The Internet is abuzz with the latest results from a couple of those massive trials that physicians who practice "evidence-based medicine" require before they'll believe in any treatment.
Although I understand why such studies are needed, I hate them, because they're studying a huge, diverse population of patients who may differ a lot in their baseline characteristics, even though the mean is usually all you can see.
Unless the outcome is black and white, for example, 100% of the patients who took the new drug dropped dead within 2 weeks, you need statistics to evaluate the study. Quite often, individual patients may be harmed or helped, but the published conclusion refers only to the average impact, as I noted here. Then physicians apply these average results to everyone.
A good example of this is the blood glucose (BG) arm of the ACCORD study, which was stopped early a couple of years ago because it appeared that the patients who used intensive treatment with a lot of drugs and lowered their A1cs to a mean of 6.5% had higher mortality than those who used standard treatment and had A1cs of about 7.3%.
This was despite the fact that patients in both groups had mortality rates lower than those of most people with diabetes.
In fact, the patients in the ACCORD study were older, had had type 2 for at least 10 years, had other risk factors for heart disease, and started with mean A1cs of 8.3. This means they had probably had poor control for years. Yet doctors are applying the conclusions to everyone.
Many patients are now reporting that their doctors tell them that their excellent A1c levels in the 5s are too low and they should increase them until they're over 7!
Furthermore, like most patients, the ACCORD patients were told to follow an ADA-type diet with less than 30% total fat and less than 10% saturated fat. This means they undoubtedly increased their consumption of carbohydrates, most likely the kind most Americans eat: potatoes, rice, white bread, processed fat-free foods. Yet a recent meta-analysis showed that there is no significant evidence to conclude that saturated fat causes heart disease. Some studies showed an increase when saturated fat was reduced, and others showed an increase. This averaged out to no effect.
The authors suggested that it might depend on what you substitute for the saturated fat, as studies with substitution of unsaturated fat tended to reduce heart disease and mortality and studies with substitution of carbohydrate tended to increase it, although no studies have been done that would actually prove this.
Yet replacing saturated fat with carbohydrate is undoubtedly what people in ACCORD were told to do, and those in the intensive treatment arm of the study got more intensive nutritional counseling and hence probably ate more carbohydrate.
Now the other two arms of the ACCORD study have been published. The blood pressure arm showed that reducing the systolic blood pressure below 120 resulted in no better cardiovascular outcomes than using fewer drugs to keep the systolic blood pressure below 140. The lower blood pressures did result in fewer strokes.
This is the same patient population as the BG arm of the study, and the same caveats apply: longstanding diabetes in an elderly population with coexisting medical problems (34% had already had a cardiovascular event), relatively high starting A1cs and fasting BG levels over 170, and multiple blood pressure drugs given to reach the goal. Also, twice as many of the intensively treated patients gained more than 10 kg during the study.
The final arm of the study was designed to see whether adding a fibrate drug to the treatment of patients already taking a statin would reduce cardiovascular events. The fibrates (they used fenofibrate) reduce triglycerides and increase HDL levels.
Again, they found no significant effect but a suggestion that the drug might help in patients who began with triglyceride levels over 204 and HDL levels under 34. Men appeared to do better and women appeared to do worse on the fibrate. Such studies can show differences that appear to be real but aren't statistically significant.
Again: same population and same caveats.
Another study, the NAVIGATOR study, was reported at the same time. This study started with patients who had prediabetes, with mean A1cs of 5.8 and also either preexisting heart disease or cardiovascular risk factors. They tested whether using valsartan (Diovan), an angiotensin-receptor inhibitor that lowers blood pressure, would reduce progression from prediabetes to diabetes. Similar drugs had been shown in the past to do so.
Again, all the patients were given "lifestyle modification" advice, although the papers don't specify exactly what that was other than the usual ADA line of reducing total and saturated fat and increasing exercise. You have to go to an Appendix, which most people won't read, and then to a reference to a Finnish study they cite to see what type of dietary advice was given.
It turns out to be the usual low fat with "lots of whole grains, fruits and vegetable." Many Americans told to eat lots of whole grains are apt to eat whole-wheat bread (which isn't whole grain) and to drink more orange juice and eat more apples and bananas, and maybe more peas and corn. Very few will up their intake of kale and broccoli and other low-carb veggies.
It turned out that the low-fat high-carb diet plus increased exercise plus the drug reduced the progression to type 2 diabetes from 36.8% to 33.1%, which they calculate is a 13% reduction in the "absolute hazard difference using an exponential model," but a pretty small absolute reduction. It didn't affect the rate of cardiovascular events.
The second arm of the NAVIGATOR trial involved the same patient population and the drug nateglinide (Starlix), which is a sulfonylurea-type drug that increases insulin secretion by the beta cells but for a shorter period than the traditional sulfs.
The rationale was that high postprandial BG levels are said to lead to beta cell deterioration, and higher A1cs are associated with increased heart disease. They tested whether or not this drug would reduce progression from prediabetes to diabetes and whether it would affect cardiovascular events.
They found it did neither.
Do these studies mean there's no point in trying to control our diabetes?
Not at all. What they really show is that you can't give people with longstanding diabetes or even a diabetic tendency and either preexisting heart disease or a lot of heart disease risk factors a low fat, and hence very high carbohydrate, diet, try to control the resulting high BG levels with a lot of drugs, and expect the heart disease to go away.
Furthermore, even though you tell people to eat lots of vegetables and whole grains, you know that in the general population, most of them -- if they modify their diet at all -- will eat high-glycemic foods, low-fat processed convenience foods, and sugary fruits. If they show the dietician that their fat consumption is down, the dietician will probably tell them they're doing great.
No one has tested whether or not trying to control diabetes with lower-carb diets and fewer drugs would reduce heart disease rates.
But I'm afraid that the results of these trials will make a lot of people simply throw up their hands and give up, figuring that heart attacks are inevitable, no matter what they do.
Even if the results from a lower-carb study showed fewer cardiovascular events, I'm afraid most Americans wouldn't make significant changes in their diets. An intelligent woman with type 2 once told me she had trouble eating just a couple of potato chips. I asked why she bought potato chips (she lived alone). She said, "Because I like potato chips."
Well, who doesn't. I also used to like blueberry pie (I probably wouldn't like it now, because it would seem overwhelmingly sweet with relatively little taste) and homemade bread slathered with butter and homemade jam. But I don't eat those things now.
What we need to learn to do is to become gourmets, seeking out foods with a lot of taste and not a lot of carbohydrate, like berries, or exotic fresh vegetables from a farmers market. This is a lot more fun and cheaper than paying $500 a month for a lot of pills to try to cover the damage from eating ho-hum potato chips and packaged snack cakes.
The intelligent people who read this blog will understand this. I worry about the other millions of people in the country who don't have access to good information. I worry about the overworked GPs who don't have time to slog through long statistical studies and try to figure out what an "absolute hazard difference using an exponential model" is.
Many of the details, like the actual dietary advice, in these papers are difficult, if not impossible, to find. If you make an effort to download the full study protocol of the ACCORD study, you find that patients were taught carb counting but it doesn't say how many carbs they were supposed to eat. They were taught self-monitoring of BG, and how to titrate their drugs according to the results. They were apparently not taught how to "titrate" their carb consumption according to the results.
