Know Your A1C: What This Blood Test Can Tell You About Your Risk for Diabetes and Cardiovascular Disease

Know Your A1C: What This Blood Test Can Tell You About Your Risk for Diabetes and Cardiovascular Disease

The higher the A1C level, the greater the risk of developing diabetes-related complications.

By Martin Tibuakuu, M.D., M.P.H. and Erin Michos, M.D., M.H.S. | Aug. 24, 2016, at 6:00 a.m.

Know Your A1C: What This Blood Test Can Tell You About Your Risk for Diabetes and Cardiovascular Disease
Man performing blood test on himself.

After a diabetes diagnosis, A1C is also used for gauging how well treatment controls blood sugar levels. MIKE WATSON IMAGES

A simple blood test can diagnose diabetes, but it also can tell you so much more, including your risk for heart attack and stroke.

Type 2 Diabetes: Who Is at Risk?

Diabetes, which causes chronically high blood sugar levels, is the seventh leading cause of death in the United States, according to the Centers for Disease Control and Prevention. It can also result in serious health complications, including heart disease, blindness, kidney failure and lower-extremity amputations. The CDC reports that close to 29.1 million people are currently living with diabetes in America, meaning about 1 of every 11 people has it. There are different types of diabetes, but Type 2 diabetes accounts for about 90 to 95 percent of all diagnosed diabetes cases.

Risk factors for Type 2 diabetes include older age, obesity, a family history of diabetes, prior history of gestational (pregnancy) diabetes, impaired glucose tolerance, physical inactivity and race/ethnicity. African-Americans, Latinos, American Indians and some Asian-Americans and Pacific Islanders are at particularly high risk for Type 2 diabetes.

What Is Prediabetes?

People with prediabetes have glucose (i.e., blood sugar) levels that do not meet the criteria for diabetes but are too high to be considered normal. These individuals have an increased risk for the development of diabetes and other serious health problems, including heart disease and stroke. According to the CDC, 86 million American adults, or more than 1 of 3 people, have prediabetes. Without lifestyle changes, such as eating healthy foods, getting regular physical activity and maintaining a healthy weight, 15 to 30 percent of these individuals will develop Type 2 diabetes within five years.

What Is the A1C Blood Test?

The term A1C is short for HbA1c, or hemoglobin A1C. It refers to glycated hemoglobin, which develops when hemoglobin – a protein within red blood cells that carries oxygen – becomes coated with glucose or sugar in the blood. The amount of glucose that combines with this protein is directly proportional to the total amount of sugar in a person’s system, and so the higher blood glucose levels are, the higher the A1C level. Red blood cells have a life span of 120 days; by measuring A1C, clinicians are able to determine average blood sugar levels over approximately two to three months. A1C is particularly important in people with diabetes because the higher the A1C level, the greater the risk of developing diabetes-related complications. After a diabetes diagnosis, A1C is also used for gauging how well treatment controls blood sugar levels. In the U.S., A1C results are given as a percentage of hemoglobin that is glycated.

How Does an A1C Test Differ From a Blood Glucose Level?

An A1C measurement is a marker of average blood sugar levels over a period of two to three months, so it is a more stable test assessing longer-term blood sugar control. This means less day-to-day fluctuations to A1C levels due to stress and illness. A1C is often tested using blood samples from the arm, but samples can also be taken from a finger prick. Fasting is not required before A1C testing like it is for the blood glucose test.

On the other hand, the blood glucose level gives us the concentration of glucose in the blood only at the time of the test.

Health care providers measure both A1C and blood glucose to ensure good diabetes control, which informs them of the long-term and day-to-day control of blood sugar levels.

How Do We Diagnose Diabetes and Prediabetes?

Both diabetes and prediabetes may be diagnosed based on either A1C or blood glucose criteria. Blood glucose criteria could either be a blood glucose level measured after an overnight fast or a two-hour blood glucose value after eating 75 grams of sugar.

An international committee of experts from the American Diabetes Association, the European Association for the Study of Diabetes and the International Diabetes Federation recommends that the A1C test be the primary test used to diagnose prediabetes and Type 2 diabetes.

What Are the A1C Criteria for Diabetes and Prediabetes Diagnosis?

A1C can indicate if people have prediabetes or diabetes based on the following:

A1C Percentage
Normal Below 5.7%
Prediabetes 5.7%–6.4%
Diabetes 6.5% or greater

An A1C level of 6.5 percent or more measured on two separate occasions indicates you have diabetes.

If your A1C test returns a reading of 5.7 to 6.4 percent, this indicates you have prediabetes and are at an increased risk of Type 2 diabetes. At this point, you need to talk to your doctor about appropriate lifestyle changes that could reduce your risk of developing full-blown Type 2 diabetes in the future.

It is important to note that normal ranges for A1C levels may vary from one lab to another, so patients who may wish to interpret their own A1C results need to keep this in mind, especially when using a lab that is different from the one used for previous testing.

What Is the Target A1C Level?

For most people with previous diagnoses of diabetes, a target A1C level of 7 percent or less is a common treatment target. However, this is a general target, and health care teams do tailor targets to meet individual goals. A1C values are not indicators of specific diabetes complications, meaning any complications could arise with any A1C value. However, the closer someone’s value is to the normal A1C range, the better. A person’s recommended A1C target should take into account his or her ability to achieve the target without any risk of serious health complications caused by blood sugar levels that are too low (called hypoglycemia).

