The Rapid Rise In Diabetes

FILED IN Type 2 Diabetes No Comments

I’m sure you’ve already heard that there is a rapid rise in diabetes all around the world. In fact, the numbers boggle the mind when you start to really study them. First of all, type 2 diabetes didn’t even exist before the 1920’s and did not exist until artificial oils were introduced into the food supply on a grand scale. Doctors were totally perplexed with it started showing up and there is a full discussion of this when you start digging into the literature. The political discourse about this before World War 2 is also very telling. By the end of the 1930’s, type 2 diabetes had risen a staggering 1000%! Now, only about 90 years later, we are told by the CDC that approximately 23.6 million people have diabetes in the United States. Another 57 million have “pre-diabetes” which is just another way of saying that their blood sugar levels are just below the official mark for diabetes.

By several accounts, one third to one half of the American population is expected to have diabetes in the next few decades. The International Diabetes Federation estimates that 7 million more people develop diabetes every year. Wow! Shouldn’t this be front page news in every major newspaper worldwide? Most of these cases of diabetes are of the type 2 variety and remember that type 2 diabetes didn’t even exist before 1920.

There is no doubt we live in a scarier world than our Grandparents grew up in. Almost every time you turn on the news you hear about someone getting shot, raped, or otherwise violently attacked. We are constantly bombarded with news about terrorist attacks, school shootings, and serial killers. This no doubt accounts for why we are so much more vigilant than our Grandparents had to be when they were kids. It’s a totally different world as they say. But… are we being as vigilant as we should be about our current health crisis? Have we become desensitized when it comes to our health?

What I don’t understand is why there isn’t more of a public outcry about the rise in diabetes and other serious medical conditions that are skyrocketing completely out of control. Why do we sit back and so passively accept this rise in diabetes? Shouldn’t we do something about it? I truly believe people need to wake up to reality and begin to question why diseases like diabetes have risen so much and why they are rising even faster now than they did only a few decades ago.

So much of what is going on with the rising rate of diabetes can be tracked to the artificial foods and other crazy things that are going on with our food supply. Why aren’t citizens demanding that our government take appropriate action to prevent this? Why does the USDA allow these artificial substances to be added to our food without them being thoroughly tested? Artificial foods are totally taking over the grocery shelves. Our bodies are not at all designed to handle this artificial food and it’s no wonder that we are developing diabetes and other serious diseases at alarming rates. If you buy pre-packaged or processed of any kind, you are almost certainly eating this artificial food. If you eat out, you are almost certainly getting it too. Even some of the food that is marketed as being extra healthy is actually artificial food. You could almost think of it as a grand scale experiment and the results do not look good for the human race.


Impaired Glucose Tolerance

FILED IN Other No Comments

Impaired glucose tolerance (IGT) as a clinical entity has gained increased attention in recent years. Three main factors can account for this. First, the recognition of increased risk for cardiovascular disease that is associated with IGT has resulted in a plea to recognize IGT as a disease state in its own right. Secondly, the role of IGT as a risk factor for diabetes has been accepted by the scientific community, despite caveats about the use of the oral glucose tolerance test (OGTT) in its diagnosis. For example, it functions as the primary screening tool and the basis for intervention in the multicenter National Institutes of Health–sponsored Diabetes Prevention Project. The increased risk in IGT amounts to a 3–9% likelihood per year of developing type 2 diabetes. Thirdly, new options for treatment of IGT have emerged. This emergence is a by-product of the dramatic increase in the availability of oral agents for treatment of type 2 diabetes, which also provides new opportunities for preventive strategies. To justify the risks of pharmacological treatment in a prediabetic state, identification of people at high risk for diabetes is required. Hence, the choice of IGT. Focus on IGT has also been associated with attempts to understand underlying mechanisms; greater understanding may help improve prediction of diabetes and enhance development of targeted therapies. In this issue, Larsson and Ahrén report on defects in islet physiology that may contribute further to our understanding of the pathogenesis of IGT.

In a population-based study of postmenopausal Swedish women, these investigators studied IGT, applying World Health Organization criteria to an OGTT. Of 108 women evaluated, 34% had IGT. This group had slightly elevated systolic blood pressure and serum triglyceride levels, although BMI measurements, waist-to-hip ratios, and body fat content were similar to those of the normal glucose tolerance group (NGT). Insulin sensitivity was measured using a glucose clamp, and insulin and glucagon secretion were evaluated using glucose and arginine infusions. Women with IGT were shown to have both insulin resistance and reduced insulin secretion; the latter was particularly evident when expressed in terms of each subject’s insulin sensitivity as a disposition index. The utility of this approach was well demonstrated, because insulin secretion, though similar in both groups, was found to be significantly reduced when evaluated in relation to the degree of insulin resistance present. The investigators also found hyperglucagonemia, manifesting as an increase in arginine-stimulated secretion and a reduced suppressibility of glucagon during hyperglycemia. A novel aspect of this study is the finding that there was an inverse relationship between insulin sensitivity and glucagon secretion in these subjects. Previous studies support the concept that glucagon may be involved in the pathogenesis of IGT. This concept derives from studies of glucagon suppressibility during oral glucose loading. The normal physiological suppression of glucagon secretion in response to elevated plasma glucose is lost in diabetes and is also impaired in IGT.

