Our study found that a low-carbohydrate diet induced greater weight loss and reductions in cardiovascular risk factors at 12 months than a low-fat diet among black and white obese adults who did not have diabetes, CVD, or kidney disease at baseline. Previous studies have examined the effects of low-carbohydrate diets on CVD risk factors, but most had small sample sizes or low completion rates, did not assess a typical low-carbohydrate diet for weight loss, or did not include diverse populations (19-24).
The underlying mechanisms that may account for differences in weight loss by diet are still not fully identified, but a recent study indicated that low-carbohydrate diets may have a more favorable effect on resting energy expenditure and total energy expenditure than low-fat diets (26). We found that a low-carbohydrate diet resulted in a significantly greater reduction in the ratio of total-HDL cholesterol, which has been identified as a strong and independent predictor of CHD (27). A major concern that has been frequently raised about low-carbohydrate diets is their potential to elevate LDL cholesterol levels, an established risk factor for CVD (8, 28).
We also observed moderate reductions in blood pressure and plasma glucose, serum insulin, and serum creatinine levels that did not differ significantly between groups. The Framingham risk score is a global index of CHD risk used in clinical settings (8, 17, 30).
Objective: To examine the effects of a low-carbohydrate diet compared with a low-fat diet on body weight and cardiovascular risk factors. Results: Sixty participants (82%) in the low-fat group and 59 (79%) in the low-carbohydrate group completed the intervention.
Conclusion: The low-carbohydrate diet was more effective for weight loss and cardiovascular risk factor reduction than the low-fat diet. According to the latest estimates, more than one third of American adults have at least 1 form of cardiovascular disease (CVD) and one third of total deaths are due to CVD (1). Low-carbohydrate diets have become a popular strategy for weight loss and weight management in recent years; however, their cardiovascular effects are unknown. We used a computer-generated, blocked randomization, stratified by sex, to allocate participants to 1 of the 2 diet groups.
Participants met with a dietitian in weekly individual counseling sessions for the first 4 weeks, followed by small group counseling sessions every other week for the next 5 months (a total of 10 sessions) and monthly for the last 6 months of the intervention. Staff provided a single set of instructions that were not altered over the course of the study. Two 24-hour dietary recalls were obtained from participants at baseline and 3, 6, and 12 months to characterize and monitor individual dietary intake of macronutrients. A detailed medical history that included assessment of hypertension, diabetes, CVD, medication use, and health behaviors (smoking habits, alcohol use, and physical activity) was obtained at the screening visit. The power assessment for the primary end point (body weight) was based on data abstracted from trials similar to this one (4, 14-16). Data on baseline characteristics of study participants were expressed as means (SDs) or numbers (percentages). The study was funded by the National Center for Research Resources of the National Institutes of Health. Dietary composition data for participants who remained on each diet and also provided 24-hour recalls are summarized in Table 2.
Weight loss from baseline values was greater in the low-carbohydrate group than in the low-fat group at 3, 6, and 12 months (Table 3). At 12 months, serum levels of total and LDL cholesterol had not significantly changed among participants in either group. Participants in the low-carbohydrate group had significant decreases in estimated 10-year risk for CHD at 6 and 12 months, whereas those in the low-fat group did not (Table 3 and Appendix Figure).
Results of sensitivity analyses using multiple imputation techniques to impute missing values were consistent with those presented in our primary analyses. Our results with regard to body weight are consistent with those of other trials (23-24) and a recent meta-analysis (25). In summary, this 12-month randomized, parallel-group trial showed that a low-carbohydrate diet resulted in greater weight loss and reduction in cardiovascular risk factors than a low-fat diet among obese black and white adults.