What Are the Benefits of Lowering A1C?

Studies have shown that reducing A1C by 1 percent in people with diabetes reduces the risk of serious health complications involving small vessels of the eyes and kidneys, as well as nerves by almost 25 percent.

Also, a study published in the journal BMJ revealed that people with Type 2 diabetes who reduce their A1C level by 1 percent are:

  • 19 percent less likely to suffer cataracts
  • 16 percent less likely to suffer heart failure
  • 43 percent less likely to suffer amputation or death due to blood vessel diseases

A lower A1C level in the blood means a lower amount of sugar in the blood on average, which reduces the risk of developing complications caused by high blood sugar levels.

Who Should Get an A1C Test?

  • Everyone with Type 2 diabetes should be offered an A1C test at least once a year.
  • Some may require an A1C test more often. This is especially true for patients who had a recent change in medication(s) or if a health care team wishes to more frequently monitor a patient’s diabetes status to get it under control.
  • For those without diabetes, experts recommend that anyone 45 or older should consider getting tested for A1C, especially if they are overweight. If they are younger than 45 but are overweight and have one or more additional risk factors for diabetes, they should consider getting tested.

What Are the Limitations to A1C Testing for Diabetes?

While A1C tests are usually reliable and widely used, it’s important to acknowledge that the test may not be accurate in people who:

• Have insufficient hemoglobin due excessive bleeding (may have a falsely low A1C reading).

• Have iron-deficiency anemia (may have a falsely high A1C test).

• Have hemoglobin genetic variations or uncommon forms of hemoglobin, commonly found in African-Americans and people of Mediterranean or Southeast Asian heritage.

• Have had a recent blood transfusion or have other forms of hemolytic anemia (may have falsely low A1C results)

• Are pregnant.

What Can You Do to Protect Yourself From Diabetes?

Anyone can benefit from a reduction of long-term diabetes complications, such as heart attack, stroke, kidney failure and diabetic nerve pain, by controlling their A1C levels through adopting healthy lifestyle practices. The benefit of reducing A1C should not be underestimated. To reduce A1C levels, you can:

Eat healthy. By keeping your post-meal blood glucose low, A1C can gradually be reduced in patients with diabetes and prediabetes. Those with diabetes and prediabetes need to eat foods that are high in nutrition and avoid excess calories. A healthy diet is rich in fruits, vegetables, fiber, lean protein and “good” monounsaturated and polyunsaturated fats in moderation. Saturated fats, refined “simple” carbohydrates and processed foods should be limited. For instance, switching white bread and white rice for whole-grain and brown rice will help reduce blood glucose spikes after a meal. Understanding what to eat and what to avoid can be challenging. Talk to a registered dietitian if you need help with food choices and meal planning. Tracking daily food intake using a diet diary or calorie-counter app can help keep things in check.

Be physically active. By keeping physically active, blood glucose is moved from the blood into cells to produce energy for the body, which lowers blood glucose levels. Also, physical activity improves our body’s sensitivity to insulin, a hormone needed to transport glucose into cells. This means that less insulin is needed to transport large amounts of glucose. Everyone should incorporate physical activity into their daily routine. For those without diabetes, being physically active will help to prevent the onset of prediabetes and Type 2 diabetes. For those with diabetes, it will help them maintain good blood sugar levels. The American Diabetes Association recommends aiming for 30 minutes of moderate- to vigorous-intensity aerobic exercise at least five days a week, or a total of 150 minutes per week. Moderate intensity means that you are working hard enough that you can talk but not sing during the activity, while vigorous intensity means you can’t say more than a few words without pausing for a breath during the activity.

Maintain a healthy weight. Losing weight through diet and exercise if you are overweight will significantly improve blood sugar levels, meaning a good A1C measurement.

Monitor your numbers. Carefully monitor both blood sugar and A1C levels if you have diabetes. Your medical team will most likely recommend regular A1C testing to monitor your overall diabetes control over a period of two to three months. However, A1C should never replace blood sugar level monitoring. For instance, people on insulin and other medications that cause hypoglycemia need regular blood glucose monitoring to ensure blood glucose doesn’t get too low.

Hepatitis C Virus Infection in African Americans

By Brian Pearlman

Hepatitis C is more prevalent among African Americans than among persons of any other racial group in the United States. However, comparatively little data are available on the natural history and treatment of hepatitis C in this population. Compared with white persons, African American persons have a lower rate of viral clearance and, consequently, a higher rate of chronic hepatitis C. Nonetheless, African American persons may have a lower rate of fibrosis progression than do white persons. African American persons with hepatitis C–related cirrhosis have higher rates of both hepatocellular carcinoma and liver cancer–related mortality than do white persons with hepatitis C–related cirrhosis. In nearly all treatment trials that enrolled a significant proportion of African American subjects, such patients had inferior treatment responses, compared with those of white subjects. The prevalence of infection with hepatitis C virus genotype 1 is higher among African American patients than white patients, although this difference does not account for a greatly dissimilar response to therapy. Some of the postulated mechanisms for these disparate treatment responses and natural histories of infection are also reviewed.

Hepatitis C virus (HCV) infection is a major public health problem for persons of all races, and it has become the most common cause of death associated with liver disease in the United States [1]. According to population-based studies, HCV infection accounts for >10,000 deaths per year [2]. Furthermore, the number of HCV-related deaths is expected to triple by the year 2020 [3].

