Health care insurance doesn’t mean access to medical care any more than car insurance means you have access to a car.
–WhiteCoat’s Call Room, October 6, 2010
Quote of the Day
Filed under Quote of the Day
Diabetes and Shortened Lifespan: “How Bad Is It, Doc?”
Diabetes mellitus for years has been linked with cardiovascular disease such as heart failure and coronary heart disease (blocked arteries in the heart, and the leading cause of death in the Western world). How scared should diabetics be?
An article in the Archives of Internal Medicine gives us one answer.
Researchers from the Netherlands and Harvard examined medical records of 5,209 people (mostly white, 64% men) enrolled in the Framingham (Massachusetts, USA) Heart Study. This cohort has been examined every other year for more than 46 years.
Study subjects who had diabetes at age 50 were identified; health outcomes going forward were then analyzed, with particular attention to lifespan and cardiovascular disease. “Cardiovascular disease” in this context means coronary heart disease, stroke, congestive heart failure, intermittent claudication (leg pain during exertion caused by blocked arteries), and transient ischemic attack (stroke-like symptoms that resolve within 24 hours).
Results
Compared to those in the cohort free of diabetes, having diabetes at age 50 more than doubled the risk of developing cardiovascular disease for both women and men.
Compared to those without diabetes, having both cardiovascular disease and diabetes approximately doubled the risk of dying, regardless of sex.
Compared to those without diabetes, women and men with diabetes at age 50 died 7 or 8 years earlier, on average.
[Specific causes of death were not reported.]
Take-Home Points
We’d likely see longer lifespans and less cardiovascular disease if we could prevent diabetes in the first place. How do we do that? Strategies include regular physical activity, avoidance or reversal of overweight and obesity, and low-glycemic-index diets.
The Mediterranean diet it linked to reduced heart attacks and strokes, and longer lifespan. That’s why I’ve been working for the last year and a half to adapt it for diabetics.
We have better treatments for cardiovascular disease and diabetes and these days, so the death rates and illness numbers shouldn’t be quite so alarming. Up-to-date management of diabetes and cardiovascular disease will prevent some acute disease events—such as heart attacks and strokes—and prolong life.
References:
Franco, O., Steyerberg, E., Hu, F., Mackenbach, J., & Nusselder, W. (2007). Associations of Diabetes Mellitus With Total Life Expectancy and Life Expectancy With and Without Cardiovascular Disease Archives of Internal Medicine, 167 (11), 1145-1151 DOI: 10.1001/archinte.167.11.1145
Knowler, W.C., et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. New England Journal of Medicine, 346 (2002): 393-403.
Tuomilehto, J., et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. New England Journal of Medicine, 344 (2001): 1,343-1,350.
Filed under coronary heart disease, Diabetes Complications, Stroke
Rosiglitazone Severely Restricted by FDA
MedPageToday reported yesterday on the U.S. Food & Drug Administration’s ruling that the diabetes drug rosiglitazone should be used in new patients only if blood sugars are not controlled with other diabetes drugs, such as pioglitazone.
It sounds as if new users and their doctors may have to jump through some paperwork hoops to get the drug, which is more reason not to prescribe it.
The problem is that scientific studies suggest that rosiglitazone increases the risk of heart attack, heart failure, and death.
Filed under Diabetes Complications, Drugs for Diabetes
Myth Busted: Alzheimer Dementia NOT Caused By Diabetes
Contrary to popular belief among the experts, type 2 diabetes is not one of the causes of Alzeimer dementia. They may indeed be associated with each other, but that’s not causation.
Brain CT scan
Dr. Emily Deans (psychiatrist) has been considering this issue recently at her Evolutionary Psychiatry blog.
The brains of Alzheimer patients, under a microscope, are characterized by many senile plaques (aka neuritic plaques) and neurofibrillary tangles. That’s the gold standard for diagnosis. Nevertheless, brain biopsies are rarely done to diagnose Alzheimer disease in living patients, and even autopsies after death are rare. The diagnosis usually is clinical, based on ruling out other illnesses, etc.