Early work with lectins clearly showed that the brains of schizophrenics bind lectins differently than the brain tissue of non-schizophrenics, which appears to make sense in that the carbohydrate content of schizophrenic brain tissue (in addition to dementia and a few other illnesses) revealed the existence of spherical deposits in the inner and middle molecular layers of the dentate gyrus in the hippocampal formation which contained fucose, galactose, n-acetyl galactosamine, n-acetyl glucosamine, sialic acid, mannose and chondroitin sulfate; many of these blood group active carbohydrates with known lectin binding affinities (link). We report the unexpected resolution of longstanding schizophrenic symptoms after starting a low-carbohydrate, ketogenic diet. I don’t suffer from schizophrenia, but I can tell you that bread is definitely bad for my head.

Compared with a low-fat diet, a low-carbohydrate diet resulted in greater improvements in body composition, HDL cholesterol level, ratio of total-HDL cholesterol, triglyceride level, CRP level, and estimated 10-year CHD risk. This finding is consistent with at least 1 previous study (23) but not others that had small sample sizes or high rates of loss to follow-up (20-21). In contrast, a recent meta-analysis showed that both low-fat and low-carbohydrate diets reduced LDL cholesterol levels, although the reduction was less for persons assigned to low-carbohydrate diets (25). In our study, participants on the low-carbohydrate diet had greater decreases in CRP levels (inflammation marker) than those on the low-fat diet. Although it was not a prespecified outcome in our study, we prospectively collected data needed to calculate it.
Prospective cohort studies have produced conflicting results regarding the association between low-carbohydrate dietary patterns and risk for CVD (2-3). After randomization, 73 participants were assigned to the low-fat diet group and 75 were assigned to the low-carbohydrate diet group. Individual sessions generally lasted about 1 hour and included dietary instruction and supportive counseling.
One recall reflected consumption on a weekday, and the other reflected consumption on a weekend day. We collected anthropometric measures, blood pressure, and blood and urine samples at the screening visit, randomization, and each follow-up visit.
Assuming a 2-sided significance level of 0.05, we needed 55 participants per group to provide 80% power to detect differences in weight change of at least 3% (SD, 5%) between the groups.
Eleven participants (5 in the low-fat group and 6 in the low-carbohydrate group) declined to have their body weight measured at randomization and were not included in the analysis of our primary outcome.
We performed sensitivity analyses to assess the robustness of our conclusions and departures from the MAR assumption. At baseline, reported dietary composition in the low-fat group was similar to that in the low-carbohydrate group. Systolic and diastolic blood pressures did not significantly decrease among participants in either group, and mean differences in change between the groups were also not significant at 12 months.
The number of participants who had symptoms, including constipation, fatigue, thirst, polyuria, diarrhea, heartburn, gas, nausea, vomiting, appetite changes, or headache, did not differ significantly between the low-carbohydrate and low-fat groups, except significantly more participants on the low-fat diet reported headaches at 3 months (18 [25%] vs. In contrast, our study tested the effects of a typical low-carbohydrate diet, had a high completion rate (approximately 80%) over 12 months of follow-up, and included a substantial sample of black persons (a group underrepresented in previous trials). In our study, participants on the low-carbohydrate diet had greater decreases in CRP levels than those on the low-fat diet. First, self-reported dietary information may be subject to memory and recall issues, and participants who complete the dietary recall may be more likely to report adhering to the interventions. All data were collected by trained and certified staff using rigorous quality control protocols. Restricting carbohydrate may be an option for persons who are seeking to lose weight and reduce cardiovascular risk factors and should be studied further. Because CVD is the most common cause of death in the United States and obesity is a particularly prevalent risk factor, our study has important clinical and public health implications. Brinkworth and colleagues (19) reported a nonsignificant difference in Framingham risk score between a modified Atkins-style low-carbohydrate diet and a low-fat diet among 118 participants with abdominal obesity and other metabolic syndrome components.
Few randomized, controlled trials thus far have examined the effects of carbohydrate restriction on CVD risk factors in a diverse population with a significant proportion of black persons.