And the authors are often sloppy. For example, sometimes they give both mean and median A1c. Sometimes they give only one. Sometimes they don't indicate which one they calculated.
I worry that the busy physicians will just read the headlines in medical magazines and the New York Times ("Diabetes Heart Treatments May Cause Harm") and conclude that they shouldn't try to treat diabetic patients with high blood pressure, high BG levels, or high lipid levels. Why bother, because they might be sued if they caused harm.
As studies become old, people who write about them tend to simplify, ignoring the many caveats that apply to the studies. For example, Gina Kolata wrote in the recent New York Times story, "It was discovered 2 years ago that rigorously controlling blood sugar did not prevent heart disease or deaths in people with type 2 diabetes." What that study actually showed was that "rigorously controlling blood sugar with a lot of drugs to cover a high-carb diet did not prevent heart disease or death in elderly patients with preexisting heart disease or at least two cardiovascular risk factors and long-standing poorly controlled diabetes."
But how many physicians have retained Kolata's interpretation? I suspect a lot. I've mentioned the many patients whose doctors told them that their diet-controlled A1cs of 5.6 were too low and they should try to get them up to 7!
I would agree that if someone had an A1c of 5.6 only because they were on 7 different expensive medications with a lot of potential side effects, it would make sense to stop several of the drugs and let the A1c go up a bit, especially if the patient was elderly with several other medical problems treated with even more drugs.
But if someone has an A1c of 4.8 because of strict diet control and a lot of exercise, and if that person doesn't go low (after all, nondiabetics don't go low when they have low A1cs), there's absolutely no reason to tell that person to increase the A1c.
Applying a "rule" for the wrong reasons is the type of faulty logic that has caused harm in a lot of diabetic patients. I know some who have been told by registered dieticians that they should put raisins in their oatmeal "to get the carb counts up."
The reason for the high-carb ADA diet is not to eat a lot of carbohydrate; it's to eat less fat. The idea is that when you eat more carbohydrate, you'll eat less fat. But adding carbohydrate to a meal instead of substituting carbohydrate for fat won't reach the ADA goals (which many people today don't agree with anyway). It will just add calories, increase insulin levels, and promote even more fat gain.
So will patients with type 2 diabetes soon be told to get their blood pressure up, not worry about lipid levels, and pay no attention to postprandial BG levels?
I certainly hope not.
The full texts of the New England Journal of Medicine articles cited are available free here.
Monday, March 15, 2010
Friday, March 5, 2010
Ancient Bacteria
It's generally agreed that low-grade chronic inflammation is related to metabolic syndrome, cardiovascular disease, and type 2 diabetes. But no one knows what causes this generalized inflammation.
Acute, localized inflammation is a good thing. It's what walls off an infection, "eats" the offending organism, and then digests it with the help of heavy-duty oxidants. Then, when things are working right, the body repairs the damage, and the cells that have been doing all this leave the scene.
Chronic inflammation, on the other hand, is not a good thing, and the more scientists can find out about it, the better.
Hence I was intrigued by a recent paper in Nature that proposed a totally new idea and confirmed an old idea. You can read a popularized description here, or a link to the original paper here.
When we are invaded by pathogens, the body mounts what is called the innate immune response. This is a nonspecific response triggered by certain chemicals on the surface of many organisms that are unique to them and are not found on our own cells. The body sends out cells called macrophages to engulf the offending organisms and sends chemical signals to recruit other cell types to help rid the body of the organisms and then repair any damage that occurred.
This response is more primitive than the adaptive immune response that uses antibodies and is more specific than the innate immune response.
Usually, the cause of the response is clear, as bacteria or viruses or other pathogens can be found in the blood. But sometimes people seem to have such a response when no pathogens can be found. This puzzled scientists for a long time.
But Carl Hauser and colleagues, the authors of the Nature paper, came up with a fascinating hypothesis. It is generally accepted that mitochondria, known as the "powerhouses of the cell" because they are where most of the cell's energy is produced, were originally bacteria that invaded the cells of other organisms and adapted to the benefit of both.
Mitochondria have their own DNA, which comes only from the mother.
Hauser and colleagues wondered if perhaps trauma that destroys cells could release mitochondria from the damaged cells into the bloodstream. Then, because the mitochondria are descended from bacteria, they might have surface molecules that our bodies would interpret as foreign, so we would mount an innate immune response, just as we do to other bacteria.
His researched suggested that this does indeed happen.
It explains why severe trauma patients sometimes get reactions that look like severe infections when no signs of infecting organisms can be found.
And I wonder if less severe chronic trauma could cause just enough of an innate immune response to trigger chronic disease. For example, we know that chronic gum disease can increase blood glucose levels, along with various signs if inflammation. Could this be because the gum disease is causing gum cells to break down and release mitochondria?
Could other hidden infections be doing the same? By reducing various chronic infections, could we reduce people's chance of getting type 2 diabetes?
I find this research exciting, not because it offers an immediate chance for a cure of type 2 diabetes, but because it's a new idea and I find new paradigm-shifting ideas much more fascinating than huge studies of drugs that rely on statistics to prove anything. Even then, although the statistics can show that the drug worked on average, it can never show whether or not it will help you in particular, as I discussed here.
Creative new ideas can suggest new research paths that may some day lead to real cures.
.
Acute, localized inflammation is a good thing. It's what walls off an infection, "eats" the offending organism, and then digests it with the help of heavy-duty oxidants. Then, when things are working right, the body repairs the damage, and the cells that have been doing all this leave the scene.
Chronic inflammation, on the other hand, is not a good thing, and the more scientists can find out about it, the better.
Hence I was intrigued by a recent paper in Nature that proposed a totally new idea and confirmed an old idea. You can read a popularized description here, or a link to the original paper here.
When we are invaded by pathogens, the body mounts what is called the innate immune response. This is a nonspecific response triggered by certain chemicals on the surface of many organisms that are unique to them and are not found on our own cells. The body sends out cells called macrophages to engulf the offending organisms and sends chemical signals to recruit other cell types to help rid the body of the organisms and then repair any damage that occurred.
This response is more primitive than the adaptive immune response that uses antibodies and is more specific than the innate immune response.
Usually, the cause of the response is clear, as bacteria or viruses or other pathogens can be found in the blood. But sometimes people seem to have such a response when no pathogens can be found. This puzzled scientists for a long time.
But Carl Hauser and colleagues, the authors of the Nature paper, came up with a fascinating hypothesis. It is generally accepted that mitochondria, known as the "powerhouses of the cell" because they are where most of the cell's energy is produced, were originally bacteria that invaded the cells of other organisms and adapted to the benefit of both.
Mitochondria have their own DNA, which comes only from the mother.
Hauser and colleagues wondered if perhaps trauma that destroys cells could release mitochondria from the damaged cells into the bloodstream. Then, because the mitochondria are descended from bacteria, they might have surface molecules that our bodies would interpret as foreign, so we would mount an innate immune response, just as we do to other bacteria.
His researched suggested that this does indeed happen.
It explains why severe trauma patients sometimes get reactions that look like severe infections when no signs of infecting organisms can be found.