A concomitant decrease in early insulin secretion in response to oral glucose is also observed. This combined defect alters the insulin-to-glucagon ratio and, as a result, leads to failure of the normal suppression of endogenous glucose production that occurs after oral glucose ingestion. This, in turn, contributes to elevated plasma glucose concentrations that are characteristic of IGT. Insulin resistance also plays a role in IGT by impairing glucose disposal and providing resistance to hepatic insulin action. However, secretory abnormalities can cause IGT in the absence of insulin resistance. Shah et al. studied normal subjects with a combined hormonal defect, i.e., insulin secretion and glucagon suppressibility were both reduced experimentally during glucose loading. This experiment resulted in a marked reduction in glucose tolerance with a failure to suppress endogenous glucose production. When normal suppressibility of glucagon was allowed to occur, endogenous glucose production and glucose tolerance were normalized. These authors suggest that improving postprandial suppressibility of plasma glucagon may be a therapeutic target in IGT. What are the mechanisms responsible for the abnormalities in glucagon secretion that occur in IGT?

Both exaggerated responses to secretagogues and failure of suppressibility of glucagon are tied to abnormal _-cell function. Types 1 and 2 diabetes and IGT each have different degrees of insulin-secretory dysfunction, and all are associated with abnormal regulation of glucagon secretion. This is explained by the inhibitory effect of insulin on glucagon release and by evidence for local control of _-cell function by insulin within the islet. Reducing the inhibitory influence of insulin can account for a difference in both the tonic control and the stimulation of glucagon secretion observed in IGT. Thus, abnormalities in glucagon that are characteristic of IGT can be explained by dysfunction in islet secretion. However, resistance to secreted products of the islets may also play a role. This was illustrated by Kulkarni et al., who demonstrated the functional importance of insulin receptors in the islets of Langerhans in a model of insulin resistance of the _-cell. Using a tissue- specific _-cell insulin-receptor knockout mouse, they found impaired insulin secretion due (presumably) to reduction of a stimulatory influence of insulin on the _-cell. If resistance to insulin action occurs in the _-cell, it may also apply to the _-cell and thereby contribute to a reduction in the ability of insulin to inhibit glucagon secretion.


Diabetes Ayurvedic Treatment

FILED IN Other No Comments

Ayurveda is a natural way to stimulate adult stem cells to regenerate damaged tissues is explained as “KSHEERA DADHI NYAYA” in ayurveda,5000years back.

Body-senses-mind & soul are the integral parts of human biological system. And body is a complex of Doshas-Dhatus & Malas; these are grosser manifestations of Panchamahabhuta.

The dhatus form the basic stuff of the body – tissues. These are of two categories –Sthayee & Asthayee & generic types of these dhatus are 7. The presence of Sthayee dhatus controls the architecting of Asthayee dhatus throughout life from the available nutrients in the human system with the help of Agni, transporting mechanisms.

If due to deficiency of any nutrition/ in any chronic disease condition any kinds of dhatu get depleted then with the help of Rasayana therapy the process of formation of that particular dhatu/ dhatus is stimulated.

These Sthayee dhatus are stem cell in modern terms & in Ayurveda system of medicines the applied aspect of this concept is elaborately discussed & used therapeutically & as preventive measures for various diseases & as an anti-ageing modality.

Rejuvenation, The Panchakarma therapeutic techniques and Traditional treatments that were used by kings-queens & allied persons in Olden Days are the most powerful methods to utilize the nutrients available within the body systems, to preserve physical-vital-energy and to save the body from decay & rejuvenation as well. Latest scientific research has confirmed findings of stem cells at the routes/systems that are touched/ reactivated following the Panchakarma technique.for more log on www.vedantayurveda.com

The physiological-psychological- nature can be transformed to retard the ageing process,health state for ever & steping towards immortility by revealing spritituality .


Treating Diabetic Ketoacidosis

FILED IN Other No Comments

Diabetes is one of the most common diseases faced with people these days. Diabetes needs a lot more care than other diseases so as to see that the blood sugar level is controlled in the body at regular intervals. If the blood sugar gets so high that ones body starts burning fats stored for energy, one may start producing ketones bodies which build up and spill over in to the urine. Ketoacidosis is a condition which is commonly found in Type 1 diabetes, where the combination of high blood glucose, ketones bodies, dehydration, and various chemical imbalances and when not taken care of results in the same. But studies have shown this is not found in Type 2 diabetes.

