The more books one reads, the stupider one becomes.
—Mao Tse-Tung, Chinese communist dictator with a lifelong hatred of formal education, as quoted in “Modern Times” by Paul Johnson
Quote of the Day
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Paleo Diet for Heart Patients With Diabetes and Prediabetes
A Paleolithic diet lowered blood sugar levels better than a control diet in coronary heart disease patients with elevated blood sugars, according to Swedish researchers reporting in 2007.
About half of patients with coronary heart disease have abnormal glucose (blood sugar) metabolism. Lindeberg and associates wondered if a Paleolithic diet (aka “Old Stone Age,” “caveman,” or ancestral human diet) would lead to improved blood sugar levels in heart patients, compared to healthy, Mediterranean-style, Western diet.
Methodology
Investigators at the University of Lund found enrolled 38 male heart patients—average age 61—patients and randomized them to either a paleo diet or a “consensus” (Mediterranean-like) diet to be followed for 12 weeks. Average weight was 94 kg. Nine participants dropped out before completing the study, so results are based on 29 participants. All subjects had either prediabetes or type 2 diabetes (the majority) but none were taking medications to lower blood sugar. Baseline hemoglobin A1c’s were around 4.8%. Average fasting blood sugar was 125 mg/dl (6.9 mmol/l); average sugar two hours after 75 g of oral glucose was 160 mg/dl (8.9 mmol/l).
The paleo diet was based on lean meat, fish, fruits, leafy and cruciferous vegetables, root vegetables (potatoes limited to two or fewer medium-sized per day), eggs, and nuts (no grains, rice, dairy products, salt, or refined fats and sugar).
The Mediterranean-like diet focused on low-fat dairy, whole grains, vegetables, fruits, potatoes, fatty fish, oils and margarines rich in monounsaturated fatty acids and alpha-linolenic acid.
Both groups were allowed up to one glass of wine daily.
No effort was made to restrict total caloric intake with a goal of weight loss.
Results
Absolute carbohydrate consumption was 43% lower in the paleo group (134 g versus 231 g), and 23% lower in terms of total calorie consumption (40% versus 52%). Glycemic load was 47% lower in the paleo group (65 versus 122), mostly reflecting lack of cereal grains.
The paleo group ate significantly more nuts, fruit, and vegetables. The Mediterranean group ate significantly more cereal grains,oil, margarine, and dairy products.
Glucose control improved by 26% in the paleo group compared to 7% in the consensus group. The improvement was statisically significant only in the paleo group. The researchers believe the improvement was independent of energy consumption, glycemic load, and dietary carb/protein/fat percentages.
High fruit consumption inthe paleo group (493 g versus 252 g daily) didn’t seem to impair glucose tolerance.
Hemoglobin A1c’s did not change or differ significantly between the groups.
Neither group showed a change in insulin sensitivity (HOMA-IR method).
Comments
The authors’ bottom line:
In conclusion, we found marked improvement of glucose tolerance in ischemic heart disease patients with increased blood glucose or diabetes after advice to follow a Palaeolithic [sic] diet compared with a healthy Western diet. The larger improvement of glucose tolerance in the Palaeolithic group was independent of energy intake and macronutrient composition, which suggests that avoiding Western foods is more important than counting calories, fat, carbohydrate or protein. The study adds to the notion that healthy diets based on whole-grain cereals and low-fat dairy products are only the second best choice in the prevention and treatment of type 2 diabetes.
This was a small study; I consider it a promising pilot. Results apply to men only, and perhaps only to Swedish men. I have no reason to think they wouldn’t apply to women, too. Who knows about other ethnic groups?
This study and the one I mention below are the only two studies I’ve seen that look at the paleo diet as applied to human diabetics. If you know of others, please mention in the Comments section.
The higher fruit consumption of the paleo group didn’t adversely affect glucose control, which is surprising. Fruit is supposed to raise blood sugar. At 493 grams a day, men in the paleo group ate almost seven times the average fruit intake of Swedish men (75 g/day). Perhaps lack of adverse effect on glucose control here reflects that these diabetics and prediabetics were mild cases early in the course of the condition—diabetes tends to worsen over time.
Present day paleo and low-carb advocates share a degree of simpatico, mostly because of carbohydrate restriction—at least to some degree—by paleo dieters. Both groups favor natural, relatively unprocessed foods. Note that the average American eats 250-300 g of carbohydrates a day. Total carb intake in the paleo group was 134 g (40% of calories) versus 231 g (55% of calories) in the Mediterranean-style diet. Other versions of the paleo diet will yield different numbers, as will individual choices for various fruits and vegetables. Forty percent of total energy consumption from carbs barely qualifies as low-carb.
