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Do High-Carbohydrate Diets Increase Heart Disease Risk?
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By James J. Kenney, PhD, RD, FACN
Good through December 2013
Introduction
Clinical Trials Show Regression on Very-Low-Fat
Diets
Replacing SFA with CHO Reduces LDL-C and CAD
But Wouldn't Replacing SFA With UFA Also Prevent
CAD?
Differences in Blood Lipids Due to Genetics
and Diet May Not Be Comparable
A Lower HDL On A High-CHO Diet May Not Be Dangerous
Fasting TG Also Return to Normal over the Long
Run on a High-CHO Diet
How a High-CHO Diet is Fed Impacts Blood Lipids
Do High-CHO Diets Increase Fasting TG and RLP?
Conclusions
References
Post Test for Do High-Carbohydrate Diets Increase Heart Disease Risk
Introduction
Yet another study by Stanford University researchers (and others) has been published which presumably shows that a diet higher in carbohydrate (CHO) and lower in unsaturated fats alters blood lipids in such a way that the risk atherosclerosis is increased.[1] This study found a lower HDL-cholesterol (HDL-C) (39 vs. 44 mg/dl) and higher fasting triglycerides (TG) (206 vs. 113 mg/dl) in 8 healthy subjects fed a high-CHO (25% fat) diet compared to those same subjects fed a high-fat (45% fat) diet for 2 weeks. This type of finding is "old hat" for this research group. The "new" finding was higher postprandial remnant lipoprotein particles (RLP) on the higher CHO diet compared to the diet higher in unsaturated fat. All of these changes in blood lipids have been associated with an increased risk of coronary artery disease (CAD) in epidemiological studies of Americans. So, the authors concluded, "Given the atherogenic potential of these changes in lipoprotein metabolism, it seems appropriate to question the wisdom of recommending that all Americans should replace dietary saturated fat with CHO." Is such a conclusion justified?
Clinical Trials Show Regression on Very-Low-Fat Diets
If high-CHO diets are more atherogenic than diets higher in fat, what are we to make of several studies that have reported that very-low-fat, near-vegetarian diets (VLFNV) cause regression of atherosclerosis in most patients who already have advanced CAD?[2] [3] [4] [5] [6] And if diets higher in CHO do result in a more atherogenic lipoprotein profile (as the Stanford group suggested), how can we reconcile such a claim with the results of a 12 year study. This study found that a VLFNV diet not only greatly reduced deaths from CAD but also markedly reduced overall mortality in 50 older subjects (all of whom had had a previous heart attack) compared to the 50 patients in the control group who maintained a typical high-fat American diet?[7] Obviously high-CHO diets are not necessarily more atherogenic than diets higher in saturated fat.
Replacing SFA with CHO Reduces LDL-C and CAD
In healthy people, the benefits of lowering serum cholesterol by reducing dietary fat and increasing dietary CHO have been well documented in terms of preventing CAD.[8] There really can be no rational debate about whether replacing dietary saturated fatty acids (SFA) with CHO will help to prevent CAD in the average American. Perhaps there are some people in America that would do better health-wise on a diet higher in unsaturated fat and lower in CHO. But until we know for sure this is the case and have cost effective diagnostic test(s) to determine who these people are, reason dictates replacing SFA and cholesterol with CHO and fiber is a safe an effective public health policy to recommend for all Americans for reducing CAD. More extreme reductions in dietary fat and cholesterol coupled with an increase in CHO and fiber has been proven to reverse atherosclerosis and reduce the overall risk of dying in many patients with advanced CAD. Those who would advocate replacing SFA with unsaturated fatty acids (UFA) should be aware that there is no such proof that diets higher in UFA reverse CAD. Therefore, it seems a leap of faith, rather than science and logic to advocate the replacement of SFA with UFA as more effective for preventing CAD in most people.
But Wouldn't Replacing SFA With UFA Also Prevent CAD?
