Archive for the ‘Diabetes’ Category

KEY POINTS: NEPHROPATHY

Nephropathy has traditionally occurred in 30-40% of people with type 1 diabetes.
Mortality from complications of nephropathy in type 1 diabetes was 80% in 1971, 40% in 1984, and 20% in 1996. With modern intensive management of glucose, blood pressure, albuminuria, and the synthesis and/or action of angiotensin II, the incidence of nephropathy and its cardiovascular complications will continue to decrease.
Intensive glucose management, with a HbAlc goal of < 7%, will decrease occurrence of microalbuminuria and subsequent diabetic nephropathy.
If microalbuminuria (> 30 mg/24 hr) is present, therapy with angiotensin-converting enzyme inhibitors leads to regression of microalbuminuria and delays the progression to clinical albuminuria (> 300 mg/24 hr) and/or end-stage renal failure. These effects are seen in normotensive as well as hypertensive type 1 diabetic patients vvith microalbuminuria.
ACE inhibitor therapy in type 1 diabetic patients with clinical albuminuria and an elevated serum creatinine leads to a 48-50% reduction in the risk of doubling of serum creatinine or progression to end-stage renal disease
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KEY POINTS: NEPHROPATHYNephropathy has traditionally occurred in 30-40% of people with type 1 diabetes.Mortality from complications of nephropathy in type 1 diabetes was 80% in 1971, 40% in 1984, and 20% in 1996. With modern intensive management of glucose, blood pressure, albuminuria, and the synthesis and/or action of angiotensin II, the incidence of nephropathy and its cardiovascular complications will continue to decrease.  Intensive glucose management, with a HbAlc goal of < 7%, will decrease occurrence of microalbuminuria and subsequent diabetic nephropathy.If microalbuminuria (> 30 mg/24 hr) is present, therapy with angiotensin-converting enzyme inhibitors leads to regression of microalbuminuria and delays the progression to clinical albuminuria (> 300 mg/24 hr) and/or end-stage renal failure. These effects are seen in normotensive as well as hypertensive type 1 diabetic patients vvith microalbuminuria.ACE inhibitor therapy in type 1 diabetic patients with clinical albuminuria and an elevated serum creatinine leads to a 48-50% reduction in the risk of doubling of serum creatinine or progression to end-stage renal disease*66\357\8*

WHAT DOES TOO MUCH INSULIN MEAN?

