [4]. The cause of such a pronounced lesion of the vascular bed is currently considered to be hyperglycemia. Meta-analysis of 20 different studies including 95,783 patients followed up for 12 years led to the conclusion that glucose is the same risk factor for the development of atherosclerosis and acute cardiovascular mortality as the level of total cholesterol and blood pressure [5].

A series of large randomized trials [6-10] have proven the importance of tight glycemic control in reducing the risk of developing diabetic vascular complications, which requires aggressive treatment of T2DM using effective and safe hypoglycemic drugs and their combinations already at the diagnosis of the disease, allowing to achieve the target level of glycemia, which, as proven by long-term observations, can prevent the rapid progression of atherosclerosis in these patients [11, 12].
However, the intensification of hypoglycemic therapy is limited by the risk of developing hypoglycemic conditions, weight gain and, as a result, increased mortality from acute vascular accidents. Hypoglycemic episodes were 3 times more common in the intensive care group compared with standard therapy in the ACCORD study [13] and 2 times more often in the VADT study [14], which was accompanied by a 22% increase in overall mortality in the ACCORD study and an increase in cases cardiovascular events in the next 3 months. after severe hypoglycemia in the elderly in the VADT study.
In connection with the above, at the end of 2011, the Russian Association of Endocrinologists proposed to individualize the target levels of glycemic control [15] depending on the patient’s age, life expectancy (LE), the risk of developing hypoglycemic conditions, and the presence/absence of severe cardiovascular complications (Table 1). 1).
T2DM is characterized by two major pathogenetic defects: decreased insulin sensitivity (or insulin resistance) and inadequate insulin secretion to overcome the barrier of insulin resistance. Insulin resistance often precedes the development of DM for many years and is genetically determined, although exacerbated by external factors such as obesity, decreased physical activity, pregnancy, and excess contrainsular hormones. Initially, existing insulin resistance is compensated by hyperinsulinemia, which maintains normal carbohydrate tolerance. Impaired carbohydrate tolerance is observed with an increase in insulin resistance or a decrease in the compensatory capabilities of insulin secretion, or with the progression of both defects [16, 17]. According to modern concepts, T2DM manifests itself in a situation where the secretory capabilities of β-cells are unable to overcome the barrier of insulin resistance. The main role in this failure of the insular apparatus is assigned to genetic disorders [17], however, the so-called “glucose toxicity phenomenon” plays an important role in reducing the secretory reserves of the insular apparatus, due to which apoptosis and death of β-cells develop. According to statistics, by the time of the disease manifestation, only 50% of the initial number of β-cells are functioning in patients, which confirms the theory of the gradual progression of carbohydrate metabolism disorders: from normoglycemia in conditions of insulin resistance and hyperinsulinemia to the manifestation of diabetes through successive stages of impaired fasting glycemia and impaired tolerance to glucose [18].
Based on the foregoing, a completely logical conclusion suggests itself that the main strategic direction in the treatment of T2DM should be the impact on insulin resistance as the main pathogenetic link in the development of the disease. By reducing insulin resistance, or, in other words, increasing insulin sensitivity, we reduce the load on the insular apparatus, thereby preserving its secretory capabilities and removing the negative effect of hyperinsulinemia on increased appetite, weight gain, and the state of the cardiovascular system. The easiest way to increase insulin sensitivity is to reduce weight through lifestyle and dietary changes, which, unfortunately, allows achieving the target level of glycemia in less than 30% of patients with newly diagnosed T2DM [6]. In such situations, agents are needed that affect the main pathogenetic link of the syndrome – insulin resistance.
Currently, the most accessible and effective drug is metformin (the original metformin drug is Glucophage®), the main mechanism of action of which is to reduce insulin resistance by increasing the activity of the insulin receptor tyrosine kinase in peripheral tissues. As a result, the utilization and oxidation of glucose in peripheral tissues improves [19, 20], and lipolysis and oxidation of free fatty acids as an alternative energy substrate are suppressed [21, 22]. It is with an increase in insulin sensitivity of the liver tissue that a decrease in gluconeogenesis and glycogenolysis is associated [23, 24]. Thus, the hypoglycemic effect of metformin is not so much hypoglycemic as antihyperglycemic, because. leads to a decrease in hepatic glucose production and fasting glucose levels. An increase in the sensitivity of peripheral tissues to insulin is also associated with a decrease in the need for insulin and an improvement in the functionality of β-cells due to a decrease in glucose toxicity [25]. In addition, as recent studies show, metformin can increase the level of glucagon-like peptide-1 (GLP-1), which, as you know, stimulates insulin secretion by improving glucose absorption in the more distal parts of the small intestine, where L-cells are mainly localized. secreting GLP-1 [26].
In case of metformin intolerance or contraindications, the latest 2011 IDF algorithm suggests, as an alternative option for patients who are not overweight, the use of sulfonylurea drugs (SUM) as the first line of treatment, based on the assumption that the main pathogenetic defect in the development of T2DM without obesity is inadequate secretion of insulin. This option of starting drug treatment is justified not only by the need for a pathogenetic approach to therapy, but also by a sufficient evidence base for the effectiveness and safety of the use of PSM, as well as the relative cheapness and availability of such an alternative treatment option.