African Americans experience complications of some chronic diseases disproportionately, compared with their white American counterparts [4, 5], and they are often underrepresented in clinical trials [6]. These differences also exist with respect to HCV infection; African American subjects represent only 5%–10% of participants in clinical trials involving HCV infection. Moreover, clinical features, such as the natural history of infection, infection prevalence, and therapeutic response, are disparate among minority and majority populations.

The African American population in the United States has a dominant ancestry from sub-Saharan West Africa [7]. However, the term “African American” has been criticized because of its imprecise geographic and cultural meaning. Furthermore, a racial classification does not necessarily convey genetic homogeneity [8]. Despite these limitations, the term “African American” will be used throughout this survey.

The aim of this review is to highlight the discrepancies in HCV infection characteristics and treatment responses between African American and white persons in the United States.

Epidemiology, Genotype, and Natural History

According to the most recent US census data, 12% of the population is African American, whereas 75% is white [9]. HCV infection is more prevalent in the African American population than in any other racial group in the United States (table 1). Although African Americans represent only 12% of the US population, they represent ∼22% of the estimated Americans with chronic HCV infection [3].

Table 1

Rates of hepatitis C seroprevalence among African American and white populations.

The mode of transmission of HCV appears to be similar for white and African American individuals. In a retrospective chart review of 355 patients with chronic HCV infection, injection drug use was the most common means of transmission for both ethnic groups, followed by receipt of a contaminated blood transfusion. In ∼25% of patients, irrespective of race, the mode of transmission was unknown [12]. In a prospective, controlled treatment trial involving >400 patients, injection drug use was also the predominant means of transmission (48%–50% of cases) in subjects of both races [13].

The prevalences of HCV genotypes also differ among racial groups. Although 70% of overall HCV isolates in the United States are of genotype 1 [14], there is a higher prevalence of genotype 1 infection among African Americans than among any other racial group (table 2). The explanation for this disparity is currently unknown.

Table 2

Prevalence of hepatitis C virus (HCV) genotype 1 among HCV-infected patients.

According to the Center for Disease Control and Prevention’ sentinel surveillance data on viral hepatitis [16], there has been a significant decrease in the number of cases of acute HCV infection since 1989. This decrement was seen in all ethnic and racial groups studied [17]. Between 1991 and 1996, African American patients accounted for 10% of patients with acute HCV infection. With respect to acute infection clinical features, African American and white subjects had nearly identical elevations in aminotransferase levels and in rates of jaundice and death [18].

Although the incidence of acute HCV infection does not seem to vary between races, the chronic HCV infection rate is higher among African American than among white individuals (table 3). Despite higher rates of chronic infection, HCV-infected African American persons may have a slower rate of fibrosis progression, compared with their white counterparts. In a retrospective chart review of 355 patients who underwent liver biopsy at a university medical center, the authors found significant differences between African American and white patients that could not be explained by age, alcohol use, or duration of infection [12]. The study suggests that histologic progression of HCV infection occurs less rapidly among African American patients than among white patients; however, there are obvious limitations of a retrospective analysis of disease progression. Furthermore, 19% of the non–African American patients were Hispanic, and a subgroup analysis was not separately performed. This factor is especially important, because Latino persons may have a faster rate of liver fibrosis than do either African American or non-Hispanic white persons [21, 22]. Nonetheless, other studies support the notion that African American persons may experience slower histologic progression than do white persons ( table 4).

Table 3

Rates of chronic hepatitis C among African American and white subjects.

Table 4

Rate of hepatitis C–related cirrhosis among African American and white subjects.

Prospective, randomized controlled trials are needed to better clarify the natural history of infection in African American persons. Discrepancies in disease severity may not necessarily correlate with differences in disease progression, as has been seen in cross-sectional and retrospective studies. Furthermore, not all studies have confirmed that natural histories of infection are dissimilar between races; preliminary data from a large multicenter treatment trial of patients with chronic HCV infection show no difference between African American and white patients with regard to the rate of fibrosis [25].

The mechanism for the possible discrepancies in the natural history of hepatitis C is unknown; however, the answer may lie in disparate HCV-specific CD4 T cell responses between African American and white persons. The strength and sustenance of HCV-specific T cell responses have already been identified as critical determinants of viral clearance during acute HCV infection [26,27–28]. In a clinical and immunologic analysis of 99 HCV-infected patients, CD4-proliferative T cell responses were observed in response to HCV-derived antigens in African American and white participants with both viral persistence and spontaneous clearance. Compared with chronically infected patients with a relatively weak HCV-specific T cell response, patients who achieved HCV clearance had a robust T cell response, irrespective of race. However, compared with chronically infected white patients, chronically infected African American patients had a significantly greater T cell proliferative response to HCV [29]. Futhermore, acute HCV infection clearance requires a potent IFN-γ response [30]. In African American patients, HCV-specific CD4 T cell proliferative responses were not accompanied by IFN-γ production, suggesting a dysregulated, virus-specific T cell function in cases of chronic infection in this population. The authors concluded that there are novel ethnicity-related differences in CD4 T cell responsiveness to HCV [29].

Other mechanisms invoked to explain the disparities in the natural history of hepatitis C among different races include the stronger association of certain human leukocyte antigen class II alleles with HCV clearance in African Americans [30] and the lack of immune system recognition of the virus in African Americans [12]. In a recent study, variants of the immunomodulatory IL-10 and IL-19/20 genes seemed to play a role in the spontaneous clearance of HCV in African American patients; no such relationship was found in white patients [31].