Study participants were mild, diet-controlled diabetics or prediabetics, not representative of the overall diabetic population, most of whom take drugs for it and have much higher hemoglobin A1c’s.
Lindeberg and associates in 2009 published results of a paleo diet versus standard diabetic diet trial in 13 diabetics. Although a small trial (13 subjects, crossover design), it suggested advantages to the paleo diet in terms of heart disease risk factors and improved hemoglobin A1c. Most participants were on glucose lowering drugs; none were on insulin. Glucose levels were under fairly good control at the outset. Compared to the standard diabetic diet, the Paleo diet yielded lower hemoglobin A1c’s (0.4% lower—absolute difference), lower trigylcerides, lower diastolic blood pressure, lower weight, lower body mass index, lower waist circumference, lower total energy (caloric) intake, and higher HDL cholesterol. Glucose tolerance was the same for both diets. Fasting blood sugars tended to decrease more on the Paleo diet, but did not reach statistical significance (p=0.08).
The paleo diet shows promise as a treatment or preventative for prediabetes and type 2 diabetes. Only time will tell if it’s better than a low-carb Mediterranean diet or other low-carb diets.
Reference: Lindeberg, S., Jönsson, T., Granfeldt, Y., Borgstrand, E., Soffman, J., Sjöström, K., & Ahrén, B. (2007). A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease Diabetologia, 50 (9), 1795-1807 DOI: 10.1007/s00125-007-0716-y
Heart and Stroke Patients: Avoid Weight-Loss Drug Sibutramine (Meridia)
The weight-loss drug sibutramine (Meridia) should be withdrawn from the U.S. market, suggests an editorialist in the September 2, 2010, New England Journal of Medicine. Based on a clinical study in the same issue, it’s more accurate to conclude that sibutramine shouldn’t be prescribed for people who aren’t supposed to be taking it in the first place.
Sibutramine is sold in the U.S. as Meridia and has been available since 1997. Judging from the patients I run across, it’s not a very popular drug. Why not? It’s expensive and most people don’t lose much weight.
The recent multi-continent SCOUT trial enrolled 9,800 male and female study subjects at least 55 years old (average age 63) who had either:
- 1) History of cardiovascular disease (here defined as coronary artery disease, stroke, or peripheral artery disease)
- 2) Type 2 diabetes plus one or more of the following: high blood pressure, adverse cholesterol levels, current smoking, or diabetic kidney disease.
- Or both of the above (which ended up being 60% of the study population)`.
Here’s a problem from the get-go (“git-go” if you’re from southern U.S.). For years, Meridia’s manufacturer and the U.S. Food and Drug Administration have told doctors they shouldn’t use the drug in patients with history of cardiovascular disease. It’s not the scary “black box warning,” but it’s clearly in the package insert of full prescribing information.
Half the subjects were randomized to sibutramine 10 mg/day and the other half to placebo. All were instructed in diet and exercise aiming for a 600 calorie per day energy deficit. They should lose about a pound a week if they followed the program. Average follow-up was 3.4 years.
What Did the Researchers Find?
Forty percent of both drug and placebo users dropped out of the study, a very high rate.
As measured at one year, the sibutramine-users averaged a weight loss of 9.5 pounds (4.3 kg), the majority of which was in the first 6 weeks. After the first year, they tended to regain a little weight, but kept most of it off.
Death rates were the same for sibutramine and placebo.
Sibutramine users with a history of cardiovascular disease had a 16% increase in non-fatal heart attack and stroke compared to placebo. To “cause” one heart attack or stroke in a person with known cardiovascular disease, you would have to treat 52 such patients.
Folks in the “diabetes plus risk factor(s)” group who took sibutramine had no increased risk of heart attack or stroke.
So What?
Average weight loss with sibutramine isn’t much. Nothing new there. [Your mileage may vary.]
People with cardiovascular disease shouldn’t take sibutramine. Nothing new there either.
Reference: James, W. Philip, et al. Effect of sibutramine on cardiovascular outcomes in overweight and obese subjects. New England Journal of Medicine, 363 (2010): 905-917.
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Filed under coronary heart disease, Drugs for Diabetes, Overweight and Obesity, Stroke, Weight Loss
Quote of the Day
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
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
Diabetic Mediterranean Diet 