Nearly all the studies associating diabetes with Alzheimers disease (and other dementias) are observational or epidimiologic. [The exception is the Honolulu-Asia Aging Study.] Establishing an association is helpful in generating theories, but establishing causation is the goal. At least five studies confirm an association.
Neurology this year reported findings of Japanese researchers who examined the brains of 135 people who died between 1998 and 2003. They lived in Hisayama, a town with an incredibly high autopsy rate of 74%. These people before death had undergone an oral glucose tolerance test. Their insulin resistance was calculated on the basis of fasting glucose and fasting insulin (HOMA-IR). None of them showed signs of dementia at the time of study enrollment in 1988.
What Did They Find?
Twenty-one of the 135 subjects developed Alzheimer-type dementia. The investigators don’t say if the diagnosis was based on the brain examination, or just a clinical diagnosis without a brain biopsy. How this got beyond the article reviewers is beyond me. [If I’m missing something, let me know in the comments section below.] It must be a clinical diagnosis because if you don’t act demented, it doesn’t matter how many senile plaques and neurofibrillary tangles you have in your brain.
Senile plaques, but not neurofibrillary tangles, were more common in those with higher levels of blood sugar (as measured two hours after the 75 g oral glucose dose), higher fasting insulin, and higher insulin resistance. People with the APOE epsilon-4 gene were at even higher risk for developing senile plaques.
The researchers did not report whether the subjects in this study had been previously during life with diabetes or not. One can only hope those data will be published in another paper. Why make us wait?
Average fasting glucose of all subjects was 106 mg/dl (5.9 mmol/l); average two-hour glucose after the oral glucose load was 149 mg/dl (8.3 mmol/l). By American Association of Clinical Endocrinologists criteria, these are prediabetic levels. Mysteriously, the authors fail to mention or discuss this. [I don’t know if AACE criteria apply to Japanese.] Some of these Japanese subjects probably had diabetes, some had prediabetes, others had normal glucose and insulin metabolism.
As with all good research papers, the authors compare their findings with similar published studies. They found one autopsy study that tended to agree with their findings (Honolulu) and three others that don’t (see references below). In fact, one of the three indicated that diabetes seems to protect against the abnormal brain tissue characteristic of Alzheimer disease.
Botton Line
Type 2 diabetes doesn’t seem to be a cause of Alzheimer disease, if autopsy findings and clinical features are the diagnostic criteria for the disease.
If we assume that type 2 diabetics have higher than normal blood sugar levels and higher insulin levels for several years, then hyperglycemia and hyperinsulinemia don’t cause or contribute to Alzheimer dementia. Myth busted. [I hope that’s not copyrighted by the “Myth Busters” TV show.]
Type 2 diabetes is, however, linked with impaired cognitive performance, at least according to many of the scientific articles I read in preparation for this post. So type 2 diabetics aren’t in the clear yet. It’s entirely possible that high blood sugar and /or insulin levels cause or contribute to that. [Any volunteers to do the literature review? Best search term may be “mild cognitive impairment.”]
Type 2 diabetes is associated with Alzheimer disease, but we have no proof that diabetes is a cause of Alzheimers. Nor do we have evidence that high blood sugar and insulin levels cause Alzheimer disease.
Alzheimer disease is a major scourge on our society. I’d love to think that carbohydrate-restricted eating would help keep blood sugar and insulin levels lower and thereby lessen the devastation of the disease. Maybe it does, but I’d like to see more convincing evidence. It’ll be years before we have a definitive answer.