And I wonder if less severe chronic trauma could cause just enough of an innate immune response to trigger chronic disease. For example, we know that chronic gum disease can increase blood glucose levels, along with various signs if inflammation. Could this be because the gum disease is causing gum cells to break down and release mitochondria?
Could other hidden infections be doing the same? By reducing various chronic infections, could we reduce people's chance of getting type 2 diabetes?
I find this research exciting, not because it offers an immediate chance for a cure of type 2 diabetes, but because it's a new idea and I find new paradigm-shifting ideas much more fascinating than huge studies of drugs that rely on statistics to prove anything. Even then, although the statistics can show that the drug worked on average, it can never show whether or not it will help you in particular, as I discussed here.
Creative new ideas can suggest new research paths that may some day lead to real cures.
.
Monday, March 1, 2010
Slow Progress
One thing that annoys me is how long it takes for new ideas and new research results to filter down to practitioners. At this rate I will have died of old age before they figure out a better way to treat type 2 diabetes.
When I was first diagnosed in 1996, because I had been a biology major and had done some research in biochemistry, I wanted to learn more about the science of type 2 diabetes.
I was puzzled because the nurse practitioner who diagnosed me told me to follow the American Diabetes Association (ADA) diet, which was chock-a-block full of carbohydrates. I knew that diabetes was caused by an inability to process carbohydrates. So why were they telling me to eat more of them? It made no sense.
So I went to the library. Remember libraries? They were places with books and preceded Internet searches and Google and all that. The library didn't have much of interest, so I searched the interlibrary loan catalogs and found and ordered a book called Insulin, edited by F. M. and S. J. H. Ashcroft. It was published in 1992, which means it was probably written around 1990, as the publishing process does take time.
The book was very interesting. A chapter author named Erol Cerasi said he and others had done a study of a large group of obese and nonobese subects both with and without diabetes and studied insulin resistance (IR) and insulin secretion.
They found that only beta-cell responsiveness could distinguish the diabetic from nondiabetic subjects. The IR could only distinguish obese from nonobese subjects.
In other words, if you're obese, you'll have IR, but you won't necessarily have diabetes. If you have diabetes, your beta cells won't secrete enough insulin, whether or not you're overweight.
They concluded that "the diabetic state is much more closely related to a failure of the secretion of insulin than to diminished efficiency of the circulating hormone level," that is, beta cell defects are more important than IR in causing type 2.
Another group did a similar study and found that those who progressed from prediabetes to diabetes had decreased insulin responses to glucose at the beginning of the study.
Yet people with type 2 diabetes continued to be told that their obesity had caused IR and the IR had caused the diabetes.
Recently, 23 years after the research published by Cerasi and others, there was a report of a study of 13 new genes increasing the risk of type 2 diabetes. The authors of the study said they were "intrigued" by the finding that most of these genes affect beta cell secretion rather than insulin resistance.
"Beta cell impairment may play a larger role in type 2 diabetes than previously recognized," the authors said, as if this was a totally new idea.
It is true that there's so much diabetes research published that no researcher can have read all of it. One report or one person's opinion isn't considered proof of anything, but it should suggest something, so researchers shouldn't be stunned 23 years later to discover the same thing.
Why is it that an amateur researcher, a newly diagnosed patient, can find information a professional apparently cannot? I'm sure the Cerasi papers were not the only ones to come to the same conclusion, and the other researchers had 23 years in which to look.
Cerasi also recommended using insulin in type 2 patients right from the beginning, to normalize blood glucose levels and reduce glucotoxicity, which he felt contributed to the IR. "Present therapeutic approaches based on initial dietary restriction followed after a period of up to several months by oral diabetic agents, seem rather unsuited" for returning the patient to mild diabetes or prediabetes.
"I propose initial, short-term (one to a few weeks) intensified insulin treatment aimed at achieving euglycemia very rapidly, in order to block down-regulation of glucose transport and inprove beta-cell function." He showed in a pilot study that when patients in whom the oral drugs had stopped working were given insulin to maintain normal BG levels for two weeks, they could then maintain good control on oral agents alone after the insulin was stopped.
Again, a recent proposal suggests essentially the same thing. Ralph DeFronzo proposed starting newly diagnosed patients with type 2 on an intensive drug regimen of metformin, a TZD, and exenatide. And he and 15 other diabetes experts proposed the same at the 2008 ADA meeting.
The ADA's response: Prove it. They just now started a 3-year study to see if early normalization of BG levels with drugs helps. But what is taking them so long? And why use drugs instead of insulin?
Other research has shown that early intensive insulin treatment is more effective than drugs in maintenance of beta cell function. So why mess around with expensive drugs that can have serious side effects when a simpler, cheaper treatment has already been shown to work?
It boggles the mind.
Another example is a 2007 paper by Frank Q. Nuttall and Mary C. Gannon. They showed in 1996 that fasting caused normalization of BG levels in people with type 2 diabetes and wondered, "Could merely a reduction in carbohydrate mimic the effect of a reduced fuel-energy diet or short-term starvation on blood glucose in people with type 2 diabetes mellitus?"
They published the results of using l0w-carb diets (20 and 30% carbohydrate), showing that BG levels and HbA1c levels were much lower. However, their request for further funding was rejected by the National Institutes of Health, which said their sample sizes were too low to show anything and "it is difficult to conceive of the diet as producing larger improvements than metformin or rosiglitazone, for example, especially if the subjects are maintaining their body weight."
"So much for open mindedness," wrote Nuttall and Gannon. The health authorities cling to their old views even in the face of new evidence. They seem to have made up their minds, and there's no more room in their tiny minds to consider alternatives.
But wait a minute. For decades, Richard K. Bernstein has been proposing low-carbohydrate diets for both type 1 and type 2 patients. His first book was published in 1984. But almost no one in the professional world listened to him either. Why did Nuttall and Gannon have to "wonder" in 1996 if the idea of reducing carbohyrate would work?
Research has been done, and it has been published, but other researchers don't seem to pay a lot of attention.
Why must the patients be the ones to ferret out the facts?
When I was first diagnosed in 1996, because I had been a biology major and had done some research in biochemistry, I wanted to learn more about the science of type 2 diabetes.
I was puzzled because the nurse practitioner who diagnosed me told me to follow the American Diabetes Association (ADA) diet, which was chock-a-block full of carbohydrates. I knew that diabetes was caused by an inability to process carbohydrates. So why were they telling me to eat more of them? It made no sense.
So I went to the library. Remember libraries? They were places with books and preceded Internet searches and Google and all that. The library didn't have much of interest, so I searched the interlibrary loan catalogs and found and ordered a book called Insulin, edited by F. M. and S. J. H. Ashcroft. It was published in 1992, which means it was probably written around 1990, as the publishing process does take time.
The book was very interesting. A chapter author named Erol Cerasi said he and others had done a study of a large group of obese and nonobese subects both with and without diabetes and studied insulin resistance (IR) and insulin secretion.
They found that only beta-cell responsiveness could distinguish the diabetic from nondiabetic subjects. The IR could only distinguish obese from nonobese subjects.
In other words, if you're obese, you'll have IR, but you won't necessarily have diabetes. If you have diabetes, your beta cells won't secrete enough insulin, whether or not you're overweight.