One has to be more careful and more aware, if one is suffering with other illness along with diabetes, as ketoacidosis have more chances to attack the body system, therefore it is vital to check ones blood glucose frequently. One should be very careful when home sick, one should always be prepared with one’s spouse or a close friend in case if emergency occurs. One should make them instruct that if in any case one may not answer the phone after frequent rings they should come to the house, give a check and if found in conscious state should be referred to hospital or they should call an ambulance without any delay.

Intravenous fluids are used to treat diabetic ketoacidosis, as they dilute the blood glucose and rehydrate you. Chemicals like potassium and sodium are used with intravenous fluid in order to balance the boy’s imbalances. Insulin is also used to push glucose out of the bloodstreams and eventually into the cells. As soon as the blood glucose level comes down to normal, the body immediately needs some fuel in the form of glucose to prevent the formation of ketones. That is why glucose is added to the intravenous fluid. In emergency situations, you will be stabilized in the emergency room by physicians and later they keep you in hospital for a day or two to make sure that your have passed the crisis period safely and there is no threat left over.

Mathew is a diabetic child and he got food poisoning or stomach flu for some reasons and began to vomit. As far as insulin is concerned, he knew nothing, but to take prescribed dose of insulin. Besides this, he had no idea about it. His condition became severe and his mother called for doctor help. Doctor suggested her to take her son immediately to emergency. Mathew was dehydrated. Doctors took some blood and began intravenous fluid treatment. He was admitted to intensive care unit as he was so dehydrated, he took eight liters of fluid before e had to urinate.

The purpose of giving this example here is to let you know that how important is your immediate response to diabetic ketoacidosis. If you show any carelessness, the things get worse for you. So, if you feel that the things are getting worse rather than improving, contact your doctor immediately.


How to Balance Blood Sugar

FILED IN Other No Comments

Diabetes is a growing problem in the population: according to Diabetes UK there are 3% (1.8 million) diagnosed cases (approximately 250 thousand with type 1 and over 1.5 million with type 2) and another estimated 750 thousand to 1 million undiagnosed cases of type 2 diabetes. No statistics are available for the athletic population.

What is diabetes?

Diabetes is a syndrome or group of symptoms arising from failure to regulate the metabolism of glucose by means of the pancreatic hormone, insulin. This occurs due to a lack of insulin because the pancreas does not produce enough, fails to produce any or the body fails to make proper use of the insulin that is available. Diabetes is classified as insulin-dependent (type 1) and non-insulin-dependent (type 2). This paper will focus on the latter and will ignore any genetic predisposition to the disease.

The glycaemic index and diabetes

The Glycaemic Index (GI) can be considered as a measure of carbohydrate quality. It measures the postprandial (after a meal) glycaemia (plasma glucose) raising potential of a single food by expressing the rise in glycaemia in response to a 50g available carbohydrate portion of that food as a percentage of the rise in response to a 50g available carbohydrate portion of a reference food (white bread or glucose).

Foods high on the GI result in a sharp rise of plasma glucose, with a high demand for insulin, followed by a more or less rapid fall of glucose. Foods that are low to moderate on the GI produce a slower rise, with a lower demand for insulin, and a more gradual decline in plasma glucose.

Those in favour of carbohydrate quality, argue that GI is a robust measurement, predicts the relative glycaemic response to mixed meals and is easy to follow and implement. In contrast, opponents who favour giving priority to carbohydrate quantity argue that GI is highly variable, not physiological, cannot reliably predict mixed meal responses and is difficult to learn or follow.

Despite some opposition to low-GI intervention in type 2 diabetes, the interventions are clinically efficacious in diabetes therapy over the mid to long-term. The Canadian Diabetes Association, Diabetes Australia, Diabetes UK and the European Association for the Study of Diabetes all support the application of the GI concept in the management of diabetes.

Insulin resistance

Insulin resistance, a component of the Insulin Resistance Syndrome, also known as Syndrome X and the Metabolic Syndrome, is associated with type 2 diabetes. No statistics for insulin resistance are available in the UK, although, according to Diabetes UK, a national register may be set up in the future.

Obesity is the most significant factor leading to insulin resistance with visceral obesity having a particularly strong negative correlation. It can be reversed with diet modification based on a low-fat intake and limiting refined carbohydrates without the need of caloric restrictions. Physical activity is an important factor in reversing the problem.

Mechanisms leading to insulin resistance are unclear, although the abnormal accumulation of certain fats in the liver (hepatic steatosis) is a contributing factor.

In a study by Pan et al, skeletal muscle triglyceride (mTG) appeared to be another important factor in predicting insulin resistance. Trained athletes and animals show the same or higher levels of muscle triglycerides as sedentary controls but have improved insulin action. The authors postulated that this could be due to the distribution of triglyceride. Endurance exercise increases both the mitochondrial volume and distribution in skeletal muscles. In trained dogs, mitochondria appear virtually in direct contact with triglyceride droplets whereas no such association with mitochondria was found in untrained animals. As a result, trained individuals may have an improved ability to mobilise fats.