As noted above, for the majority of people with T2DM, lifestyle interventions fail to achieve carbohydrate goals, either because of insufficient weight loss, weight gain, disease progression, or a combination of these and other factors. Therefore, it is recommended to start metformin therapy along with lifestyle changes immediately after diagnosis. In the absence of specific contraindications, metformin is recommended primarily due to its effect on glycemia, lack of weight gain and hypoglycemic conditions, generally good tolerability with a low incidence of side effects, high adherence, and relatively low cost. The dose of metformin should be gradually (over 1-2 months) increased to the maximum effective and tolerated.
Second line therapy
At the same time, even the maximum doses of metformin do not always make it possible to achieve the target level of glycemia and reduce the level of Hb A1c <7.0% during the first 2-3 months. treatment as recommended by the authors of the latest IDF algorithm (2011). If persistent hyperglycemia persists, the question of the rapid addition of other hypoglycemic drugs should be addressed. A clear consensus on a second drug added to metformin does not yet exist, and the choice is between SSM and DPP-4 or TZD inhibitors and α-glucosidase blockers as an alternative (Fig. 1). In particular, when the risk of hypoglycemia is especially dangerous (for example, in patients engaged in heavy physical labor), it is advisable to additionally prescribe DPP-4 inhibitors or the drug of the TZD class, pioglitazone. In cases where one of the main goals of treatment is weight loss, and the level of Hb A1c is <8.0%, it is preferable to prescribe α-glucosidase blockers.
As a second line of drugs, if it is impossible to achieve the target level of glycemic control with the use of SSM, the use of metformin is suggested, if it has not been previously prescribed, or DPP-4 inhibitors, or TZD, or α-glucosidase blockers as an alternative option (Fig. 1).
Third line therapy
If lifestyle modification, metformin, and the second drug did not lead to the achievement of the target parameters of carbohydrate metabolism control, the next step is to start or intensify insulin therapy (Fig. 1). If the A1c level is close to the target (< 8.0%), a third oral antidiabetic drug can be added as an alternative. As an additional hypoglycemic agent, the 2011 IDF algorithm suggests either α-glucosidase blockers or DPP-4 inhibitors, or TZD, or, as an alternative, GLP-1 agonists (exenatide, liraglutide) when one of the main goals of treatment is to reduce weight, and the level of Hb A1c <8.0%. However, this approach is more expensive and not always effective compared to switching to insulin therapy or its intensification.
Fourth line therapy
Intensive insulin therapy usually consists of additional injections of short-acting or ultra-rapid-acting insulin before individual meals to reduce postprandial glycemic fluctuations (Fig. 1). When switching to intensive insulin therapy with short-acting or rapid-acting insulin injections, insulin secretogens (PSM or glinides) should be discontinued, since they have a synergistic effect with injected insulin.
However, endocrinologists often face the problem of not being able to achieve the target level of glycemic control within 2-3 months. treatment. This is due to the fact that the initial level of Hb A1c in patients can range from 6.5 to 10% or more, which, of course, complicates the ability to quickly and effectively achieve the goal.
Stratification of treatment tactics
according to the Algorithm of the RAE 2011
In this regard, the Russian Association of Endocrinologists (RAE) at the end of 2011 proposed a differentiated approach to prescribing and correcting hypoglycemic therapy depending on the initial level of Hb A1c, followed by a change in treatment if the goal is not achieved no earlier than after 6 months. from the start of therapy. Indeed, if the initial level of Hb A1c does not exceed 7.5%, it is quite possible to achieve the target level of <6.5% with monotherapy with metformin, pioglitazone, DPP-4 inhibitors (dipeptidyl peptidase) or α-glucosidase, as shown in Figure 2. The double combination with the ineffectiveness of monotherapy involves the addition of drugs that somehow stimulate insulin secretion either due to a direct effect on the β-cell (PSM, glinides and GLP-1 analogues), or indirectly, due to blockade of the cleavage of native GLP-1 by inhibitors of the DPP- 4. In any case, this combination affects both pathogenetic links in the development of T2DM: insulin resistance and inadequate secretion of insulin, resulting in adequate glycemic control not only in terms of fasting glycemia, but also after meals, leading to rapid achievement of the goal.
Which combination is preferred in patients with baseline Hb A1c between 6.5% and 7.5%? Based on the tolerability and safety criteria, the possible risk of hypoglycemia when using secretogens in patients with initially low levels of Hb A1c exceeds the severity of side effects from the gastrointestinal tract and edematous syndrome associated with the use of incretins and TZD, respectively. That is why the authors of the RAE algorithm suggest, first of all, the combination of metformin with DPP-4 inhibitors or GLP-1 analogues, and secondly, metformin with secretogens (PSM or glinides), as the most rational combinations. If lifestyle modification, metformin, and the second drug did not lead to the achievement of the target parameters of carbohydrate metabolism control, the next step is to start or intensify insulin therapy (Fig. 2). If the A1c level is close to the target (<7.5%), a third oral hypoglycemic agent can be added. However, this approach is more expensive and not always effective compared to switching to insulin therapy or its intensification [27].
Case Management
with A1c level from 7.6 to 9%