They concluded that "the diabetic state is much more closely related to a failure of the secretion of insulin than to diminished efficiency of the circulating hormone level," that is, beta cell defects are more important than IR in causing type 2.
Another group did a similar study and found that those who progressed from prediabetes to diabetes had decreased insulin responses to glucose at the beginning of the study.
Yet people with type 2 diabetes continued to be told that their obesity had caused IR and the IR had caused the diabetes.
Recently, 23 years after the research published by Cerasi and others, there was a report of a study of 13 new genes increasing the risk of type 2 diabetes. The authors of the study said they were "intrigued" by the finding that most of these genes affect beta cell secretion rather than insulin resistance.
"Beta cell impairment may play a larger role in type 2 diabetes than previously recognized," the authors said, as if this was a totally new idea.
It is true that there's so much diabetes research published that no researcher can have read all of it. One report or one person's opinion isn't considered proof of anything, but it should suggest something, so researchers shouldn't be stunned 23 years later to discover the same thing.
Why is it that an amateur researcher, a newly diagnosed patient, can find information a professional apparently cannot? I'm sure the Cerasi papers were not the only ones to come to the same conclusion, and the other researchers had 23 years in which to look.
Cerasi also recommended using insulin in type 2 patients right from the beginning, to normalize blood glucose levels and reduce glucotoxicity, which he felt contributed to the IR. "Present therapeutic approaches based on initial dietary restriction followed after a period of up to several months by oral diabetic agents, seem rather unsuited" for returning the patient to mild diabetes or prediabetes.
"I propose initial, short-term (one to a few weeks) intensified insulin treatment aimed at achieving euglycemia very rapidly, in order to block down-regulation of glucose transport and inprove beta-cell function." He showed in a pilot study that when patients in whom the oral drugs had stopped working were given insulin to maintain normal BG levels for two weeks, they could then maintain good control on oral agents alone after the insulin was stopped.
Again, a recent proposal suggests essentially the same thing. Ralph DeFronzo proposed starting newly diagnosed patients with type 2 on an intensive drug regimen of metformin, a TZD, and exenatide. And he and 15 other diabetes experts proposed the same at the 2008 ADA meeting.
The ADA's response: Prove it. They just now started a 3-year study to see if early normalization of BG levels with drugs helps. But what is taking them so long? And why use drugs instead of insulin?
Other research has shown that early intensive insulin treatment is more effective than drugs in maintenance of beta cell function. So why mess around with expensive drugs that can have serious side effects when a simpler, cheaper treatment has already been shown to work?
It boggles the mind.
Another example is a 2007 paper by Frank Q. Nuttall and Mary C. Gannon. They showed in 1996 that fasting caused normalization of BG levels in people with type 2 diabetes and wondered, "Could merely a reduction in carbohydrate mimic the effect of a reduced fuel-energy diet or short-term starvation on blood glucose in people with type 2 diabetes mellitus?"
They published the results of using l0w-carb diets (20 and 30% carbohydrate), showing that BG levels and HbA1c levels were much lower. However, their request for further funding was rejected by the National Institutes of Health, which said their sample sizes were too low to show anything and "it is difficult to conceive of the diet as producing larger improvements than metformin or rosiglitazone, for example, especially if the subjects are maintaining their body weight."
"So much for open mindedness," wrote Nuttall and Gannon. The health authorities cling to their old views even in the face of new evidence. They seem to have made up their minds, and there's no more room in their tiny minds to consider alternatives.
But wait a minute. For decades, Richard K. Bernstein has been proposing low-carbohydrate diets for both type 1 and type 2 patients. His first book was published in 1984. But almost no one in the professional world listened to him either. Why did Nuttall and Gannon have to "wonder" in 1996 if the idea of reducing carbohyrate would work?
Research has been done, and it has been published, but other researchers don't seem to pay a lot of attention.
Why must the patients be the ones to ferret out the facts?
Saturday, January 30, 2010
Fuzzy Fats
Fats have been in the news lately, with publication of a meta-analysis mentioned in a previous blogpost showing that there's no statistical evidence that saturated fat is associated with deaths from cardiovascular disease (CVD).
Well, let me qualify that statement. Fats have been in the low-carb news lately. I haven't seen much discussion of this study by people like Dean Ornish who support very low fat diets.
Note that the study showed that they found no evidence that saturated fat intake was associated with CVD mortality. They didn't study whether or not eating other fats were associated with CVD mortality.
But what does saturated fat intake mean? Does it mean the amount of saturated fat you eat? Or does it mean what percentage of your diet consists of saturated fat? These two things can be quite different. Yet many research reports, written by scientists who should be precise about such things, don't make it clear.
Fat intake is often reported as a percentage. For example, low fatters want us to keep our dietary fat under 30% and saturated fat under 10%. But I don't know anyone who goes into a restaurant and sits down with a calculator and a scale to make sure they don't eat more than 30% fat at that meal. (Actually, people with type 1 diabetes used to have to do just that.) Trying to calculate total fat and also saturated fat is even more difficult.
I once bought a little hand-held gizmo that allowed you to punch in your menu and it would, indeed, calculate the macronutrients in the meal. If you ate the same meals over and over again, it might have been useful. But if you ate the same meals over and over again it would have been equally useful to do the calculations on a real computer or even by hand with the aid of a book and then write them down to refer to when you had that meal.
When you ate something different at each meal, you had to locate that food among thousands of foods, decide what description best fit it and how much it weighed, and then input that.
I don't eat the same meal over and over again. I think variety is the spice of eating as well as the spice of life. When it's mealtime, I go to the fridge to see what's there and then try to make something interesting from it.
And the biggest problem I had with any nutritional gizmo was trying to decide which of the myriad choices to input for various foods. Let's say I roast a leg of lamb.
Do I want "Lamb, Australian, imported, fresh, leg, center slice, bone in, separable lean and fat, trimmed to 1/8 inch fat, raw" or do I want "Lamb, domestic, leg, shank half, separable lean and fat, trimmed to 1/4 inch fat, Choice, cooked, roasted, USDA"? I counted 44 different versions of leg of lamb in the nutrition program I have on my computer: Computer Planned Nutrition.
And how do I know how the nutritional information from lambs raised by my neighbors are closer to those of the Australian, New Zealand, or domestic lamb in this program? The lamb I eat comes from free-range animals. Do the animals used in the nutritional program? I don't know.
So even assuming I have time to comb through all 44 choices every time I sit down to eat a slice of lamb (which would probably be cold by the time I figured out the best one), I have no confidence that the lamb I'm eating has the same nutritional composition as the lamb in the program.
Some lambs are fatter than others. Of course I could trim them all evenly. But I could trim the lamb to 1/4 inch or 1/8 inch and then eat or not eat the remaining fat. Or I could leave some of the lamb and a lot of the fat that oozed out of the lamb on my plate.
I see some of the precise calculations some people do with nutritional programs as GIGO: garbage in, garbage out. The computational ability of the computer programs exceeds the accuracy of the data you put in.
The same is true of other foods. Foods have different nutritional compositions depending not only on the particular variety and size but on the condition of the soil, fertilizer, growing season, and so forth.