Research into sucrose and fructose on animals has consistently shown that high sucrose and fructose diets decrease insulin sensitivity. Studies on humans have been inconsistent.

In a large cohort study by Janket et al, 38,480 initially healthy postmenopausal women were followed for an average of 6 years. The researchers accrued 918 incident cases of type 2 diabetes but found no definitive influence of sugar intake on the risk of developing type 2 diabetes. It was noted, however, that the median follow-up time of 6 years might not have been long enough to detect a very subtle relationship between sugar intake and incidence of type 2 diabetes.

Assessment on humans is thought to be more complicated because of other factors affecting insulin sensitivity. Some studies found that those consuming a diet consisting of large amounts of sweets and desserts were at increased risk of developing diabetes. However, the diet also included high amounts of saturated fats (red meat, fries and dairy products) which is known to be associated with decreased insulin sensitivity.

No studies have shown a negative effect of sucrose on insulin sensitivity. One explanation for this lack of correlation could be that recruitment of volunteers for nutrition studies is notoriously difficult and many studies have a young or a highly health-orientated population. Both groups are likely to be physically active. Given the strength of the positive influence of physical exertion on insulin sensitivity, such persons are inclined to be resistant to the negative effects of diet. However, this does suggest that the promotion of physical activity may have a greater influence on insulin sensitivity than diet.

Another possible explanation is that the GI concerns only the first 2 hours of the postprandial period. It is postulated that a GI defined by a 4-6 hour postprandial period would alter the ranking of sucrose in a GI table to a higher level. Neither sucrose (a disaccharide: glucose bonded to fructose) nor fructose (a monosaccharide) is high on the GI.

Studies based on high fructose versus high glucose diets have shown that the high fructose diets produce an increase in plasma triacylglycerol, plasma cholesterol, VLDL and LDL cholesterol concentrations, all of which are a risk factor in cardiovascular disease. In addition, some of these effects were seen in men but not women. The reason for this difference is not clear. Although not all studies are consistent with these findings, the positive data cannot and should not be dismissed as it may be of considerable clinical importance. It is also important to note that some individuals are more sensitive to fructose than others.

The risk for athletes

Are athletes at risk of developing type 2 diabetes as a result of their high intake of fructose, sucrose and high glycaemic foods? Although the scientific evidence to-date does not support this notion, athletes may be at risk of developing insulin resistance which is associated not only with diabetes but also with coronary heart disease, hypercholesterolaemia, hypertension, dysglycaemia, osteoarthritis and impaired glucose tolerance.

An over-consumption of refined carbohydrates, over-processed foods, saturated fats and processed vegetable fats are all associated with insulin resistance. The majority of adult athletes we have consulted to-date, over-consume the above with the possible exception of saturated fats. However all our adolescent athletes consumed large amounts of saturated fats.

Although some athletes are becoming more informed on the importance of nutrition for both their long-term health and their performance, there are still a large number who are uninformed or misinformed on nutritional issues. Particularly distressing is the lack of knowledge amongst adolescent athletes which needs to be urgently addressed, not only by nutritionists and dieticians, but also by coaches and parents.

One procedure that can be immediately implemented by everybody is that of chewing our food thoroughly and eating more slowly: it appears that prolonging absorption time by increasing the length of time to complete a meal, consuming smaller and more frequent meals or drinking a beverage over a prolonged period of time all improve glucose tolerance.

In summary, to minimise the risk of insulin resistance, the following points should be adhered to:

  • Limit sugars and high GI carbohydrates to just before, during and just after exercise.
  • At other times, consume a large variety of foods avoiding repeating the same food on any one day.
  • Try to include colourful foods at every meal.
  • Eat fresh rather than ready-made as often as possible.
  • Limit all saturated fats found in dairy products and fatty meats.
  • Avoid fried foods.
  • Avoid junk foods.
  • Dilute fruit juices.
  • 22Sep

    Living With Type 2 Diabetes

    FILED IN Type 2 Diabetes No Comments

    Type 2 diabetes is a disease characterized by high levels of sugar in the bloodstream. The most common form of diabetes, type 2 diabetes today affects over 25,000,000 Americans and in 2006 was the 7th leading cause of death in the United States. People with type 2 diabetes have what’s known as insulin resistance. This is the inability of liver, fat and muscle cells to respond normally to insulin. As a result the sugar in your blood can’t get into the cells so it can be used as energy.

    The basic fuel that the body uses is called glucose. Glucose is created when the body breaks down the sugar in your food. Insulin created by the pancreas then takes the sugar from the blood and carries it to the cells. The problem arises when there isn’t enough insulin to carry the glucose or when the cells don’t take the glucose in. When the sugar doesn’t get into the cells, the sugar in the blood starts to build up resulting in a condition called hyperglycemia. As levels of glucose in the blood increase, the pancreas responds by producing more and more insulin, but not enough to keep up with demand.