Although fibrosis may evolve more slowly in African Americans, the rate of hepatocellular carcinoma is increasing more quickly in this population. Compared with non-Hispanic white men, among whom the incidence of hepatocellular carcinoma increased from 2.3 to 2.8 cases per 100,000 persons (for 1981–1985 vs. 1991–1995), the age-adjusted incidence among African American men increased from 5.3 to 6.1 cases per 100,000 persons in the same time period [32].

Not only is the rate of hepatocellular carcinoma among African American persons 2-fold higher than the rate among white persons [33], but the rate of liver cancer–related mortality is 2–3 times higher among African American patients than among white patients [32]. More recent data confirm that the risk of hepatocellular carcinoma is twice as high among African American men than it is among white men [34].


Although the prevalence of chronic HCV is higher in the African American population than in the white population, African American subjects are usually underrepresented in clinical trials. Moreover, despite improvements in antiviral therapy, rates of sustained response to treatment among African American patients are relatively poor ( figure 1).

Figure 1

Progressive improvement in rates of sustained response to therapy for chronic hepatitis C virus infection in white and African American (AA) subjects. PegIFN, pegylated IFN; R, ribavirin.

Older therapies. Several authors have reported inferior response rates in chronically HCV-infected African American patients who have received standard or consensus IFN therapy, with or without ribavirin ( table 5).

Table 5

Summary of trials that included a significant number of African American patients with chronic hepatitis C virus infection who received older therapies.

Therapy today. In trials of pegylated IFN monotherapy treatment, there were inadequate numbers of African American subjects to make meaningful conclusions about the role of race in treatment outcomes [40, 41]. Likewise, in the registration trials of treatment with pegylated IFN and ribavirin, too few African American subjects were enrolled to make outcome assessments [42, 43].

Fortunately, 2 recent prospective trials have examined the effect of pegylated IFN treatment in a large number of African American subjects. Not only did these studies use pegylated IFN with ribavirin— today’ standard of care— but they also enrolled the largest number of HCV-infected African American patients of any other trial to date. Both of these studies will be analyzed in detail.

The first trial [44] compared a group of 100 African American patients with a control group of 100 non-Hispanic white patients, both of which were treated with pegylated IFN-α -2b (1.5 µ g/kg per week) and ribavirin (1000 mg per day for 3 months, followed by 800 mg per day until week 48). Both groups were treatment naive and were equally matched with regard to infecting genotype, with each group including 98 genotype 1–infected patients. The groups were also well matched with respect to age, duration of infection, viral load, alanine aminotransferase level, education level, and the presence of steatosis, fibrosis, and cirrhosis.

Treatment was well tolerated; 81% of African American and 79% of white patients completed therapy. Rates of adherence to treatment and of adverse events were also similar in both groups, and depression was the most common reason for discontinuation of therapy, regardless of ethnicity. Twenty-four percent of white patients and 22% of African American patients required dose reductions, with similar numbers of patients having the doses reduced because of neutropenia and anemia.

Compared with non-Hispanic white subjects, African American subjects had substantially poorer rates of sustained virologic response (19% vs. 52%; P <.001). The only predictor of sustained virologic response in multivariate analysis was race. Also analyzed was the predictive value of an early virologic response, defined as a ⩾ 2-log10 reduction in HCV RNA level at week 12 of therapy. None of the subjects who did not achieve an early virologic response at week 12 reached a sustained virologic response, irrespective of ethnicity. Thus, the negative predictive value of early virologic response was 100%. However, fewer African American patients than white patients achieved an early virologic response (40% vs. 69%; P <.001). Moreover, there was a discrepant positive predictive value for patients who did achieve early virologic response (48 [83%] of 58 white patients with an early virologic response had a sustained virologic response, compared with only 18 [64%] of 28 such African American patients).

Study limitations included differences in sex, body weight, and diabetes status, some of which may have impacted response rates. Furthermore, alcohol use and abstinence were not documented in the study. Because alcohol affects response to IFN-based therapy [45], discrepancies in the 2 groups’ rates of alcohol consumption may have influenced results. Finally, the ribavirin doses used were less than those customarily used for HCV genotype 1–infected patients. Although this may have impacted rates of sustained virologic response, it would have not engendered any outcome differences between ethnic groups.

The second study [46] was a prospective, multicenter trial that enrolled 78 African American subjects and 28 white subjects who were infected with HCV genotype 1 and were treatment naive. All subjects received pegylated IFN-α -2a (180 µ g per week) and ribavirin (1000–1200 mg per day, dosed on the basis of weight) for 48 weeks. Unlike the study mentioned above, this trial allowed the use of growth factors. Sustained virologic response was the primary end point, but early virologic response was assessed at week 12 of the study. Pre- and posttreatment liver biopsy specimens (for 69 patients) were also evaluated for histologic improvement.

Patient characteristics, including age, viral load (high), alanine aminotransferase level, fibrosis score, and rate of cirrhosis, were similar in the 2 groups. However, there were discrepancies in the percentages of male participants and in mean body weight.

Rates of adverse events, especially injection site reactions, vomiting, alopecia, and xerosis, were higher among white patients. Thirty-nine percent of white subjects discontinued therapy, compared with 23% of African American subjects. Severe neutropenia (neutrophil count, <0.5 × 109 cells/L) occurred more frequently among African American subjects, and more patients in this group had their IFN treatment dose reduced for this reason (37% vs. 18%).