Furthermore, most nutritional studies rely on people's recollection of what they ate last week or last month or last year. I often can't remember what I had for breakfast, much less last week.
But I digress. I was talking about fat.
Most people don't estimate the percentage of fat in every meal they eat. You can get an estimate of what you need every day by calculating the number of calories you need every day to keep your weight stable, or to lose weight if that's what you're trying to do. Then you can calculate how many calories or grams of a food you should eat each day to reach that percentage.
For example, let's say you're trying to eat about 2000 calories a day with 30% fat. That would be 600 calories of fat. Because there are about 9 calories per gram of fat, that would be 66 grams of fat. Divide that by 28.35 (1 ounce = 28.35 grams), and you get about 2.35 ounces of fat per day, or 1.175 tablespoons (1 oz = 2 Tb). That includes the fat in your meat as well as the oil you cook in or pour on your salad.
But how do you really know how much fat is in the meat you eat?
What if you're eating a lot more or a lot less than 2000 calories a day? What if you're a large man and you're very athletic and you eat 5000 calories a day. Then you could eat 1000 calories of fat (111 grams) of day and still say you were eating a very low fat diet, only 20%.
What if you're a small woman trying to lose weight? You might eat only 1000 calories a day. Then the same amount of fat (1000 calories, or 111 grams) would constitute 100% of your diet, obviously not a likely choice for anyone. If you ate only 400 calories of fat (44 grams), you'd still be eating 40% fat, considered a high-fat diet.
You could get your fat percentage down by eating more carbohydrate calories. Let's say you increased your total calories to 2000. Then you'd be on a "nice healthy 20% fat diet." But does that many any sense? Not to me.
Now let's look at what often happens when people go on a low carb diet. Let's say your previous lunch every day was a hamburger on a bun with french fries and a regular soda. I chose ground beef and a large hamburger bun (this had less fat than a fast-food burger, but I wanted to be able to compare it with a burger without the bun), a "serving" of Burger King fries, and a 32-ounce soda. Most people would probably also add catsup, or the fast-food burger would come with a sweet sauce, but I'm ignoring that. According to my nutritional program, without those extras, you have a meal with 1358 calories, 38 grams of fat, 10 grams of saturated fat, and 200 grams of carbohydrate.
Now let's say you go on a low-carb diet. You still eat at the hamburger place because all your friends do, but now you get a large burger without the bun. In place of the bun, you order a salad of mixed greens (I used 2 cups), with ranch dressing, and water or a sugarfree soda. This meal results in 324 calories, 15 grams of fat, 3 grams of saturated fat, and 4 grams of carbohydrate.
The first meal results in 25% fat (38 grams of fat x 9, divided by 1358), because of all the calories in the soda and the potato. The second meal results in 42% fat (15 x 9, divided by 324), because the total calories are so much lower that the fat makes up a larger proportion of the meal.
But would anyone claim that a meal that included french fries and a large soda (25% fat) was healthier than a meal that included salad greens and ranch dressing (42% fat)?
I don't think so.
This is why measuring a diet by the percentage of fat can be so misleading. This is why worrying about the fat content of low-carb diets can be so misleading.
Although my current low-carb diet includes about 60% fat, I don't think I'm eating any more fat than I used to eat. What I'm not eating is all the carbohydrate I used to put underneath that pat of butter or tablespoon of oil.
Biochemist Richard Feinman said all this in a more concise and more academic way when he wrote here, ". . . it is important to recognize that percentages are misleading. There are really three degrees of freedom in design or analysis of a weight loss experiment: two of the three macronutrients and the total calorie intake. It is unlikely that the percentage rather than the absolute amount of macronutrients is the controlling variable and at least three published studies show that carbohydrate reduction is not necessarily accompanied by replacement with either fat or protein but rather caloric reduction due to the carbohydrate removed."
In trying to unravel the very complex picture of the role of fat in human health, and for us its role in diabetes control, remember to scrutinize any research articles you read to see if the reseachers were measuring absolute amounts of nutrients or their percentages.
If only percentages, take the results with a grain of salt . . . or maybe a piece of cheese.
Also see how they determined the various nutritional intakes. Did they isoloate people in a ward and feed them carefully controlled meals? Or did they provide all the food on a take-out basis and trust that the participants weren't eating anything else? Or did they just provide "guidance" by a nutritionist who told them what kinds of foods they should be eating? Or did they just ask people to fill out food questionnaires after the fact?
You also need to see how the researchers defined their terms. They can differ a lot. For example, some people call a diet that has 45% carbohydrate (225 grams on a 2000-calorie diet) instead of 55 or 60% a low-carb diet and then claim that low-carb diets do this or that. Often this information cannot be found in the abstract of the article. You have to obtain and read the whole thing.
If you're reading an article about the effects of fat, you need to determine what other foods the subjects were eating. If you're on a low-carb diet, you'll burn a lot more fat than if you're eating both fats and carbs.
Unfortunately, the news media can't deal with these subtleties. They want interesting stories. And simplistic interpretations make for better stories. A story headlined "Whortleberries cure cancer" would get more readers than a story headlined "When fed a diet of 98% whortleberry, small percentage of highly inbred white mice see improvements in obscure cancer type that never affects humans ."
But you're smarter than the average reporter. So reader beware. Read and learn. But don't take any nutritional study as the last word. And especially, don't accept fuzzy fat words like "fat intake."
Well, let me qualify that statement. Fats have been in the low-carb news lately. I haven't seen much discussion of this study by people like Dean Ornish who support very low fat diets.
Note that the study showed that they found no evidence that saturated fat intake was associated with CVD mortality. They didn't study whether or not eating other fats were associated with CVD mortality.
But what does saturated fat intake mean? Does it mean the amount of saturated fat you eat? Or does it mean what percentage of your diet consists of saturated fat? These two things can be quite different. Yet many research reports, written by scientists who should be precise about such things, don't make it clear.
Fat intake is often reported as a percentage. For example, low fatters want us to keep our dietary fat under 30% and saturated fat under 10%. But I don't know anyone who goes into a restaurant and sits down with a calculator and a scale to make sure they don't eat more than 30% fat at that meal. (Actually, people with type 1 diabetes used to have to do just that.) Trying to calculate total fat and also saturated fat is even more difficult.
I once bought a little hand-held gizmo that allowed you to punch in your menu and it would, indeed, calculate the macronutrients in the meal. If you ate the same meals over and over again, it might have been useful. But if you ate the same meals over and over again it would have been equally useful to do the calculations on a real computer or even by hand with the aid of a book and then write them down to refer to when you had that meal.
When you ate something different at each meal, you had to locate that food among thousands of foods, decide what description best fit it and how much it weighed, and then input that.
I don't eat the same meal over and over again. I think variety is the spice of eating as well as the spice of life. When it's mealtime, I go to the fridge to see what's there and then try to make something interesting from it.
And the biggest problem I had with any nutritional gizmo was trying to decide which of the myriad choices to input for various foods. Let's say I roast a leg of lamb.
Do I want "Lamb, Australian, imported, fresh, leg, center slice, bone in, separable lean and fat, trimmed to 1/8 inch fat, raw" or do I want "Lamb, domestic, leg, shank half, separable lean and fat, trimmed to 1/4 inch fat, Choice, cooked, roasted, USDA"? I counted 44 different versions of leg of lamb in the nutrition program I have on my computer: Computer Planned Nutrition.