References:
Matsuzaki T, Sasaki K, Tanizaki Y, Hata J, Fujimi K, Matsui Y, Sekita A, Suzuki SO, Kanba S, Kiyohara Y, & Iwaki T (2010). Insulin resistance is associated with the pathology of Alzheimer disease: the Hisayama study. Neurology, 75 (9), 764-70 PMID: 20739649
Heitner, J., et al. “Diabetics do not have increased Alzheimer-type pathology compared with age-matched control subjects: a retrospective postmortem immunocytochemical and histofluorescent study.” Neurology, 49 (1997): 1306-1311. Autopsy study, No. of subjects not in abstract. They looked for senile plaques and neurofibrillary tangles, etc. The title says it all.
Beeri, M.S., et al. “Type 2 diabetes is NEGATIVELY [emphasis added] associated with Alzheimer’s disease neuropathology.” J. Gerontol A. Biol Sci. Med. Sci. 60 (2005): 471-475. 385 autopsies. The title again says it all.
Arvanitakis, Z., et al. “Diabetes is related to cerebral infarction but NOT [emphasis added] to Alzheimers disease pathology in older persons.” Neurology, 67 (2006): 1960-1965. Autopsy study of 233 Catholic clergy, about 50:50 women:men.
Filed under Carbohydrate, Diabetes Complications
Do We Really Need to Cut Salt?
Dr. Paul Maher just finished a two-part series on dietary salt that is well worth a read, especially if you are convinced we need to cut our consumption.
Polititians and public health mandarins have been on the low-salt bandwagon again for the last couple years. Some researchers question whether it’s even possible to reduce salt consumption as low as they would have us.
I’ll consider the polititians’ opinions on my salt intake as soon as they produce reasonable wait times at the post office, reasonable service times at the Department of Motor Vehicles, improve public school student achievement scores to a respectable level, balance state and federal budgets, and drastically reduce corruption in their hallowed halls.
Filed under coronary heart disease, Stroke
Drug Review: Insulin
Insulin is life-saving for type 1 diabetics. Many type 2 diabetics will eventually, if not at the outset, need to take insulin for adequate control of blood sugars, which should help prevent diabetes complications.
My comments here are simply a brief review of insulins used by type 2 diabetics. Anyone taking insulin must work closely with a physician or diabetes nurse educator on proper dosing, injection technique, and recognition and management of hypoglycemia (low blood sugar).
This is NOT an insulin rig! Modern insulin injections barely hurt, if at all.
Insulin is made by the pancreas to keep blood sugars from rising above a fairly strict range: 70-140 mg/dl or 3.89-7.78 mmol/l. [It has many other actions that I won’t bother to outline here.] When we eat a meal containing carbohydrates (and proteins to a lesser extent), blood sugar starts to rise as we digest the carbs. Insulin drives the sugar into our body’s cells for use as immediate energy or conversion to fat as stored energy. About half of the insulin produced by a healthy body is “basal,” meaning it’s secreted into the bloodstream in a steady, low-volume amount, to keep the liver from making too much sugar (glucose) and controlling fasting sugar levels. The other half is secreted in to the bloodstream in response to meals.
In type 2 diabetes, the body’s tissues, at first, are resistant to the effect of insulin. So the pancreas has to secrete more than usual (hyperinsulinism). As the illness progresses, the pancreas cannot keep up with demand for more insulin and starts to “burn out,” producing less insulin. This is when many type 2 diabetics need to start insulin injections. [These are generalities; there are exceptions.]
Types of Insulin
Specific names of insulins vary by manufacturer and by country. By convention, I capitalize only the brand names below, plus NPH and NPL.
We could break them down into two types: human (identical in structure to human insulin) and analogs (minor molecular modifications to the usual human insulin molecule). But most people don’t care about that. It’s more helpful to distinguish them by the timing of their action:
- Rapid acting: lispro (e.g., Humalog), aspart (e.g., Novolog), glulisine (e.g., Apidra)
- Short acting: regular (e.g., Novolin R, Humulin R)
- Intermediate to long acting: NPH, glargine (e.g., Lantus), detemir (e.g., Levemir), degludec (e.g., Tresiba), NPL (neutral protamine lispro)
Rapid-acting insulins have onset of action between 5 and 15 minutes, peak effect in 30 to 90 minutes, and duration of action of 2 to 4 hours.