Assume you eat a carbohydrate-rich meal, perhaps a simple one of two slices of pizza and a bottle of cola. If you’re a normal person, four or five hours will pass before you become hungry again. If you’re a carbohydrate addict, however, you might feel hungry only two hours later—with a craving for more sweets or starchy foods (because of the excess insulin released into the bloodstream). Some carbohydrate addicts report that they feel hungry immediately after eating carbohydrates. They never feel satisfied.
Carbohydrate addicts recognize the desire to eat isn’t logical, because they know they’re not really hungry in the sense of requiring nourishment. But the drive to eat is hard to deny. You may find yourself eating out of habit, almost unconsciously satisfying a compulsion. You may snack, realizing to your surprise that you are eating out of boredom or to relieve stress. Simple fatigue may provoke hunger, too. Sometimes the desire to eat can be overwhelming, virtually compelling you to satisfy it. Sometimes you may be unable to identify any apparent cause.
Many carbohydrate addicts report that their cravings grow stronger each time they eat carbohydrates. In short order, they find themselves in a continuous cycle of eating, craving, and eating again.
For carbohydrate addicts, consuming carbohydrate-rich foods produces a compulsion to eat. At first the consumption of high-carbohydrate snacks or meals produces a feeling of pleasure or satisfaction. Shortly, however, pleasure is followed by an anxious sensation, perhaps a feeling of weakness. Hunger, tiredness, and a desire to snack often follow.
Unfortunately, the problem doesn’t end there. In the presence of the excess insulin, the body also becomes very good at conserving energy. So while the carbohydrate addict gets hungrier with each carbohydrate-rich meal, the body gets better at storing energy—in the form of fat.
When we talk to our professional colleagues, we use terminology such as “mesolimbic dopamine system” and “decreased cellular insulin receptors.” Yet the bottom line can be stated quite simply: In carbohydrate addiction, the carbohydrate-insulin/carbohydrate-serotonin connection has gone awry.
While other research scientists have reported this phenomenon, we were the first to recognize how the mechanism could be “corrected,” and the experience of hunger cravings and fat storage could be minimized. We acted on these discoveries and created the Carbohydrate Addict’s Diet.
In the past, diet experts have failed to treat the problem—whether they knew it by these names or others—by reducing the total daily intake of carbohydrates and distributing carbohydrates equally to all meals. We know that these strategies don’t work for carbohydrate addicts.
Between 95 and 98 percent of the people on standard weight-loss diets regain all lost weight within one year. Until now, no one has found any alternative to these nearly sure-to-fail treatments. Through our research we discovered that it isn’t only the amount of carbohydrates eaten that matters—it is also how frequently they are eaten. Frequency governs, in large measure, the hunger response for millions of people. Personally and professionally, we discovered that any weight-loss diet that prescribes three or more small meals each day containing anything more than minor amounts of carbohydrates will ultimately fail with the carbohydrate addict. Such a diet will trigger the insulin response and signal the carbohydrate addict to eat once again.
In general, we direct our dieters to eat two low-carbohydrate meals each day and to confine their carbohydrate-rich foods to one, daily sixty-minute sitting that makes up the third meal. In this way, the fundamental mechanism causing excessive hunger, recurring cravings, and weight gain is corrected. Insulin release is dramatically reduced. The carbohydrate addict feels satisfied—and stays satisfied for many hours. Weight drops off naturally, fat deposits decrease, and the addictive cycle is broken.
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WHAT DOES TOO MUCH INSULIN MEAN?Assume you eat a carbohydrate-rich meal, perhaps a simple one of two slices of pizza and a bottle of cola. If you’re a normal person, four or five hours will pass before you become hungry again. If you’re a carbohydrate addict, however, you might feel hungry only two hours later—with a craving for more sweets or starchy foods (because of the excess insulin released into the bloodstream). Some carbohydrate addicts report that they feel hungry immediately after eating carbohydrates. They never feel satisfied.Carbohydrate addicts recognize the desire to eat isn’t logical, because they know they’re not really hungry in the sense of requiring nourishment. But the drive to eat is hard to deny. You may find yourself eating out of habit, almost unconsciously satisfying a compulsion. You may snack, realizing to your surprise that you are eating out of boredom or to relieve stress. Simple fatigue may provoke hunger, too. Sometimes the desire to eat can be overwhelming, virtually compelling you to satisfy it. Sometimes you may be unable to identify any apparent cause.Many carbohydrate addicts report that their cravings grow stronger each time they eat carbohydrates. In short order, they find themselves in a continuous cycle of eating, craving, and eating again.For carbohydrate addicts, consuming carbohydrate-rich foods produces a compulsion to eat. At first the consumption of high-carbohydrate snacks or meals produces a feeling of pleasure or satisfaction. Shortly, however, pleasure is followed by an anxious sensation, perhaps a feeling of weakness. Hunger, tiredness, and a desire to snack often follow.Unfortunately, the problem doesn’t end there. In the presence of the excess insulin, the body also becomes very good at conserving energy. So while the carbohydrate addict gets hungrier with each carbohydrate-rich meal, the body gets better at storing energy—in the form of fat.When we talk to our professional colleagues, we use terminology such as “mesolimbic dopamine system” and “decreased cellular insulin receptors.” Yet the bottom line can be stated quite simply: In carbohydrate addiction, the carbohydrate-insulin/carbohydrate-serotonin connection has gone awry.While other research scientists have reported this phenomenon, we were the first to recognize how the mechanism could be “corrected,” and the experience of hunger cravings and fat storage could be minimized. We acted on these discoveries and created the Carbohydrate Addict’s Diet.In the past, diet experts have failed to treat the problem—whether they knew it by these names or others—by reducing the total daily intake of carbohydrates and distributing carbohydrates equally to all meals. We know that these strategies don’t work for carbohydrate addicts.Between 95 and 98 percent of the people on standard weight-loss diets regain all lost weight within one year. Until now, no one has found any alternative to these nearly sure-to-fail treatments. Through our research we discovered that it isn’t only the amount of carbohydrates eaten that matters—it is also how frequently they are eaten. Frequency governs, in large measure, the hunger response for millions of people. Personally and professionally, we discovered that any weight-loss diet that prescribes three or more small meals each day containing anything more than minor amounts of carbohydrates will ultimately fail with the carbohydrate addict. Such a diet will trigger the insulin response and signal the carbohydrate addict to eat once again.In general, we direct our dieters to eat two low-carbohydrate meals each day and to confine their carbohydrate-rich foods to one, daily sixty-minute sitting that makes up the third meal. In this way, the fundamental mechanism causing excessive hunger, recurring cravings, and weight gain is corrected. Insulin release is dramatically reduced. The carbohydrate addict feels satisfied—and stays satisfied for many hours. Weight drops off naturally, fat deposits decrease, and the addictive cycle is broken.*5\236\2*