At week 72, in the African American group, the rate of sustained virologic response was 26% (95% CI, 16%–35%), which was significantly lower than the rate for the white group (39%; 95% CI, 21%–57%). The rate of sustained virologic response for white subjects was somewhat lower than that seen in registration trials [42, 43], but the authors attribute this anomaly to the high rate of premature discontinuation of therapy and to the small size of the cohort of patients. Significant predictors of sustained virologic response in multivariate analysis were age of <41 years, low pretreatment viral load, and an alanine aminotransferase level of ❤ times the upper limit of normal.

With regard to histologic response, examination of paired biopsy specimens revealed improvement in fibrosis scores in 25% of African American patients. More than 90% of patients whose paired biopsy specimens were examined in both groups showed improvement or at least stabilization of fibrosis. of the 36 African American patients who did not achieve sustained virologic response and who underwent both biopsies, 22% achieved fibrosis improvement. These data may support the concept that some patients may achieve reversal in fibrosis, irrespective of whether they achieved a sustained virologic response [47].

Study limitations included the high rate of treatment discontinuation in the white group, the lower rate of sustained virologic response in the white group, and higher weights in the African American group, which may have contributed to the poor response to IFN. Nonetheless, multivariate analysis failed to show a significant association between body mass index and nonresponse to treatment. Another limitation of the study was that racial disparity in histological outcomes did not reach statistical significance, because too few of the patients underwent paired liver biopsies. Like the previous study, this study did not indicate differences in alcohol use between patient groups.

Despite some limitations of the aforementioned studies, some important conclusions can be drawn from both. African American persons have lower rates of sustained virologic response to pegylated IFN combination therapy than do white persons, even when controlling for genotype 1 infection. Furthermore, the negative predictive value of not achieving an early virologic response at week 12 is reliable for both races. Despite the fact that early virologic response had an inferior positive predictive value for African American patients, patients of both ethnicities should be treated for 48 weeks if early virologic response is achieved.

Preliminary findings from the weight-based dosing of Peg-Intron and Rebetrol (WIN-R) trial demonstrate that weight-based dosing of ribavirin confers a significant advantage in the treatment of African American persons infected with genotype 1, compared with fixed dosing of ribavirin [25]. WIN-R is a prospective trial of 5000 treatment-naive HCV-infected patients from >200 US study centers designed to study weight-based versus fixed-dose ribavirin therapy. Patients were randomized to receive either pegylated IFN-α -2b, 1.5 µ g/kg per week, plus ribavirin, 800 mg per day, or the same amount of pegylated IFN-α -2b plus ribavirin, 800–1400 mg per day, depending on weight. Baseline characteristics in the study’ 2 arms were not significantly different. Three hundred eight-seven genotype 1–infected African American patients were among those treated. Sixty-four percent of the African American patients had high viral loads, and 31% had at least bridging fibrosis (determined by biopsy), which is significantly more advanced disease than has been seen in previous trials. Erythropoietin or ribavirin reduction was permitted.

Although dose reductions occurred more frequently for patients who received weight-based doses of ribavirin than for those who received standard doses (12% vs. 8%), the rate of discontinuations of treatment for adverse events was not significantly different (18% vs. 17%). Anemia was no more common among patients who received 1400 mg of ribavirin per day than among those who received lesser doses. of the 362 African American subjects who weighed ⩾ 65 kg, those who received weight-based ribavirin dosing had better end-of-treatment and sustained virologic response rates than did those who received flat dosing; in fact, rates of sustained virologic response were more than doubled (sustained virologic response rate, 21% vs. 10%; P =.004). However, even though African American patients achieved higher response rates with weight-based doses of ribavirin, rates of sustained virologic response were still inferior to the rates for white patients.

A summary of the large treatment trials of African American persons who received pegylated IFN and ribavirin is shown in table 6.

Table 6

Findings from large trials of African American patients with chronic hepatitis C virus (HCV) infection who were treated with pegylated IFN-α -2b (Peg-IFN) and ribavirin (R).

Mechanisms for inferior treatment response. A multitude of hypotheses have been promulgated to explain the dissimilar treatment responses among ethnic groups. As discussed previously, dysregulated CD4 function has been described in African Americans [29]. Other possibilities include discrepant viral kinetics, cytokine production, and iron stores.

An initial decrease in the HCV RNA level, referred to as “phase 1,” occurs hours after the administration of IFN; it represents blocking of viral replication. The subsequent, slower decrease in the viral level (phase 2) represents the clearance of HCV-infected hepatocytes and usually occurs days to months after IFN therapy is initiated. The phase 2 decrease is the better predictor of ultimate HCV RNA clearance [48, 49]. Ethnicity may influence these phases. In a kinetics study that compared African American and white subjects who received combination therapy, the former had both small phase 1 and phase 2 decreases in the viral load [50]. A significant difference was found between African American and white subjects with regard to inhibition of viral production on the first day of treatment. The findings for phase 2 decreases in the viral load were also discordant; the rate of loss of infected cells was lower in African American subjects. The authors believed that the inadequate phase 1 decrease among African American patients accounted for the limited phase 2 decrease; thus, their poor response to therapy may be related to an impaired ability to block viral production early in treatment. However, when controlled for treatment effectiveness, differences in the decrease in the viral load were not statistically significant. More studies are clearly needed.