The vast majority of patients with T2DM have an A1c level of >7.6% at the time of disease diagnosis. To date, there are no drugs that can achieve the target level of control in monotherapy for 2-3 months. (Table 2).
That is why the authors of the algorithm propose to initially use combined “double” therapy to achieve rapid and effective glycemic control (Fig. 3). This approach is based on the data of numerous studies showing that the simultaneous administration of drugs with different points of application of action provides a more significant decrease in A1c not only in a shorter time, but also at significantly lower dosages than the initial metformin monotherapy followed by the addition of a second drug [28– thirty]. Metformin is the basis of all possible combinations, of which the combination of metformin with incretin mimetics is the safest, due to the absence of the risk of hypoglycemic conditions and weight gain, and the most effective is the combination of metformin with PSM, since these drugs most significantly reduce the level of A1c, and their combination provides good control not only of glycemia, but also of cholesterol and blood lipid spectrum [30].
In case of ineffectiveness of “dual” therapy, it is recommended to add a third drug, based on the principles of efficiency and safety in this case: Metformin is considered the basis of therapy in this situation, while the safest in terms of the risk of developing hypoglycemic conditions is the addition to the combination of metformin with incretin TZD mimetics, and the most effective is the addition of PSM to a combination of metformin with incretin mimetics. Thus, in patients with A1c levels close to 7.5%, it is more appropriate to prescribe a combination of metformin with TZD and incretin mimetics, while in patients with higher A1c levels, it is more logical to use a combination of metformin with SM and incretin mimetics. The next step in achieving the target level of glycemia with the ineffectiveness of the “triple” combination is the appointment of insulin therapy, first in the background, and then in the background-bolus mode, upon transition to which it is necessary to cancel drugs that somehow stimulate insulin secretion.
Case Management
at A1c >9%
In clinical practice, situations are not uncommon in which, already at the stage of T2DM diagnosis, patients have significant hyperglycemia and the Hb A1c level exceeds 9%, but there are no clinical symptoms of the disease, which indicates sufficient secretory activity of the insular apparatus. The tactics of choice in this situation, at the suggestion of the authors of the algorithm, may not be intensive insulin therapy, which is absolutely indicated for A1c > 10% and severe clinical symptoms, but the initial “triple” therapy. In this case, the combination of metformin with PSM and incretin mimetics is considered the most effective, the most safe in terms of the risk of hypoglycemia is the combination of metformin with incretin mimetics and TZD (Fig. 4).
However, practitioners are well aware of the adverse effect of complex hypoglycemic regimens on patient adherence to medical prescriptions in daily practice. According to the results of the DARTS study [31], only 30% of patients are firmly adherent to single-drug therapy and less than 13% adhere to multiple drugs and high doses (separate combination). It is this fact that explains the emergence of official combined hypoglycemic drugs, consisting of a combination of metformin with various drugs of other classes. The most effective is the combination of metformin with PSM, which allows to achieve the most rapid and significant decrease in the level of A1c, while using smaller doses of each of the components, which, of course, reduces the risk of development and severity of side effects (gastrointestinal disorders, weight gain, hypoglycemic conditions) .
One of the drugs of this group, registered in Russia, is Glyukovance®, the only combination drug in Russia that contains the original metformin and glibenclamide in a micronized form, which provides a number of advantages compared to the usual form of glibenclamide, confirmed in clinical trials, including: hours, lower risk of hypoglycemia and safer action compared to the conventional form of glibenclamide [28, 33]. In addition, the faster release of glibenclamide from the Glucovance® tablet is more effective in preventing an increase in glycemia in the first 3 hours after a meal compared to the standard form of glibenclamide [34, 35]. The calibrated particle size technology used in the creation of Glucovance® provides controlled release of drug components in accordance with the physiological needs of the patient [34]. Thus, the target values ​​of glycemia are achieved with the use of lower doses of metformin and glibenclamide in the composition of Glucovance® in comparison with the doses used in monotherapy [33].
The drug is available in two dosages containing 2.5/500 mg of glibenclamide/metformin and 5.0/500 mg of glibenclamide/metformin, respectively, which makes it possible to titrate the dose of glibenclamide to reduce the risk of developing hypoglycemic conditions. Thus, using Glucovance in the treatment of T2DM, it is possible to achieve the target level of glycemic control both in patients with ineffectiveness of higher doses of metformin or in case of its intolerance, and in patients who are initially indicated for “double” therapy with A1c> 8.0% or ” triple” therapy at the level of A1c> 90% in combination with incretin mimetics or TZD. The use of Glucovans not only provides an effect on both major pathogenetic defects in T2DM, but also allows to achieve an effect at lower doses with a lower risk of side effects and with greater patient compliance with the prescribed therapy [36]. Glucovance can be used in any cohort of patients with T2DM, regardless of the initial HbA1c level, of course, taking into account individual treatment goals that exclude the risk of developing hypoglycemic conditions, in the absence of severe vascular complications, taking into account age and life expectancy.