And how do I know how the nutritional information from lambs raised by my neighbors are closer to those of the Australian, New Zealand, or domestic lamb in this program? The lamb I eat comes from free-range animals. Do the animals used in the nutritional program? I don't know.
So even assuming I have time to comb through all 44 choices every time I sit down to eat a slice of lamb (which would probably be cold by the time I figured out the best one), I have no confidence that the lamb I'm eating has the same nutritional composition as the lamb in the program.
Some lambs are fatter than others. Of course I could trim them all evenly. But I could trim the lamb to 1/4 inch or 1/8 inch and then eat or not eat the remaining fat. Or I could leave some of the lamb and a lot of the fat that oozed out of the lamb on my plate.
I see some of the precise calculations some people do with nutritional programs as GIGO: garbage in, garbage out. The computational ability of the computer programs exceeds the accuracy of the data you put in.
The same is true of other foods. Foods have different nutritional compositions depending not only on the particular variety and size but on the condition of the soil, fertilizer, growing season, and so forth.
Furthermore, most nutritional studies rely on people's recollection of what they ate last week or last month or last year. I often can't remember what I had for breakfast, much less last week.
But I digress. I was talking about fat.
Most people don't estimate the percentage of fat in every meal they eat. You can get an estimate of what you need every day by calculating the number of calories you need every day to keep your weight stable, or to lose weight if that's what you're trying to do. Then you can calculate how many calories or grams of a food you should eat each day to reach that percentage.
For example, let's say you're trying to eat about 2000 calories a day with 30% fat. That would be 600 calories of fat. Because there are about 9 calories per gram of fat, that would be 66 grams of fat. Divide that by 28.35 (1 ounce = 28.35 grams), and you get about 2.35 ounces of fat per day, or 1.175 tablespoons (1 oz = 2 Tb). That includes the fat in your meat as well as the oil you cook in or pour on your salad.
But how do you really know how much fat is in the meat you eat?
What if you're eating a lot more or a lot less than 2000 calories a day? What if you're a large man and you're very athletic and you eat 5000 calories a day. Then you could eat 1000 calories of fat (111 grams) of day and still say you were eating a very low fat diet, only 20%.
What if you're a small woman trying to lose weight? You might eat only 1000 calories a day. Then the same amount of fat (1000 calories, or 111 grams) would constitute 100% of your diet, obviously not a likely choice for anyone. If you ate only 400 calories of fat (44 grams), you'd still be eating 40% fat, considered a high-fat diet.
You could get your fat percentage down by eating more carbohydrate calories. Let's say you increased your total calories to 2000. Then you'd be on a "nice healthy 20% fat diet." But does that many any sense? Not to me.
Now let's look at what often happens when people go on a low carb diet. Let's say your previous lunch every day was a hamburger on a bun with french fries and a regular soda. I chose ground beef and a large hamburger bun (this had less fat than a fast-food burger, but I wanted to be able to compare it with a burger without the bun), a "serving" of Burger King fries, and a 32-ounce soda. Most people would probably also add catsup, or the fast-food burger would come with a sweet sauce, but I'm ignoring that. According to my nutritional program, without those extras, you have a meal with 1358 calories, 38 grams of fat, 10 grams of saturated fat, and 200 grams of carbohydrate.
Now let's say you go on a low-carb diet. You still eat at the hamburger place because all your friends do, but now you get a large burger without the bun. In place of the bun, you order a salad of mixed greens (I used 2 cups), with ranch dressing, and water or a sugarfree soda. This meal results in 324 calories, 15 grams of fat, 3 grams of saturated fat, and 4 grams of carbohydrate.
The first meal results in 25% fat (38 grams of fat x 9, divided by 1358), because of all the calories in the soda and the potato. The second meal results in 42% fat (15 x 9, divided by 324), because the total calories are so much lower that the fat makes up a larger proportion of the meal.
But would anyone claim that a meal that included french fries and a large soda (25% fat) was healthier than a meal that included salad greens and ranch dressing (42% fat)?
I don't think so.
This is why measuring a diet by the percentage of fat can be so misleading. This is why worrying about the fat content of low-carb diets can be so misleading.
Although my current low-carb diet includes about 60% fat, I don't think I'm eating any more fat than I used to eat. What I'm not eating is all the carbohydrate I used to put underneath that pat of butter or tablespoon of oil.
Biochemist Richard Feinman said all this in a more concise and more academic way when he wrote here, ". . . it is important to recognize that percentages are misleading. There are really three degrees of freedom in design or analysis of a weight loss experiment: two of the three macronutrients and the total calorie intake. It is unlikely that the percentage rather than the absolute amount of macronutrients is the controlling variable and at least three published studies show that carbohydrate reduction is not necessarily accompanied by replacement with either fat or protein but rather caloric reduction due to the carbohydrate removed."
In trying to unravel the very complex picture of the role of fat in human health, and for us its role in diabetes control, remember to scrutinize any research articles you read to see if the reseachers were measuring absolute amounts of nutrients or their percentages.
If only percentages, take the results with a grain of salt . . . or maybe a piece of cheese.
Also see how they determined the various nutritional intakes. Did they isoloate people in a ward and feed them carefully controlled meals? Or did they provide all the food on a take-out basis and trust that the participants weren't eating anything else? Or did they just provide "guidance" by a nutritionist who told them what kinds of foods they should be eating? Or did they just ask people to fill out food questionnaires after the fact?
You also need to see how the researchers defined their terms. They can differ a lot. For example, some people call a diet that has 45% carbohydrate (225 grams on a 2000-calorie diet) instead of 55 or 60% a low-carb diet and then claim that low-carb diets do this or that. Often this information cannot be found in the abstract of the article. You have to obtain and read the whole thing.
If you're reading an article about the effects of fat, you need to determine what other foods the subjects were eating. If you're on a low-carb diet, you'll burn a lot more fat than if you're eating both fats and carbs.
Unfortunately, the news media can't deal with these subtleties. They want interesting stories. And simplistic interpretations make for better stories. A story headlined "Whortleberries cure cancer" would get more readers than a story headlined "When fed a diet of 98% whortleberry, small percentage of highly inbred white mice see improvements in obscure cancer type that never affects humans ."
But you're smarter than the average reporter. So reader beware. Read and learn. But don't take any nutritional study as the last word. And especially, don't accept fuzzy fat words like "fat intake."
Friday, January 29, 2010
Banana Cream
I've always loved custard of any kind, and banana cream pie was a real treat.
Alas, I don't eat custard anymore, except for custard sauce I make with low-carb milk in the summer when my raspberry bushes are producing. They don't raise my BG very much.
I recently invented a banana cream substitute when I was trying to use up some ricotta cheese I'd bought for another recipe.
Basically, you stir some DaVinci sugarfree banana flavoring into full-fat ricotta cheese. (I find the Maggio brand is the creamiest I can get here.) Top with sugarfree whipped cream. And that's it. Pretty simple.
The ricotta has a smooth texture somewhat like custard, and when topped with sugarfree whipped cream, it really gave me the feeling I was eating banana cream.