No one knows for sure at this point, although changes in blood lipids certainly suggest that this would be the case. Replacing SFA with UFA does lower serum total cholesterol (TC) and LDL-C levels about as much as replacing SFA with CHO. However, no one has shown that a diet high in UFA would actually cause regression of atherosclerosis in most CAD patients. Indeed, in one monkey study, a diet high in monounsaturated fatty acids (MUFA) did improve TC and other blood lipid levels compared to a diet high in SFA. The changes in blood lipids in the monkeys were in the same direction as seen in humans fed similar diets. However, despite what appeared to be "improved blood lipids", atherosclerosis progressed to a similar degree in the monkeys fed the high-MUFA diet as those fed the high-SFA diet.[9] So at least in animal models, "improving blood lipids" does not necessarily slow the progression of atherosclerosis. The results of this study call into question the wisdom of assuming that changes in blood lipids in response to dietary changes mean the same thing as differences in blood lipids observed in individuals who are all consuming a similar diet. In this latter case, the differences in blood lipids would be primarily due to genetic factors.
Differences in Blood Lipids Due to Genetics and Diet May Not Be Comparable
Data from Framingham and other epidemiological studies have shown that an increased risk of CAD was correlated with a lower HDL-C and often a higher-fasting TG level. Few people doubt that higher fasting TG and lower HDL-C are usually associated with an increased risk of CAD in people eating a typical high-fat Western diet. Nor does there appear to be much doubt that higher levels of postprandial RLP are associated with a more rapid progression of atherosclerosis in people eating high-fat, Western-style diets. However, there are no studies to show that higher levels of fasting TG and postprandial RLP and lower HDL-C that result from switching to a diet higher in CHO and lower in fat actually promotes atherosclerosis. The Stanford group apparently believes that such changes observed in blood lipids, during their short-term clinical trials, are detrimental. But, there is no solid clinical research that demonstrates that such lipid changes really do promote atherosclerosis and increase the risk of CAD in people who adhere to high-CHO diets for a prolonged period of time.
Another problem with the idea that high-CHO diets could be promote changes in blood lipids, that increase the risk of CAD, is that it seems to conflict with most epidemiological cross-cultural observations. Population studies of people consuming high-CHO diets have shown that CAD is far less common in those populations than it is in America and other countries where high-fat diets are the norm. However, in these populations not only is the intake of dietary CHO higher but the intake of SFA and cholesterol are much lower and fiber intake is often much higher than they are in Americans. There may also be differences in activity and other lifestyle factors that could account for at least some of the differences in CAD risk between Americans and high-CHO consuming populations.
A Lower HDL On A High-CHO Diet May Not Be Dangerous
The Stanford group and others have suggested that the drop in HDL-C seen in short-term studies should be expected to increase the risk of CAD over the long run. There are 2 reasons to be skeptical of such a claim. First, there is growing evidence that the drop in HDL-C that results from restricting dietary fat intake does not lead to a permanently lower HDL-C. This is because replacing high-fat foods with high-CHO foods usually reduces ad libitum energy intake. This results in weight loss and a lower body weight is usually associated with an increase in HDL-C. For example, when a group of hypercholesterolemic men were placed on an ad libitum VLFNV diet for 3 months their energy intake decreased and they lost about 16.5 lbs. On this low-fat diet, their LDL-C dropped from 236 to 139 mg/dl (or -41%) and their TG dropped from 170 to 145 mg/dl (or -15%). But their average HDL-C was essentially unchanged (36 to 37 mg/dL or +3%).[10] Those who continued to consume a very-low-fat intake for another 9 months saw their HDL-C continue to increase. It should be noted that fasting plasma TG levels also fell on average in this study which is the opposite of what the Stanford group has repeatedly observed in short-term studies where both the high-fat and high-CHO diets are fed isocalorically. The results of this and many other studies make it clear that when a VLFNV diet, that is high in fiber, is fed ad-libitum to patients at high risk of CAD, that the changes in blood lipids are usually favorable. Indeed, in many patients such a diet leads to regression of atherosclerotic plaque.
The reason a lower HDL-C on a low-fat diet is not necessarily more atherogenic may be because it has been shown that the fractional clearance rate of cholesterol is different on a VLF diet than it is on a diet higher in fat.[11] This means that it is likely that the amount of cholesterol transported back to the liver from the arteries may not be impaired on a high-CHO diet despite a lower HDL-C level. The return of cholesterol from tissues and blood to the liver is known as reverse cholesterol transport. In animals this reverse cholesterol transport was not impaired despite a much lower HDL-C on a high-CHO diet compared to a high-fat diet.[12]
So while HDL-C does often fall initially when most people first adopt a VLFNV diet, it is not clear that this lower HDL-C level necessarily increases the risk of CAD. Furthermore, in most patients, the adoption of a VLFNV diet will result in weight loss over the long run and this weight loss will eventually result in HDL-C returning to baseline levels (or even higher) levels in most patients.