    Genetics play a big role in determining who will develop type 2 diabetes as it tends to run in families. Because excess fat interferes with the body’s ability to use insulin, being excessively overweight can greatly increase your chances of developing type 2 diabetes. Other prominent factors in developing the disease are a sedentary lifestyle and bad diet.

    Managing your weight and eating a nutritious diet are critically important to living with diabetes. If diet is brought under control some people with type 2 diabetes can even progress to the point where they can stop taking medications after the losing weight. They still must be vigilant and keep the weight off because they still have diabetes.

    Regular exercise is another important method of preventing and dealing with the effects of diabetes. Exercise lowers your blood sugar level and helps burn off excess calories and fat and helps to keep your weight under control. Even without the benefit of burning fat, exercise can help you fight diabetes by improving your blood flow and blood pressure. Increased energy, lower tension and an improvement in your ability to handle stress can also do a lot to improve your overall health.

    If diet and exercise don’t do enough to maintain normal blood glucose levels your doctor may have to prescribe medication. These drugs help to lower your blood sugar levels and often work in different ways. This means that often you may need to take more than one of them.

    You can help prevent type 2 diabetes by keeping a healthy body weight and an active lifestyle. If you have a family history of diabetes you should be especially careful about your diet and exercise and make sure you visit your doctor twice a year to monitor you blood sugar levels.


    Diabetes, Glycemic Control: Results

    FILED IN Other No Comments

    Baseline characteristics of the study population (n = 839) are outlined in Table 1. Mean age was 67 years, and 200 patients (23.8%) had diabetes.

    Table 1

    No diabetes Diabetes P value
    n 639 200
    Age (years) 67.4 ± 11.0 65.3 ± 10.3 0.02
    Sex, male (%) 528 (82.6) 161 (80.5) 0.49
    Race, white (%) 416 (65.2) 88 (44.0) <0.001
    BMI (kg/m2) 27.9 ± 4.7 29.9 ± 6.0 <0.001
    Smoking (%) 124 (19.4) 34 (17.0) 0.44
    Heavy alcohol use (%) 215 (33.8) 38 (19.0) <0.001
    Physical inactivity (%) 221 (33.1) 85 (42.5) 0.02
    LDL cholesterol (mg/dl) 106 (34) 100 (32) 0.03
    A1C (%) 5.5 ± 0.5 7.1 ± 1.4 <0.001
    Systolic blood pressure (mmHg) 132 ± 20 137 ± 23 0.003
    Medical history
    Myocardial infarction (%) 313 (49.1) 106 (53.8) 0.25
    Revascularization (%) 367 (57.4) 104 (52.3) 0.20
    Medication use
    ACE inhibitor/ARB (%) 261 (40.8) 136 (68.0) <0.001
    β-Blocker (%) 343 (53.7) 129 (64.5) 0.007
    Baseline LVEF (%) 62.7 ± 8.6 63.1 ± 8.8 0.59
    Diastolic function (%) 0.22
    Normal 361 (63.2) 116 (63.7)
    Impaired 151 (26.4) 40 (22.0)
    Pseudo/restricted 59 (10.3) 26 (14.3)
    Exercise-induced wall motion abnormalities (%) 128 (21.5) 44 (24.4) 0.40
    Creatinine clearance (ml/min) 82.4 ± 26.9 82.0 ± 31.2 0.87
    CRP (mg/l) 4.0 ± 6.8 4.8 ± 7.0 0.11

    Data are means ± SD unless otherwise indicated. CRP was log-transformed for statistical analysis.

    Diabetes as a predictor of heart failure hospitalizations

    During a mean ± SD follow-up of 4.1 ± 1.2 years, 30 (15.0%) patients with diabetes and 47 (7.4%) patients without diabetes developed heart failure. Between baseline and end of follow-up (either heart failure event or end of study), 52 patients (6.2%) had a myocardial infarction. In Fig. 1, Kaplan-Meier analysis shows the proportion of patients with hospitalizations for heart failure divided into patients with and without diabetes. In Table 2, results of the Cox regression models are presented. Diabetes was a significant predictor of heart failure hospitalization (HR 2.17 [95% CI 1.37–3.44]; P = 0.001). Diabetes remained a strong predictor of heart failure while adjustments were made for other predefined predictors of heart failure. Thus, adjustment for age, sex, race, smoking, physical inactivity, BMI, LDL cholesterol, systolic blood pressure, myocardial infarction during follow-up, LVEF, exercise-induced wall motion abnormalities (i.e., ischemia), diastolic dysfunction, or CRP did not attenuate the strength of the relationship between diabetes and heart failure. In the fully adjusted model, diabetes was associated with an increased HR for hospitalization because of heart failure (3.34 [1.65–6.76]; P = 0.001). Other significant multivariable predictors were age (years, HR 1.06), smoking status (3.01), physical inactivity (2.18), LVEF (percent, 0.94), exercise-induced wall motion abnormalities (2.34), diastolic dysfunction (1.26–4.97, depending on the grade of diastolic dysfunction), and logCRP (2.10).