I like the sugarfree whipped cream that comes in a can, made by Land O'Lakes, because I can use just a little at a time. You can get it at Walmart superstores. When I buy heavy cream and whip it, then I have to use up the rest of the cream or it will go bad. So I end up eating more heavy cream than I really want.
You do have to be careful with ricotta cheese, as it does contain some carbs, so small portions are in order. It was so good I went overboard, and my BG levels did reflect that.
But it made a nice change for me, and next time I'll be more careful.
Alas, I don't eat custard anymore, except for custard sauce I make with low-carb milk in the summer when my raspberry bushes are producing. They don't raise my BG very much.
I recently invented a banana cream substitute when I was trying to use up some ricotta cheese I'd bought for another recipe.
Basically, you stir some DaVinci sugarfree banana flavoring into full-fat ricotta cheese. (I find the Maggio brand is the creamiest I can get here.) Top with sugarfree whipped cream. And that's it. Pretty simple.
The ricotta has a smooth texture somewhat like custard, and when topped with sugarfree whipped cream, it really gave me the feeling I was eating banana cream.
I like the sugarfree whipped cream that comes in a can, made by Land O'Lakes, because I can use just a little at a time. You can get it at Walmart superstores. When I buy heavy cream and whip it, then I have to use up the rest of the cream or it will go bad. So I end up eating more heavy cream than I really want.
You do have to be careful with ricotta cheese, as it does contain some carbs, so small portions are in order. It was so good I went overboard, and my BG levels did reflect that.
But it made a nice change for me, and next time I'll be more careful.
Monday, January 18, 2010
Saturated Fat and Heart Disease
I'm on a low-carb diet. I believe in LC diets for people with diabetes.
However, I also have an open mind. It's possible that new evidence will show that LC diets, although they improve blood glucose (BG) levels in people with diabetes, also make something else worse.
Richard Bernstein, the physician and author of LC diet book The Diabetes Solution, has lived with type 1 diabetes for many decades, most of those years on a LC diet. And the fact that he is in excellent health in his 70s argues against this possibility. However, Bernstein has type 1 diabetes, and very little insulin resistance. There's some evidence that fat increases insulin resistance. Hence, for those of us for whom insulin resistance is a big problem, perhaps fat of any kind, or maybe only certain kinds of fat, is not a great idea.
So, I have an open mind. But unfortunately, many people in the LC community seem not to. Many of them don't have diabetes, and they have gotten great results losing a lot of weight with LC diets. So they think the LC diet with a lot of fat is the answer for everyone.
And unfortunately, the LC world is just as guilty of spinning the news as the popular science writers who blame red meat for all our problems when some study showed that people eating red meat, hot dogs, french fries, no vegetables, and sweet desserts don't fare so well on some health factor.
A good example is the blogosphere response to this recent study, a meta-analysis of the association between saturated fat and cardiovascular disease (CVD). A meta-analysis is a study in which researchers combine the results from a lot of studies, some of which aren't statistically significant because of their small size, so that the overall results are statistically significant because of the larger populations in the combined studies.
Meta-analyses are notoriously questionable, because the researchers have to decide which studies to include. If you did a meta-analysis of the percentage of the population that watched the Super Bowl (assuming lots of people had studied this fascinating question) but excluded everyone who shaved every morning, the results wouldn't be very accurate.
Nevertheless, sometimes meta-analyses can suggest possible conclusions that other scientists can then investigate more thoroughly.
And that is what this study, titled Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, did.
The authors' conclusion was that "there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD [coronary heart disease] or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat."
Two things are important here.
First, the fact that there's no significant evidence for something doesn't mean it's not true. It just means no one has proved that it's true. Several studies have concluded that there's no significant evidence that BG testing in people with type 2 diabetes results in lower A1c's, but most of us know that it does when patients are educated about how to use the results from their meters to change their diets and their exercise patterns. But no one has done the study that would show this.
And second, this study was about association, not cause. Something can be associated with something else but not be the cause of it. For example, coffee drinking is often associated with smoking, but drinking coffee doesn't make you smoke, and vice versa.
The types of studies this meta-analysis looked at were not the types of studies that can show cause.
What the authors found was that some studies showed that saturated fat consumption was associated with higher rates of CVD (heart attacks and strokes), and other studies showed that saturated fat consumption was associated with lower rates of CVD. When you combined the higher rates and the lower rates, you got rates that weren't significantly different.
However, they also noted another recent study that showed that when saturated fat was replaced by polyunsaturated fat, CVD rates went down. When saturated fat was replaced by carbohydrates (what dieticians have been recommending that we all do), CVD rates went up. They said there was some evidence that the ratio of unsaturated to saturated fats was more important than the amount of saturated fat. Hence they suggest that studies are needed that would investigate whether the other elements of the diet have more effect on CVD than the saturated fat.
The authors of Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease never say that saturated fat definitely doesn't cause CVD. They also say that "the available data were not adequate for determining whether there are CHD or stroke associations with saturated fat in specific age and sex subgroups." In other words, the jury is still out.
Nevertheless, the Internet is awash in blogs with titles like "Two major studies conclude that saturated fat does NOT cause heart disease" and "Saturated Fats Are Not Harmful."
The following are just my opinions, and I won't cite studies to back them up. I suspect that saturated fat is fine in moderation. If you want to put a couple of teaspoons of something on your vegetables, I suspect it doesn't matter if it's butter or olive oil. People on LC diets can probably eat more saturated fat because they're burning fats instead of carbohydrates for energy. I don't think eating a lot of polyunsaturated fats (vegetable oils), which are easily oxidized (damaged), is healthy.
But I don't think eating gargantuan amounts of fat of any kind is healthy, even on a LC diet. I once measured my triglyceride levels after eating an extremely high fat breakfast. You can see the results here. The triglyceride levels were astronomical.
People with diabetes probably have a disturbed lipid metabolism, so it's possible that nondiabetics would not have such astronomical triglyceride levels after pigging out on fats (for example, eating half a pizza). But headlines proclaiming that saturated fat isn't harmful will be interpreted by many people to mean that fat isn't harmful. They won't stop eating all those carbohydrates, the doughnuts and french fries and white bread. They'll just add more fat because they remember that they saw headlines saying fat doesn't cause heart disease.
The study showing no association between saturated fat consumption and CVD, despite its many limitations, is important. It should lead to more studies that will attempt to show causation or lack thereof.
I just hope the misinterpretations don't result in more unhealthy eating.
However, I also have an open mind. It's possible that new evidence will show that LC diets, although they improve blood glucose (BG) levels in people with diabetes, also make something else worse.
Richard Bernstein, the physician and author of LC diet book The Diabetes Solution, has lived with type 1 diabetes for many decades, most of those years on a LC diet. And the fact that he is in excellent health in his 70s argues against this possibility. However, Bernstein has type 1 diabetes, and very little insulin resistance. There's some evidence that fat increases insulin resistance. Hence, for those of us for whom insulin resistance is a big problem, perhaps fat of any kind, or maybe only certain kinds of fat, is not a great idea.
So, I have an open mind. But unfortunately, many people in the LC community seem not to. Many of them don't have diabetes, and they have gotten great results losing a lot of weight with LC diets. So they think the LC diet with a lot of fat is the answer for everyone.