Fasting TG Also Return to Normal over the Long Run on a High-CHO Diet
It appears to take some time for the body to adapt to a higher CHO intake. The Stanford study, like all studies showing adverse effects on blood lipids, lasted no more than a few weeks. Figure 1 below shows what happened to fasting serum TG levels in a group of about 50 postmenopausal women who were placed on a low-fat, high-CHO diet consisting largely of whole foods.[13]
Figure 1. Effect of increasing dietary CHO at the expense of fat on fasting plasma triglyceride levels in postmenopausal women.
(Adapted from Parks EJ. Am J Clin Nutr 2000;71:424)
During the first 4 months of this study, dietary CHO gradually replaced dietary fat in the diet but subjects were required to consume enough calories to prevent weight loss. During this time fasting serum TG levels rose from 151 to 204 mg/dl. The increase in fasting TG levels was less than that observed by the Stanford study (113 vs 206 mg/dl). Part of the reason for this greater rise in TG levels observed in the Stanford study was that Stanford researchers used more refined high-CHO foods (which raise TG levels more than natural high-CHO foods). Another reason was that the Stanford study only kept their subjects on the experimental diets for two weeks. Two weeks is not long enough for the body to fully adapt to the higher CHO intake. Also, the subjects in this study lost a little weight during the first 4 months of the study despite the researchers best attempts to get them to maintain their initial body weights. Weight loss tends to lower TG levels so even the loss of a few pounds can blunt the TG raising effects of adopting a high-CHO diet.
During the next 8 months of this study, the subjects continued to consume the same high-CHO, low-fat (15% of energy) diet. During this phase, the researchers no longer tried to control how much their subjects ate or weighed. During this phase the subjects' calorie intake was ad libitum. During this second phase of the study, average fasting TG levels gradually returned to baseline level. Not surprisingly, in this 8-month period the subjects lost another 4.5 pounds while consuming a self-selected VLF diet (ad libitum). If most people were taught to consume a VLFNV diet which consisted largely of natural foods, not only would their blood lipids improve and their risk of heart disease fall but they would also lose weight without any need to count calories.
How a High-CHO Diet is Fed Impacts Blood Lipids
The new finding by the Stanford researchers was not that HDL-C dropped and fasting TG increased on the higher CHO diet. They have shown this many times before and so have other researchers using a similar research protocol.[14] [15] The new finding was higher levels of RLP on the high-CHO diet compared to the high-UFA diet. However, this finding is also probably simply an artifact of a flawed experimental design. In general, higher RLP are seen in people with higher fasting and postprandial TG levels and often lower HDL-C as well. We have already seen that fasting TG and HDL-C usually return to baseline levels if the higher CHO is fed ad libitum and for a long enough time for the body to adapt to the higher CHO intake.
Two studies have examined the potentially adverse metabolic effects of a VLF diet (15% fat) compared to a moderate-fat (30% of energy) diet when the VLF diet was fed either isocalorically with the higher fat diet or ad libitum. Both studies found that it was only when the VLF diet was fed at the same calorie level as the higher fat diet that the VLF diet produced a potentially more atherogenic blood lipid profile.[16] [17] It seems likely that it is only when subjects are required (by researchers) to eat past satiety on a higher CHO diet in order to prevent weight loss that the subjects are likely to experience much higher fasting TG levels and also higher postprandial TG and RLP.[18] It should be noted that a high-CHO diet, that is high in sugar and refined white flour and contains a high calorie density, may not lead to a reduced energy intake and may be detrimental for some people.[19]
Every study published by the Stanford group and others which has shown detrimental effects of high-CHO diets required subjects to consume the same energy level and/or maintain the same body weight on both a high-fat and a high-CHO diet. Since a diet consisting of more high-fat foods is generally more calorie-dense, it would be expected to lead most people to consume more calories than they would on a diet higher in CHO.[20] This is the main reason the results of the Stanford group and others have little relevance to the real world of clinical dietetic practice. This design flaw in their studies would render their results clinically meaningless even if they should show in the future that the presumably atherogenic changes in blood lipids they have observed on diets higher in CHO really do promote atherosclerosis and/or increase the risk of CAD.