Ethnicity-associated cytokine production may also explain dissimilar treatment responses. A study compared cytokine production in phytohemaglutinin-stimulated PBMCs obtained from infected and control participants, both African American and white. Relative to healthy white control subjects, African American subjects produced higher levels of proinflammatory (TH1) cytokines IL-2 and TNF-α and lower levels of down-regulatory (TH2) cytokine IL-10. Furthermore, HCV-infected white patients who responded to treatment produced less IL-10 and more transforming growth factor–β than did white subjects who did not respond to treatment. Because there were no African American patients who responded to therapy in this study, cytokine profiles could not be correlated with therapeutic outcome in this population. The authors postulated that the “subnormal” cytokine production among white responders may be more “permissive” to IFN-based therapy, as well as that the relatively more robust immune response among African American patients may yield inferior treatment results [51].

Elevated hepatic iron stores have also been invoked to explain resistance to IFN-based therapy in African Americans. Ioannou et al. [52] found that the risk of having increased iron stores, defined as elevated serum ferritin and transferrin saturation, was >5 times greater among HCV RNA–positive African American subjects than among HCV RNA–positive non–African American subjects. After adjustment for age, alcohol intake, sex, body mass index, and education level, HCV-positive African American patients with elevated aminotransferase levels had higher iron stores than did white patients. Because the response to standard IFN monotherapy may be influenced by hepatic iron content [53,54–55], the authors surmised that the discrepant iron stores may mirror discrepant treatment results. Limitations of the study include the assumptions that response rates to combination therapy with pegylated IFN and ribavirin are limited in the face of excess iron and that peripheral iron studies accurately reflect hepatic iron content.

Neutropenia. African American persons have significantly lower mean concentrations of leukocytes and neutrophils than do white persons [56]. Lower neutrophil counts before commencement of treatment may lead to a greater likelihood that the IFN dose will be reduced during treatment or even that the patient will be excluded from participation in clinical trials.

In a multivariate analysis of a National Institutes of Health treatment study of 119 patients with chronic HCV infection who received standard IFN combination therapy, only African American race was associated with baseline neutropenia. Unlike prior treatment trials, neutropenia was not used as an exclusion criterion for therapy. Although African Americans have a >2-fold chance of developing neutropenia during treatment, none of the neutropenic patients developed serious bacterial infections. Furthermore, those with neutropenia had minimal additional cell count decrements during treatment. Thus, the authors recommended that constitutional (benign) neutropenia should not be an exclusion criterion for IFN-based therapy [57]. Similar results were evident in the preliminary analysis of the WIN-R trial [25]. Some authorities have even suggested lowering neutrophil thresholds for dose modifications in African American patients [58].

Finally, in the 2 large treatment trials of African Americans [44, 46], severe neutropenia was not associated with serious infection. However, in one study [46], neutropenia was the most common reason for modification of the IFN dose among African American patients (for 37% in this group). In the second trial [44], both races had similar rates of neutropenia episodes (13%–14%).

HCV-HIV coinfection. Approximately one-third of all HIV-infected persons in the United States are coinfected with HCV. One hundred eighty HCV-HIV–coinfected patients in an inner city area were evaluated for suitability for combination therapy with IFN plus ribavirin. African Americans were more than twice as likely to be ineligible than eligible for HCV treatment. Concomitant medical problems, psychiatric problems, poor adherence to treatment, and/or ongoing substance abuse were factors that led to patients being ineligible for therapy [59].

Of the 3 recent large trials that have focused on HCV treatment in HCV-HIV–coinfected persons, only 2 enrolled a significant percentage of African American subjects. However, race was not predictive for sustained response in either univariate or multivariate analyses in both studies [60, 61].


A summary of key differences between HCV-infected African American patients and white patients is shown in table 7. Despite lower rates of sustained response to contemporary therapy, therapeutic nihilism is not warranted when treating HCV-infected African American patients. With few exceptions, the African American population has been underrepresented in clinical trials of HCV infection, despite having a higher rate of infection; clearly, more clinical studies are needed, particularly those that investigate the mechanisms for disparate treatment responses. Likewise, prospective studies of African American patients are needed to clarify rates of disease progression in cases of chronic HCV infection. Later in 2006, final results are expected from a multicenter study sponsored by the National Institute of Diabetes and Digestive and Kidney Disease. This trial, called the Viral Resistance to Antiviral Therapy for Chronic Hepatitis C (VIRAHEP-C), has enrolled ∼200 African American subjects and ∼200 white subjects who will be treated with pegylated IFN and ribavirin. The purposes of the study are to assess response rates to therapy, as well as to analyze both viral factors and host factors, including genetic and immunologic variables that may influence treatment results.

How does a CBC test for a leukemia patient usually look like?

My answer to How does a CBC test for a leukemia patient usually look like?

Answer by Connie b. Dellobuono:

High WBCs.

How does a CBC test for a leukemia patient usually look like?

Biomarker in blood may help predict recovery time for sports concussions

Researchers at the National Institutes of Health found that the blood protein tau could be an important new clinical biomarker to better identify athletes who need more recovery time before safely returning to play after a sports-related concussion. The study, supported by the National Institute of Nursing Research (NINR) with additional funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), published online in the Jan. 6, 2017 issue of Neurology(link is external), the medical journal of the American Academy of Neurology.