We used t tests or chi-square tests to compare baseline characteristics between the groups. We used Markov-chain Monte Carlo techniques to impute missing values, including additional covariates (age, sex, race, marital status, education, and employment status), in the model to make the MAR assumption more plausible (18). Although 2 trials have examined cardiovascular effects in samples with a majority of black persons, they included only diabetic patients or those with severe obesity, most of whom (83%) also had type 2 diabetes or the metabolic syndrome (4-5). Two previous studies that examined CRP levels found no difference between the diets (19, 29); however, both had relatively small sample sizes and may have been underpowered. However, we collected these within 24 hours of consumption and used multiple 24-hour dietary recalls to reflect weekday and weekend eating patterns.
In contrast, in our study, participants randomly assigned to the low-carbohydrate diet had greater decreases in 10-year CHD risk score than those assigned to the low-fat diet; however, the overall level of risk was low in our sample (about 4% over 10 years at baseline).

The few that have either did not assess a typical low-carbohydrate diet or included severely obese participants, most of whom had type 2 diabetes or the metabolic syndrome (4-6). We recruited, enrolled, and followed participants and collected data and specimens from 2008 through 2011 at the Tulane University Health Sciences Center in New Orleans, Louisiana.
We calculated dietary nutrient intakes using the food composition tables of the Nutrition Data System for Research (10). We measured body composition using whole-body bioelectrical impedance analysis (RJL Systems) while the participant was in a supine position.
The POUNDS LOST (Preventing Overweight Using Novel Dietary Strategies) study, which examined the effects of 4 diets with different macronutrient compositions, included a substantial number of black persons but did not test a typical low-carbohydrate diet. In addition, this study had high rates of dietary adherence, as shown by 24-hour recall and urinary ketone levels (31).
We measured blood pressure 3 times with a mercury sphygmomanometer using procedures recommended by the American Heart Association (11). We used a random-effects linear model that was fitted to continuous outcomes (primary and secondary).
In POUNDS LOST, participants on the low-carbohydrate diet (which was high in protein and fat) aimed for 35% of daily energy intake from carbohydrate and achieved approximately 43%.
To avoid potential differences in dietary counseling due to this, we used specific and detailed scripts for all counseling sessions and trained staff to deliver the scripts without deviation. The proportion of participants with detectable urinary ketone levels was significantly higher in the low-carbohydrate group than in the low-fat group at 3, 6, and 12 months (data not shown). These different findings may be due to different population characteristics or completion rates (roughly 80% in our study vs.
The systolic and diastolic blood pressures were recorded as the first and fifth Korotkoff sounds, respectively. Each random-effects model consisted of a random intercept and a random slope to adjust for the within-participant correlation among the observed longitudinal data. Typical low-carbohydrate diets for weight loss restrict carbohydrate to less than 20% of daily energy intake (6). Dietary sessions for both groups were intermittently observed for consistency by an independent registered dietitian consultant who was not a regular part of the study staff, and all outcome assessors were blinded to the diet group assignment. Finally, our study included a substantial proportion of black participants, a group underrepresented in previous trials. To examine the change in each study end point, we included an indicator variable in the model for time (3, 6, and 12 months), diet group, an interaction term for diet group by time, and baseline level of the corresponding end point. Over 12 months, participants in the low-carbohydrate group in our study achieved an average of 30% of daily energy from carbohydrate. Third, conclusions from our study are limited by the lack of CVD clinical end points; however, we assessed CVD risk factors extensively. We assayed serum total cholesterol, high-density lipoprotein (HDL) cholesterol, and triglyceride levels according to procedures recommended by the National Heart, Lung, and Blood Institute and the Centers for Disease Control and Prevention (12). In a post hoc analysis, we also examined the estimated 10-year risk for coronary heart disease (CHD) by Framingham risk score between groups (17). Low-density lipoprotein (LDL) cholesterol level was calculated using the Friedewald formula (13). We measured plasma glucose, serum creatinine, and high-sensitivity C-reactive protein (CRP) levels using standard methods. We calculated physical activity as the sum of hours of moderate to vigorous activities per week (walking, sports, dance, and conditioning) multiplied by each activity's individual metabolic equivalent value.
Urinary ketone levels were measured by dipstick at each behavioral session attended and each clinic visit for data collection.

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