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What is the analysis for glycated hemoglobin A1c

Contents

• What is the best HbA1c value?
• How often should the HbA1c test be done?
• What is the difference between A1c and eAG?

The glycated hemoglobin (hemoglobin A1c, HbA1c) test is a complete blood test used to diagnose diabetes and monitor its treatment. This test is usually done to detect type 1 and type 2 diabetes.

HbA1c test shows the average blood sugar level over the past two to three months. It shows how much hemoglobin has been glycated (i.e., has been combined with glucose).

Hemoglobin is the protein in red blood cells that carries oxygen from the lungs to other parts of the body. Glucose enters the red blood cells and glycates (combines) with hemoglobin molecules. The more glucose in the blood, the more hemoglobin will be glycated.

The average amount of glucose in the blood can be determined by measuring the level of hemoglobin A1c. If your glucose level has been high for the past two to three months, the A1c test will show this with great accuracy.

A high A1c test indicates a high glucose level, which in turn increases the risk of diabetes.

See high blood sugar diet.

According to the National Institutes of Health (USA), the most common complications in patients with high blood glucose levels are:0090

Researchers at Bloomberg University (JHSPH, USA) report in the journal NEJM that glycated hemoglobin can predict disease risk with greater accuracy than conventional fasting glucose .

What is the best HbA1c value?

HbA1c test results show the following:

• between 4% and 5.6% – people are healthy , the risk of developing diabetes is minimal
• between 5.7% and 6.4% – the person has a high risk of developing diabetes
• 6.5% or more – the person has diabetes nemia and host vitamin supplements (vitamins C and E), patients with high blood cholesterol, and people with liver or kidney disease may have poor HbA1c test results. If you are taking vitamin supplements, tell your doctor.

  Non-caregivers (diabetes) with high HbA1c levels have a much higher risk of developing complications.

  The American Diabetes Association considers the maximum glycated hemoglobin for diabetic patients to be 7%.

  How often should the HbA1c test be done?

  If you have type 2 diabetes, you need to have your hemoglobin A1c tested every quarter of (three months) to make sure your level is below 7%.

  If your blood sugar levels are good for a certain amount of time, your doctor may allow you to get tested once every six months.

  What is the difference between A1c and eAG?

  Some doctors may tell you your A1c result as an eAG (mean blood glucose) test. eAG is directly related to A1c.

  • A1c is calculated as a percentage, eg 7%
  • eAG is calculated in millimoles per liter (mmol/l, mmol/L) in blood glucose meters, eg 5.4 ml/dl.
  • A1c having a value of 5 is equal to 4.5 eAG; A1c, having a value of 7, is equal to 8.3 eAG; A1c having a value of 8 is equal to 10.0 eAG; A1c, having a value of 9, is equal to 11.6 eAG.

  A study published in The Lancet in 2010 suggests that for diabetic patients, low HbA1c levels can be just as dangerous as high . It also contributes to the development of cardiovascular diseases and, often, with a fatal outcome. After reviewing the research, the Society of Endocrinologists of the United States stated that any changes in glycemic indicators are dangerous.