And unfortunately, the LC world is just as guilty of spinning the news as the popular science writers who blame red meat for all our problems when some study showed that people eating red meat, hot dogs, french fries, no vegetables, and sweet desserts don't fare so well on some health factor.
A good example is the blogosphere response to this recent study, a meta-analysis of the association between saturated fat and cardiovascular disease (CVD). A meta-analysis is a study in which researchers combine the results from a lot of studies, some of which aren't statistically significant because of their small size, so that the overall results are statistically significant because of the larger populations in the combined studies.
Meta-analyses are notoriously questionable, because the researchers have to decide which studies to include. If you did a meta-analysis of the percentage of the population that watched the Super Bowl (assuming lots of people had studied this fascinating question) but excluded everyone who shaved every morning, the results wouldn't be very accurate.
Nevertheless, sometimes meta-analyses can suggest possible conclusions that other scientists can then investigate more thoroughly.
And that is what this study, titled Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, did.
The authors' conclusion was that "there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD [coronary heart disease] or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat."
Two things are important here.
First, the fact that there's no significant evidence for something doesn't mean it's not true. It just means no one has proved that it's true. Several studies have concluded that there's no significant evidence that BG testing in people with type 2 diabetes results in lower A1c's, but most of us know that it does when patients are educated about how to use the results from their meters to change their diets and their exercise patterns. But no one has done the study that would show this.
And second, this study was about association, not cause. Something can be associated with something else but not be the cause of it. For example, coffee drinking is often associated with smoking, but drinking coffee doesn't make you smoke, and vice versa.
The types of studies this meta-analysis looked at were not the types of studies that can show cause.
What the authors found was that some studies showed that saturated fat consumption was associated with higher rates of CVD (heart attacks and strokes), and other studies showed that saturated fat consumption was associated with lower rates of CVD. When you combined the higher rates and the lower rates, you got rates that weren't significantly different.
However, they also noted another recent study that showed that when saturated fat was replaced by polyunsaturated fat, CVD rates went down. When saturated fat was replaced by carbohydrates (what dieticians have been recommending that we all do), CVD rates went up. They said there was some evidence that the ratio of unsaturated to saturated fats was more important than the amount of saturated fat. Hence they suggest that studies are needed that would investigate whether the other elements of the diet have more effect on CVD than the saturated fat.
The authors of Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease never say that saturated fat definitely doesn't cause CVD. They also say that "the available data were not adequate for determining whether there are CHD or stroke associations with saturated fat in specific age and sex subgroups." In other words, the jury is still out.
Nevertheless, the Internet is awash in blogs with titles like "Two major studies conclude that saturated fat does NOT cause heart disease" and "Saturated Fats Are Not Harmful."
The following are just my opinions, and I won't cite studies to back them up. I suspect that saturated fat is fine in moderation. If you want to put a couple of teaspoons of something on your vegetables, I suspect it doesn't matter if it's butter or olive oil. People on LC diets can probably eat more saturated fat because they're burning fats instead of carbohydrates for energy. I don't think eating a lot of polyunsaturated fats (vegetable oils), which are easily oxidized (damaged), is healthy.
But I don't think eating gargantuan amounts of fat of any kind is healthy, even on a LC diet. I once measured my triglyceride levels after eating an extremely high fat breakfast. You can see the results here. The triglyceride levels were astronomical.
People with diabetes probably have a disturbed lipid metabolism, so it's possible that nondiabetics would not have such astronomical triglyceride levels after pigging out on fats (for example, eating half a pizza). But headlines proclaiming that saturated fat isn't harmful will be interpreted by many people to mean that fat isn't harmful. They won't stop eating all those carbohydrates, the doughnuts and french fries and white bread. They'll just add more fat because they remember that they saw headlines saying fat doesn't cause heart disease.
The study showing no association between saturated fat consumption and CVD, despite its many limitations, is important. It should lead to more studies that will attempt to show causation or lack thereof.
I just hope the misinterpretations don't result in more unhealthy eating.
Monday, December 28, 2009
Biased Reports
Now that Santa has come and gone and we don't need to worry about being good for another year, I can stop worrying that I might say something unkind in a season of joy and get back to sniping about the biased reporting we see every day.
This time it's a study suggesting that a diet high in methionine might increase your risk of Alzheimer's disease. According to the ScienceDaily summary, foods typically high in methionine include red meats, fish, beans, eggs, garlic, lentils, onions, yogurt, and seeds.
So does the researcher interviewed for the article suggest that people eat less fish, beans, lentils, and garlic?
Of course not. Instead he blames the problem on red meat:
"But people who have a diet high in red meat, for instance, could be more at risk because they are more likely to develop this high level of circulating homocysteine, [lead researcher Domenico Pratico] said."
Well, he did at least say "for instance," but you know that most readers will come away with the idea that "artery-clogging red meat" will cause Alzheimer's, and they'll forget that fish, beans, lentils, and garlic may have the same effect.
Sometimes I think it's hopeless. These people aren't real scientists, who seek the truth, whether it's what they were expecting or not. Instead, these people start out with a preconception of what healthy eating is and then do experiments to try to prove they're right. When the answers don't come out the way they want them to, sometimes they don't publish them.
I was once in a study of the cholesterol-lowering drugs Lipitor vs Zocor. At the time, Lipitor was gaining market share, and the Zocor people hoped to prove that even though Lipitor might be better for the general public, Zocor would be better for people with diabetes.
However, according to a nurse, it turned out that Lipitor worked better for the people with diabetes. And as far as I know, the results of this study have never been published.
I hope the people who read this blog are smarter than average and know how to read between the lines in these popular science reports.
We'll never get the answers if we have to rely on these biased popular reports.
This time it's a study suggesting that a diet high in methionine might increase your risk of Alzheimer's disease. According to the ScienceDaily summary, foods typically high in methionine include red meats, fish, beans, eggs, garlic, lentils, onions, yogurt, and seeds.
So does the researcher interviewed for the article suggest that people eat less fish, beans, lentils, and garlic?
Of course not. Instead he blames the problem on red meat:
"But people who have a diet high in red meat, for instance, could be more at risk because they are more likely to develop this high level of circulating homocysteine, [lead researcher Domenico Pratico] said."
Well, he did at least say "for instance," but you know that most readers will come away with the idea that "artery-clogging red meat" will cause Alzheimer's, and they'll forget that fish, beans, lentils, and garlic may have the same effect.
Sometimes I think it's hopeless. These people aren't real scientists, who seek the truth, whether it's what they were expecting or not. Instead, these people start out with a preconception of what healthy eating is and then do experiments to try to prove they're right. When the answers don't come out the way they want them to, sometimes they don't publish them.
I was once in a study of the cholesterol-lowering drugs Lipitor vs Zocor. At the time, Lipitor was gaining market share, and the Zocor people hoped to prove that even though Lipitor might be better for the general public, Zocor would be better for people with diabetes.
However, according to a nurse, it turned out that Lipitor worked better for the people with diabetes. And as far as I know, the results of this study have never been published.
I hope the people who read this blog are smarter than average and know how to read between the lines in these popular science reports.
We'll never get the answers if we have to rely on these biased popular reports.
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