    Figure 1

    Proportions of patients free of hospitalization for heart failure divided into patients with diabetes (· · · ·) and patients without diabetes (——).

    Table 2

    Diabetes and A1C as risk factors for heart failure hospitalization (multivariable Cox regression)

    Diabetes as predictor for heart failure P value A1C ≥6.5% as predictor for heart failure P value A1C (%) as predictor for heart failure P value
    n 839 832 832
    Univariable analysis 2.17 (1.37–3.44) 0.001 1.61 (0.96–2.71) 0.071 1.36 (1.17–1.58) <0.001
    Model 1 2.50 (1.57–4.01) <0.001 1.72 (1.02–2.92) 0.043 1.46 (1.24–1.73) <0.001
    Model 2 2.65 (1.61–4.36) <0.001 1.58 (0.90–2.78) 0.114 1.50 (1.26–1.79) <0.001
    Model 3 2.53 (1.58–4.07) <0.001 1.72 (1.02–2.92) 0.043 1.48 (1.25–1.76) <0.001
    Model 4 2.79 (1.74–4.50) <0.001 2.03 (1.18–3.47) 0.010 1.46 (1.24–1.71) <0.001
    Model 5 2.19 (1.29–3.71) 0.003 1.50 (0.82–2.73) 0.189 1.33 (1.09–1.61) 0.004
    Model 6 2.60 (1.55–4.36) <0.001 2.02 (1.16–3.52) 0.014 1.48 (1.24–1.75) <0.001
    Model 7 2.42 (1.50–3.90) <0.001 1.71 (1.01–2.92) 0.047 1.39 (1.17–1.64) <0.001
    Model 8 2.49 (1.52–4.08) <0.001 1.67 (0.98–2.84) 0.061 1.45 (1.22–1.72) <0.001
    Model 9 (full) 3.34 (1.65–6.76) 0.001 2.27 (1.06–4.87) 0.036 1.40 (1.13–1.74) 0.003

    Data are HR (95% CI) unless otherwise indicated. Model 1: age, sex, and race. Model 2: age, sex, race, smoking, BMI, physical inactivity, LDL cholesterol, and systolic blood pressure. Model 3: age, sex, race, and myocardial infarction during follow-up. Model 4: age, sex, race, and LVEF. Model 5: age, sex, race, and exercise-induced wall motion abnormalities. Model 6: age, sex, race, and diastolic dysfunction. Model 7: age, sex, race, and logCRP. Model 8: age, sex, race, ACE inhibitor/ARB and β-blocker use. Model 9: age, sex, race, smoking, BMI, physical inactivity, LDL cholesterol, systolic blood pressure, myocardial infarction during follow-up, LVEF, exercise-induced wall motion abnormalities, diastolic dysfunction, logCRP, and ACE inhibitor/ARB and β-blocker use.


    Diabetes, Glycemic Control: Research Design and Methods

    FILED IN Other No Comments

    The Heart and Soul Study is a prospective cohort study of psychosocial factors and health outcomes in patients with stable CAD. Design of the study has been published previously. In summary, patients were recruited from outpatient clinics of 12 different centers in the San Francisco Bay area if they met one or more of the following inclusion criteria: prior myocardial infarction, angiographic evidence of ≥50% stenosis in one of the coronary arteries, prior coronary revascularization, and exercise-induced ischemia (treadmill or nuclear scintigraphy). Exclusion criteria were acute coronary syndrome within the past 6 months, the inability to walk one block, and plans to move out of the area within 3 years.

    Between September 2000 and December 2002, 1,024 patients were enrolled in the study. For the current investigation, 185 patients (18.1%) were excluded because they had a history of heart failure (n = 179) or heart failure status was unknown (n = 6).

    Baseline study variables

    All patients completed a daylong baseline study visit that included a medical history interview, physical examination, questionnaire, laboratory analysis, exercise test, and echocardiogram. Diabetes was defined as self-reported diabetes or the use of antidiabetes medication. Alcohol use was determined by questionnaire. Participants rated their physical activity during the previous month using a 6-point Likert scale. Those responding “not at all active” or “a little active” were classified as physically inactive. An estimate of chronic glycemia was provided by serum A1C measurement. Serum glucose level, A1C, LDL cholesterol, and C-reactive protein (CRP) were assessed by standard routine biochemistry analysis after an overnight fast (except for taking their regularly prescribed medication with water) using a venous blood sample, drawn via a 21-gauge butterfly needle. Subjects were considered to have metabolic syndrome if they met the criteria of the National Cholesterol Education Program. Echocardiography was performed with an Acuson Sequoia Ultrasound System (Siemens Medical Solutions USA, Malvern, PA), with a 3.5-MHz transducer. Left ventricular ejection fraction (LVEF) was calculated using the modified Simpson rule as recommended by the American Society of Echocardiography. In addition, a full description of diastolic function was performed according to predefined established criteria (normal, impaired, pseudonormal, or restrictive diastolic function). An exercise treadmill test (standard Bruce protocol) was performed. Immediately after exercise, echocardiographic analysis was performed to investigate exercise-induced wall motion abnormalities, which served as an indicator of myocardial ischemia. Details pertaining to acquisition and analyses of echocardiographic data were reported elsewhere. The institutional review board at each of the sites approved the study protocol, and all participants provided written informed consent.