Do High-CHO Diets Increase Fasting TG and RLP?
A crossover design study that compared the effects of a VLF diet to a diet higher in fat on blood lipids may help put the Stanford study in better perspective. In this study, a VLF (15%), high-CHO diet was compared to a 30% fat diet. In this study the VLF diet was first fed isocalorically with the more moderate-fat diet (as was done in all the Stanford studies). However in this study, the same high-CHO diet was also fed ad libitum to the same subjects.16
When a VLF (15% of energy) diet was fed isocalorically with a moderate fat diet, the fasting TG levels were much higher (188 vs. 115 mg/dl) on the higher CHO diet than on the moderate fat diet. Just as the Stanford researchers observed in their most recent study, the results of this study also showed that postprandial TG (and presumably RLP) were also much higher on the higher CHO diet than on the diet higher in fat (see Figure. 2 below). HDL-C was also lower (42 vs. 35 mg/dl) in this study on the higher CHO diet just as it was in the Stanford study. LDL-C was somewhat higher on the VLF (134 vs. 128 mg/dl) than the moderate fat diet when both diets were fed isocalorically. However, when the VLF, high-CHO diet was fed ad libitum, the LDL-C was now lower (119 vs. 128 mg/dl) than on the 30% fat diet. Remarkably, this lower LDL occured despite a much higher PUFA content (11.2% vs. 2.5% energy) and polyunsaturated to saturated fat (P/S) ratio (1.6 vs. 0.5) on the 30% fat diet compared to the VLF diet. The P/S ratio in the Stanford study was also higher on their higher fat diet than on their higher CHO diet. And while the fasting TG levels were still a little higher (130 vs 115 mg/dl) on the VLF diet when fed ad libitum compared to the moderate fat diet, the postprandial TG level was already considerably lower on the VLF diet compared to the 30% fat diet.
Figure 2. Effect of an AHA-Style Diet and a VLF Diet (Fed either Ad Libitum or Isocalorically with the AHA-Style Diet) on Serum TG Levels
As we have seen, an increased fasting and postprandial TG level may be associated with more potentially atherogenic RLP. As Figure 2 above clearly shows, even when fasting TG levels are somewhat higher on a higher CHO diet, they may still be much lower during most of the day. Because most people spend most of the day in the postprandial state, it seems clinically more relevant to study the impact of dietary changes on postprandial blood lipids rather than just fasting blood lipid levels. This study clearly shows that a diet higher in CHO can result in lower serum TG levels over a 2 year period even though fasting levels may be somewhat higher. This is because the postprandial rise in TG levels (and presumably RLP) will be much less with an ad libitum VLF diet than it would be on an ad libitum diet with added fats and oils. It seems likely that potentially atherogenic RLP would also be lower on a VLF diet fed ad libitum but these were not measured in this study. It should be clear that clinicians can't assume the higher risk of CVD, often associated with higher fasting and postprandial TG levels (in people consuming high-fat Western-style diets), would be comparable to the risk of CVD with a similar fasting TG level in people consuming a VLF diet. While it seems likely that RLP would fall along with fasting and postprandial TG levels on a low-fat diet fed ad libitum over the long-term this remains to be proven. This is an area that deserves more attention from researchers.
Conclusions
It appears that the presumably adverse impact of high-CHO diets on blood lipids is limited primarily to short-term clinical trials in which the research subjects' calorie intake is artificially manipulated (ie, controlled by researchers) and the high-CHO diet is composed largely of sugar and other refined CHOs with little fiber. This is the Stanford model. The flaw in their experimental design was all explained to the Stanford group in a letter to the editor.[19] Unfortunately, Dr. Reaven's (point man for the Stanford group) replied, "In an effort to make results meaningful, we maintained energy intake and output constant throughout the study." Clearly he missed my main criticism of their experimental design.[21] Apparently Dr. Reaven and other academic researchers just don't get it. These and other researchers should compare a high-CHO diet consisting largely of natural foods high in fiber, like fruits, vegetables, whole grains, and beans, with a similar diet to which olive oil or other unsaturated oils are added. They should also allow their research subjects to consume both diets ad libitum (rather than imposing artificial controls on how much people eat). Then they would likely find that a VLFNV diet does not produce adverse changes in blood lipids that increase the risk of CAD as they imply. Indeed, any changes in blood lipids that such a diet causes must be viewed as favorable simply because such a diet has been proven to reverse atherosclerosis. High-fat diets have not been shown to regress atherosclerosis and are usually associated with its progression.