Despite the millions of sports-related concussions that occur annually in the United States, there is no reliable blood-based test to predict recovery and an athlete’s readiness to return to play. The new study shows that measuring tau levels could potentially be an unbiased tool to help prevent athletes from returning to action too soon and risking further neurological injury.

“Keeping athletes safer from long-term consequences of concussions is important to players, coaches, parents and fans. In the future, this research may help to develop a reliable and fast clinical lab test that can identify athletes at higher risk for chronic post-concussion symptoms,” said NINR Director Patricia A. Grady Ph.D., R.N.

Athletes who return to play before full recovery are at high risk for long-term symptoms like headaches, dizziness, and cognitive deficits with subsequent concussions. About half of college athletes see their post-concussive symptoms resolve within 10 days, but in others, the symptoms become chronic.

Tau is also connected to development of Alzheimer’s and Parkinson’s diseases, and is a marker of neuronal injury following severe traumatic brain injuries.

In the study, led by Dr. Jessica Gill, NIH Lasker Clinical Research Scholar and chief of the NINR Division of Intramural Research’s Brain Injury Unit, researchers evaluated changes in tau following a sports-related concussion in male and female collegiate athletes to determine if higher levels of tau relate to longer recovery durations.

“Incorporating objective biomarkers like tau into return-to-play decisions could ultimately reduce the neurological risks related to multiple concussions in athletes,” said Gill.

To measure tau levels, a group of 632 soccer, football, basketball, hockey, and lacrosse athletes from the University of Rochester first underwent pre-season blood plasma sampling and cognitive testing to establish a baseline. They were then followed during the season for any diagnosis of a concussion, with 43 of them developing concussions during the study. For comparison, a control group of 37 teammate athletes without concussions was also included in the study, as well as a group of 21 healthy non-athletes.

Following a sports-related concussion, blood was sampled from both the concussed and control athletes at six hours, 24 hours, 72 hours, and seven days post-concussion.

Concussed athletes who needed a longer amount of recovery time before returning to play, (more than 10 days post-concussion) had higher tau concentrations overall at six, 24, and 72-hours post-concussion compared to athletes who were able to return to play in 10 days or less. These observed changes in tau levels occurred in both male and female athletes, as well as across the various sports studied.

Together, these findings indicate that changes in tau measured in as short a time as within six hours of a sports-related concussion may provide objective clinical information to better inform athletes, trainers, and team physicians’ decision-making about predicted recovery times and safe return to play.

Further research will test additional protein biomarkers and examine other post-concussion outcomes.

About the National Institute of Nursing Research (NINR): NINR supports basic and clinical research that develops the knowledge to build the scientific foundation for clinical practice, prevent disease and disability, manage and eliminate symptoms caused by illness, and enhance end-of-life and palliative care. For more information about NINR, visit the website at

About the Eunice Kennedy Shrive National Institute of Child Health and Human Development (NICHD): NICHD conducts and supports research in the United States and throughout the world on fetal, infant and child development; maternal, child and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit NICHD’s website.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit

Diffuse large B-cell lymphoma , blood cancer in older adults and aspartame -sugar

Diffuse large B-cell lymphoma (DLBCL or DLBL) is a cancer of B cells, a type of white blood cell responsible for producing antibodies. It is the most common type of non-Hodgkin lymphoma among adults,[1] with an annual incidence of 7–8 cases per 100,000 people per year.[2][3] This cancer occurs primarily in older individuals, with a median age of diagnosis at approximately 70 years of age,[3] though it can also occur in children and young adults in rare cases.[4] DLBCL is an aggressive tumor which can arise in virtually any part of the body,[5] and the first sign of this illness is typically the observation of a rapidly growing mass, sometimes associated with B symptomsfever, weight loss, and night sweats.[6]

The causes of diffuse large B-cell lymphoma are not well understood. Usually DLBCL arises from normal B cells, but it can also represent a malignant transformation of other types of lymphoma or leukemia. An underlying immunodeficiency is a significant risk factor.[7] Infection with Epstein–Barr virus has also been found to contribute to the development of some subgroups of DLBCL.[8]

Diagnosis of DLBCL is made by removing a portion of the tumor through a biopsy, and then examining this tissue using a microscope. Usually a hematopathologist makes this diagnosis.[9] Several subtypes of DLBCL have been identified, each having a different clinical presentation and prognosis. However, the usual treatment for each of these is chemotherapy, often in combination with an antibody targeted at the tumor cells.[10] Through these treatments, more than half of patients with DLBCL can be cured,[11] and the overall five-year survival rate for older adults is around 58%.

Aspartame – sugar

  • The longest ever human aspartame study, spanning 22 years, found a clear association between aspartame consumption and non-Hodgkin’s Lymphoma and leukemia in men
  • Leukemia was associated with diet soda intake in both sexes
  • The study was done out of Harvard but after caving to pressure from industry, a press release was issued that minimized the impact of the study
  • The long-term nature of this study is crucial as one of the primary tricks companies use to hide the toxicity of their products is short-term tests of a few weeks. The longest study prior to this one was only four and half months, far too short to reveal any toxicity from chronic exposure
  • Another trick, especially with aspartame, is to use animal models and not humans. This is problematic because animals are protected from methanol toxicity, unlike humans
  • Another recent study found that compared with sucrose (regular table sugar), saccharin and aspartame caused greater weight gain in adult rats, and this weight gain was unrelated to caloric intake.