    End points

    The main study outcome was time to hospitalization for heart failure, as was previously reported for the whole cohort in detail. Heart failure was diagnosed according to established criteria using clinical and radiological evaluation. Potential events were recorded annually by telephonic interviews. Additional information (e.g., medical records and death certificates) was collected and reviewed by two independent and blinded adjudicators. Discrepancies were discussed, and decisions were made by unanimity. In case of disagreement, a third blinded adjudicator was consulted. Follow-up was completed for all patients.

    Statistical analysis

    The study sample comprised 839 patients. Baseline differences between participants with diabetes and without were compared using t tests for continuous variables and χ2 tests for dichotomous variables.

    In addition to the association of diabetes per se with hospitalization for heart failure, we investigated the role of glycemic control in the development of heart failure. A1C was used as a proxy measure for glycemic control (both dichotomized and continuous, per 1% change). For the former categorization, a cutoff of ≥6.5% and <6.5% was used because this cutoff was recently used to redefine the diagnosis of diabetes. The following analyses were conducted with diabetes and A1C as independent variables. First, Kaplan-Meier analysis was used to estimate the time from baseline to heart failure hospitalization in patients with or without diabetes and in patients with low or high A1C. The log-rank test was used for bivariate significance testing. In addition, given the influence of antidiabetes medication on A1C levels, we compared the effect of glycohemoglobin on heart failure in patients taking antidiabetes medication. Second, Cox proportional hazard regression analyses were performed to investigate the impact of diabetes and A1C level, respectively, on the time to first hospitalization for heart failure. To study the impact of diabetes and A1C on heart failure in the context of several potential confounders, we made a selection of the most important risk factors for heart failure based on recent guidelines. We then applied the following series of a priori determined Cox regression models in which we sequentially controlled for the following groups of confounders: model 1: age, sex, and race; model 2: smoking, physical inactivity, BMI, LDL cholesterol, and systolic blood pressure; model 3: myocardial infarction during follow-up; model 4: LVEF; model 5: exercise-induced wall motion abnormalities (i.e., ischemia); model 6: diastolic dysfunction; model 7: logCRP; and model 8: ACE inhibitor/angiotensin receptor blocker (ARB) and β-blocker-use. All models included age, sex, and race. In the final model (model 9) we include all the variables that were used in models 1–8. Finally, in sensitivity analyses, the relationship between several other definitions of diabetes and time to onset of heart failure were tested.

    These definitions were 1) self-reported diagnosis of diabetes (irrespective of antidiabetes medication use, 2) fasting blood glucose >126 mg/dl, and 3) fasting blood glucose >126 mg/dl or use of antidiabetes medication. Moreover, the presence of metabolic syndrome was tested in sensitivity analyses. P < 0.05 was used for all tests to indicate statistical significance. Hazard ratios (HRs) with 95% CIs are reported. All statistical analyses were performed using SPSS (version 17.0 for Windows; SPSS, Chicago, IL).

    , , ,


    Diabetes, Glycemic Control, and New-Onset Heart Failure

    FILED IN Other No Comments


    Diabetes is a predictor of both coronary artery disease (CAD) and heart failure. It is unknown to what extent the association between diabetes and heart failure is influenced by other risk factors for heart failure.


    We evaluated the association of diabetes and A1C with incident heart failure in outpatients with stable CAD and no history of heart failure (average follow-up 4.1 years).


    Of 839 participants, 200 had diabetes (23.8%). Compared with patients who did not have diabetes, those with diabetes had an increased risk of heart failure (hazard ratio [HR] 2.17 [95% CI 1.37–3.44]). Adjustment for risk factors for CAD (age, sex, race, smoking, physical inactivity, obesity, blood pressure, and LDL cholesterol), interim myocardial infarction, and myocardial ischemia did not alter the strength of the association between diabetes and heart failure. After inclusion also of other risk factors for heart failure (left ventricular ejection fraction, diastolic dysfunction, and C-reactive protein) and medication use, diabetes remained an independent predictor of heart failure (HR 3.34 [95% CI 1.65–6.76]; P = 0.001). Each 1% increase in A1C concentration was associated with a 36% increased HR of heart failure hospitalization (HR 1.36 [95% CI 1.17–1.58]).