Blood lipids are simply the messenger about what is going on in the artery wall. The message that patients are looking for from their health professionals is how does one prevent or reverse atherosclerosis and CAD. The Stanford researchers appear to be so preoccupied with the messenger (short-term changes in fasting blood lipids which don't always get the message straight) that they have lost sight of the message. New medical technology may soon make it possible to accurately measure the health and function of arteries. Research should now be shifting from what is happening to fasting blood lipids to what is happening to the arteries themselves.
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[1] Abbasi F, McLaughlin T, Lamendola C, et al. High carbohydrate diets, triglyceride-rich lipoproteins, and coronary heart disease risk. Am J Cardiol 2000;85:45-8
[2] Rutledge JC, Hyson DA, Garduno D, et al. Lifestyle modification program in management of patients with coronary artery disease: the clinical experience in a tertiary care hospital. J Cardiopulm Rehabil 1999;19:226-34
[3] Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary artery disease? Lancet 1990;336:129-33
[4] Ornish D. Serum lipids after a low-fat diet. JAMA 1998;279:1345-6
[5] Ornish D, Sherwitz LW, Billings JH, et al. Intensive life style changes for reversal of coronary heart disease. JAMA 1998;280:2001-7.
[6] Schueler G, Hambrecht R, Schrief G, et al. Regular physical exercise and a low-fat diet. effects on progression of coronary artery disease. Circulation 1992;86:1-11
[7] Morrison L. Diet and coronary atherosclerosis. JAMA 1960; 173:884-8
[8] Castelli WP. The triglyceride issue: a view from Framingham. Am Heart J 1986;112:432-40
[9] Rudel LL, Parks JS, Sawyer JK. Compared with dietary monounsaturated and saturated fat, polyunsaturated fat protects African green monkeys from coronary artery atherosclerosis. Arterioscler Thrombo Vasc Biol 1995;15:2101-10
[10] Thuesen L, Henriksen LB, Engby B. One-year experience with a low-fat, low-cholesterol diet in patients with coronary heart disease. Am J Clin Nutr 1986;44:212-9
[11] Brinton EA, Eisenberg S, Breslow JL. A low-fat diet decreases high density lipoprotein(HDL) cholesterol levels by decreasing HDL apoprotein transport rates. J Clin Invest 1990;85:144-51
[12] Woolett LA, Kearney DM, Spady DK. Diet modification alters plasma cholesterol concentrations but not the transport of HDL cholesteryl esters to the liver in hamsters. J Lipid Res 1997;38:2289-302
[13] Kasim-Karakas SE, Lane E, Almario R, et al. Effects of dietary fat restriction on particle size of plasma lipoproteins in postmenopausal women. Metabolism 1997;46:431-6
[14] Garg A, Bantle JP, Henry RR, et al. Effects of varying carbohydrate content of diet in patients with non-insulin-dependent diabetes mellitus. JAMA 1994;271:1421-8
[15] Jeppensen J, Schaaf P, Jones C, et al. Effects of low-fat, high-carbohydrate diets on risk factors for heart disease in postmenopausal women. Am J Clin Nutr 1997;55:1027-33
[16] Lichtenstein AH, Ausman LM, Carrasco W, et al. Short-term consumption of a low-fat diet beneficially affects plasma lipid concentrations only when accompanied by weight loss. Arterioscler Thromb 1994; 14:1751-60
[17] Schaefer EJ, Lichtenstein AH, Lamon-Fava S, et al. Body weight and low-density lipoprotein changes after consumption of a low-fat ad libitum diet. JAMA 1995; 274:1450-5
[18] Parks EJ, Hellerstein MK. Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms. Am J Clin Nutr 2000;71:412-33
[19] Kenney JJ. Low-fat, high-carbohydrate diets and risk for ischemic heart disease. Am J Clin Nutr 1997;66:1293
[20] Kenney JJ. Research points to a more effective strategy for long-term weight control without hunger. http:www.foodandhealth.com/continuingeducation.htm
[21] Reaven G. Reply to J Kenney. Am J Clin Nutr 1997;66:1294
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