A number of animal studies have clearly documented the association between aspartame and cancer, as the study points out. But what most researchers do not appreciate is that humans are the only animals that do NOT have the protective mechanism to compensate for methanol toxicity. So evaluating methanol toxicity in animals is a flawed model for testing human toxicity.

This is due to alcohol dehydrogenase (ADH). In humans, methanol is allowed to be transported in the body to susceptible tissues where this enzyme, ADH, then converts it to formaldehyde, which damages protein and DNA that lead to the increased risk of cancer and autoimmune disease.

Interestingly, the previous AARP Diet and Health Study, which did not find an association with aspartame and cancer, used fruit juice as the control. Most are unaware that canned or bottled fruit juice is loaded with methanol that dissociates from the pectin over time and can actually cause similar problems as aspartame. This does not occur in freshly consumed fruits and vegetables, only ones that are bottled or canned. Hence no major difference could be discerned between the aspartame and the control group.

10 blood tests for your physical check up


    • Female Comprehensive Hormone Panel
    • Item Catalog Number: LC100011
    This panel contains the following tests:

    • Chemistry Panel (Complete metabolic panel with lipids)
    • CBC
    • DHEA-S
    • Estradiol
    • Total Estrogen
    • Progesterone
    • Pregnenolone
    • Total and Free Testosterone
    • Sex Hormone Binding Globulin (SHBG)
    • TSH
    • Free T3
    • Free T4
    • Cortisol

    Sample Report

    As women enter the menopausal years, their bodies’ production of estrogen, progesterone, and other hormones needed to maintain youthful vitality rapidly declines. Continual assessment of hormone levels is necessary for women seeking to maintain a healthy hormonal balance.

    This comprehensive hormone panel is designed by Life Extension® for women looking to monitor their hormone status.

    An 8 to 12 hour fast is required for this blood test. However, drink plenty of water and take your medications as prescribed.

    Special Note:
    If you are supplementing with any hormones, it is important to take them approximately 2 hours prior to having your blood drawn. Any type of contraceptives that contain hormones will invalidate hormone results.

  • Male Comprehensive Hormone Panel
  • Item Catalog Number: LC100010
This panel contains the following tests:

  • Chemistry Panel (complete metabolic panel with lipids)
  • CBC
  • DHEA-S
  • DHT
  • Estradiol
  • PSA
  • Pregnenolone
  • Total and Free Testosterone
  • Sex Hormone Binding Globulin (SHBG)
  • TSH
  • Free T3
  • Free T4
  • Cortisol

Sample Report

As men enter the andropause years, their bodies’ production of dehydroepiandrosterone (DHEA), free and total testosterone, and other hormones needed to maintain youthful vitality rapidly declines, while PSA and estrogen may rise.

This comprehensive hormone panel is designed by Life Extension® for men looking to monitor their hormone status.

An 8 to 12 hour fast is required for this blood test. However, drink plenty of water and take your medications as prescribed.

Special Note:
If you are supplementing with any hormones, it is important to take them approximately 2 hours prior to having your blood drawn. Ejaculation within 48 hours preceding the blood draw may elevate the PSA in some men.

Email for more info and free personalized diet plan.

Newborn genetic screening in one blood test

American College of Medical Genetics recommendations

Core panel

The following conditions and disorders were recommended as a “core panel” by the 2005 report of the American College of Medical Genetics (ACMG).[1] The incidences reported below are from the full report, though the rates may vary in different populations.[2]

Blood cell disorders

Inborn errors of amino acid metabolism

Inborn errors of organic acid metabolism

Inborn errors of fatty acid metabolism

Miscellaneous multisystem diseases

Newborn screening by other methods than blood testing

Secondary targets

The following disorders are additional conditions that may be detected by screening. Many are listed as “secondary targets” by the 2005 ACMG report.[1] Some states are now screening for more than 50 congenital conditions. Many of these are rare and unfamiliar to pediatricians and other primary health care professionals.[1]

Blood cell disorders

Inborn errors of amino acid metabolism

Inborn errors of organic acid metabolism

Inborn errors of fatty acid metabolism

Miscellaneous multisystem diseases


As additional tests are discussed for addition to the panels, issues arise. Many question if the expanded testing still falls under the requirements necessary to justify the additional tests.[50] Many of the new diseases being tested for are rare and have no known treatment, while some of the diseases need not be treated until later in life.[50] This raises more issues, such as: if there is no available treatment for the disease should we test for it at all? And if we do, what do we tell the families of those with children bearing one of the untreatable diseases?[51] Studies show that the more rare the disease is and the more diseases being tested for, the more likely the tests are to produce false-positives.[52] This is an issue because the newborn period is a crucial time for the parents to bond with the child, and it has been noted that ten percent of parents whose children were diagnosed with a false-positive still worried that their child was fragile and/or sickly even though they were not, potentially preventing the parent-child bond forming as it would have otherwise.[51] As a result, some parents may begin to opt out of having their newborns screened. Many parents are also concerned about what happens with their infant’s blood samples after screening. The samples were originally taken to test for preventable diseases, but with the advance in genomic sequencing technologies many samples are being kept for DNA identification and research,[50][51]increasing the possibility that more children will be opted out of newborn screening from parents who see the kept samples as a form of research done on their child.

Connie’s comments: In the past, it takes 5 years or more to do one test at a time for any metabolic or newborn health screens. Now with the latest medical device and biotech technologies, multiple health screens (genetic) can be done in one blood test.