    In patients with stable CAD who are free from heart failure at baseline, diabetes and glycemic control are independent risk factors for new-onset heart failure. The mechanisms by which diabetes and hyperglycemia lead to heart failure deserve further study, as the association is independent of baseline functional assessment of ischemia, systolic and diastolic function, and interim myocardial infarction.

    Heart failure is an enormous burden of disease, leading to substantial health care costs. Despite advances in treatment, the number of heart failure hospitalizations has increased steadily. The 2005 Heart Failure Guidelines of the American College of Cardiology/American Heart Association and European Society of Cardiology emphasized the importance of identification and treatment of risk factors. Among the patients classified in the highest risk group are patients with diabetes. Diabetes is associated with incident heart failure in the general population  and with adverse outcomes among patients with already existing heart failure. Diabetes also predicts heart failure in patients with acute coronary syndromes. Whether diabetes predicts heart failure in patients with stable coronary artery disease (CAD) has not been evaluated in detail.

    The precise underlying mechanism by which diabetes portends heart failure is unclear. In fact, it remains to be elucidated whether in this context the diagnosis of diabetes per se is more important than just the presence of inadequate glycemic control. CAD is the number one risk factor for heart failure in the developed world. Because diabetes is strongly associated with CAD, it is plausible to attribute the risk of heart failure associated with diabetes to the effects of CAD. However, although it is known that hyperglycemia predicts heart failure among diabetic patients with CAD (7), it is not known whether this risk is independent of CAD severity, CAD progression, or the presence of myocardial ischemia. Even in the absence of CAD, patients with diabetes show changes in myocardial performance that put them at risk for heart failure (diabetic cardiomyopathy).

    To determine to what extent the association between diabetes and heart failure is influenced by other risk factors for heart failure (including interim myocardial infarction and the presence of baseline myocardial ischemia), we evaluated the risk of heart failure associated with diabetes in a cohort of outpatients with stable CAD. The cohort is derived from the Heart and Soul Study, which allows thorough investigation of the strength of the association between diabetes (both the diagnosis per se and the level of glycemic control) and future heart failure episodes, while taking into account the above-mentioned established and presumed risk factors.

    , ,


    Fighting Diabetes With Diet

    FILED IN Dieting No Comments

    We live in a world where preventable diseases are affecting more people every year. In fact 24 million Americans have diabetes. At the current rate, one out of every three people born in 2000 will develop diabetes, putting them at higher risk for other medical problems. What is going on? It cannot be all about genetics. Something in our day-to-day lives is making us sicker.

    Before pointing fingers, let’s look at what diabetes is. It’s a disease in which the body does not produce or properly use insulin-a hormone that is needed to convert sugar, starches and other food into energy needed for daily life. A common precursor to diabetes is hypoglycemia-the body’s inability to handle large amounts of sugar. Hypoglycemia can be caused by an overload of sugar, alcohol, caffeine, tobacco and stress. This condition is triggered when the pancreas secretes too much insulin in response to a rapid rise in blood sugar, which in turn causes blood sugar levels to plummet, starving the body’s cells of needed fuel. When we need fuel, our body’s natural response is to crave something sweet, and that is where we get into trouble.

    Most people’s reaction when they crave something sweet is to run to the vending machine for a candy bar or soda. This fix may provide instant gratification, but it can cause your blood sugar levels to spike right after a meal and then crash to abnormally low levels several hours after a meal. This roller-coaster effect is implicated in the onset of type 2 diabetes. It may take years for hypoglycemia to develop into full-blown diabetes, so the earlier you intervene the better.

    Since overconsumption of refined sweets and added sugars has led to the increase in obesity, hypoglycemia and diabetes, diet is an important preventative measure. We’ve got to literally clean up the junk in our diets. I like to say, eat less sugar and chemical-filled artificial junk food, more vegetables, whole grains and fruit. Instead of that doughnut for breakfast, try a complex carbohydrate like oatmeal for sustainable energy. By eating something without added sugar your body will be able to maintain its natural balance and you will be less likely to crave those processed sweets. Another way to think about it is to eat less food in brightly colored packages and boxes and more colorful foods from the produce section.

    Sugar cravings are as natural as our desire for air, so let’s not fight our body’s natural instincts. Instead of hitting the vending machine for sweets, alleviate your cravings with these naturally sweet foods:

    • Corn
    • Carrots
    • Onions
    • Beets
    • Sweet potatoes
    • Yams
    • Turnips
    • Red cabbage

    Doctors are realizing the importance of exercise in preventing disease as well. Exercise doesn’t have to be going to the gym every night. It could be taking a walk, parking at the back of a parking lot, taking the stairs, or going out dancing. Find ways you like to move and you will also help prevent your body from breaking down. By incorporating more movement into your daily routine, as well as more whole foods, you will be less likely to need operations and medications later on in life.