THE G.I. FACTOR: WITH A WAVE OF THE FAT WAND…

The other undesirable aspect of the modern diet is its high fat content Food manufacturers, bakers and chefs know we love to eat fat. We love its creaminess and mouth feel and find it easy to consume in excess. It makes our meat more tender, our vegetables and salads more palatable and our sweet foods even more desirable. We prefer potatoes as French fries or potato crisps, to have our fish battered and fried and our pastas in rich creamy sauces. With a wave of the fat wand, bland high carbohydrate foods like rice and oats are magically transformed into very palatable, kilojoule-laden foods such as fried rice and toasted muesli. In fact, when you analyse it, much of our diet today is an undesirable but delicious combination of both fat and quickly digested carbohydrate.

What’s wrong with our way of eating?

? The modern diet is too high in fat and therefore not high enough in carbohydrate.

? The carbohydrate we eat is digested and absorbed too quickly because most modern starchy foods have a high G.I. factor.

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DIABETES: UNDERSTANDING OF COMPLICATIONS’ RISK

What are the late complications of diabetes?

Late complications may occur many years after diagnosis of diabetes. They are most worrying because they may result from damage to vital organs of the body such as eyes, kidneys, heart, blood circulation or the nervous system. On the other hand, these complications are often treatable and early detection may help to prevent their harmful effect.

How can complications develop?

They may develop in a number of ways:

1.     By weakening and blockage of small blood vessels that supply blood to the organs of the body. This is called ‘microvascular disease’ and can lead to impaired vision if they affect the eyes or reduce kidney function if they affect the kidneys.

2.     By thickening the wall of large arteries that supply blood to large organs such as the heart or the feet. This is called ‘macrovascular disease’.

3.     By changes within the cells of the body. This can lead to the ways that the body’s nervous system functions. This is called ‘neuropathy’. A similar process within the lens of the eye can cause clouding of the lens called a cataract.

Why do complications develop?

We do not always understand why complications develop. There is no doubt that constant high levels of glucose in the blood over a period of time leading to poor diabetic control, is a major factor in increasing the risk of complications.

Some people seem more at risk than others through no fault of their own. Perhaps this is because there is an inherited risk for some people to develop the complications of diabetes.

Other factors that can increase the risk of complications include physical inactivity, smoking, becoming overweight, high blood pressure and inappropriate diet.

What is the risk of myself or my child developing complications?

We cannot answer this question. We can only estimate risk on the basis of statistics from groups of people who have had diabetes a long time. New treatment that is now available will have diminished that risk so that the statistics may not apply to people developing diabetes now. A prediction based on a statistical risk also cannot reliably apply to an individual person in predicting their future.

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