Short-acting “regular insulin” has onset in 30 minutes, peaks in 2 to 4 hours, and works for 5 to 8 hours.
Intermediate to long-acting insulins start working in 2 hours, don’t have a well-defined peak of action, and may keep working for 20 or more hours (glargine), for 6 to 24 hours (detemir), or 30 to 42 hours (degludec).
All these times are gross approximations. Once the insulin is injected into the fat below the skin, it has to be absorbed into the bloodstream and transported to the tissues where it does its magic. Lots of factors affect this process. For instance, the thicker the fat tissue at the injection site, the slower the absorption. Absorption tends to be faster from the abdominal wall, slower from the arms, even slower from the thighs or buttocks. Absorption can vary from day to day in an individual even when injection site and technique are identical.
As you might have guessed, the short- and rapid-acting insulins are usually injected before a meal in anticipation of blood sugar rising as food is digested. The intermediate- and long-acting insulins imitate the healthy body’s “basal” insulin.
Manufacturers also supply premixed insulins, combining intermdiate or long-acting insulin with a short- or rapid-acting insulin. Examples are Humalog 75/25, Humulin 70/30, and Novolog 70/30.
Dose and Selection of Insulin
See your physician or diabetes nurse educator for details. Many type 2 diabetics get started just with an intermediate or long-acting insulin once or twice daily, with or without diabetes drugs by mouth. Nearly all type 1’s will need a long-acting “basal” insulin (one-third to one-half of their total daily insulin requirement, plus meal-time “bolus” dosing with a rapid-acting insulin. Insulin pumps are a topic for another day.
Side Effects
By far the most common and worrisome is hypoglycemia.
Last update: August 1, 2016
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Filed under Drugs for Diabetes
Rosiglitazone On the Ropes
A week ago, MedPageToday reported that a British advisory commission recommended the diabetes drug rosiglitazone (Avandia) be withdrawn from the market.
On July 6, I wrote about evidence that rosiglitazone users seem to incur a higher risk of stroke, heart failure, and death.
If I were taking Avandia, I’d be asking my doctor about alternatives.
Filed under Drugs for Diabetes
Had a Stroke? Statin Drug May Prevent Next One
When taken by properly selected patients, statin drugs prevent strokes. The American Heart Association’s published stroke treatment guidelines specify which stroke patients benefit from ongoing statin usage. Find the details at my last Self/NutritionData Heart Health Blog post.
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Filed under Uncategorized
Chocolate Fights Heart Failure
My recent post at the Self/NutritionData Heart Health Blog outlines late-breaking evidence that chocolate seems to reduce both deaths and hospitalizations from heart failure among women.
You’ll also find my thoughts on milk versus dark chocolate and the healthy “dose.”
Filed under Diabetes Complications
Mediterranean Diet Lowers Risk of Breast Cancer
A study in the current issue of the American Journal of Clinical Nutrition associates the Mediterranean diet with lower risk of breast cancer in postmenopausal women.
The data derive from the Greek portion of the massive EPIC study: European Prospective Investigation Into Cancer and nutrition. Investigators followed almost 15,000 women for 10 years. No protective effect was seen for premenopausal women eating Mediterranean-style. The study at hand adds to prior evidence that the Mediterranean diet seems to protect against cancer of the breast, prostate, uterus, and colon/rectum.
Reference: Trichopoulou, Antonia, et al. Conformity to traditional Mediterranean diet and breast cancer risk in the Greek EPIC (European Prospective Investigation into Cancer and nutrition) cohort. American Journal of Clinical Nutrition, published July 14, 2010. doi: 10.3945/ajcn.2010.29619
Filed under cancer, Health Benefits, Mediterranean Diet
Diabetic Mediterranean Diet 