It is possible that this mood stability is due to steadier blood sugar in the LCK group, as blood sugar variability has been found to be related to poor mood. Other mood effects did not seem to show statistically significant differences or even clear trends, between groups. Both groups were less likely to eat when upset, which may be related to the psychological tools to support behavior change that both groups received. There are several important limitations of our study. An important limitation is that this trial was designed with primary outcomes at 3 months, although we aim to continue follow-up to 12 months. Larger scale trials with longer-term follow-up are clearly needed to better address 
the long-term feasibility of follow a low carbohydrate diet for type 2 diabetes, as well better establishing the long-term outcomes and possible adverse effects. We did not stratify randomization by sex. Due to chance, about 56% of the LCK group was female compared to 89% of the MCCR group. This could possibly have affected our results, but adjustments for sex did not dramatically alter our primary outcome. We included both individuals receiving diabetes medications or not on medication, but we excluded people taking insulin, so our results may not extend to individuals using insulin. We included a small group of individuals with prediabetes. While we believe that extending the results to persons with prediabetes requires further study due to the small numbers studied, the inclusion of persons with prediabetes likely made it more difficult to detect a difference in HbA1c between diet groups because we included individuals with more limited room for improvement than individuals with frank type 2 diabetes. Finally, as in most similar studies, we collected dietary intake data before and after randomization to the two diet groups. While we and our participants made an earnest effort to collect these data, there is a rich literature indicating that there are important inaccuracies this data that limit our ability to relate specific changes in self-reported diet content to outcomes. While our diet data are reported in Table 2, at least 20% of daily energy intake is ”missing” at baseline. It is well established that the typical ambulatory adult expends between 30–35 kcal per kg daily. Our participants at baseline should thus have required 3000–3500 kcal daily to be in energy balance, yet they reported 2200–2400 kcal of daily intake. Furthermore, at 3 months our subjects reported daily energy deficits of about 700 kcal per day, whereas their weight losses reflected a substantially smaller energy Paclitaxel Microtubule inhibitor deficit. We thus believe the dietary intake data are likely to reflect in part what participants understood we wanted to hear. Due to concerns about reporting bias in a study in which the subjects knew that we were NSC-718781 inquirer contrasting carbohydrate intakes, we did not try to assess a quantitative relationship between selfreported dietary carbohydrate intake and outcomes such as weight loss. Despite these limitations, our data suggest that, in overweight and obese individuals with type 2 diabetes, a very low carbohydrate, high fat, non calorie-restricted diet may be more effective at improving blood glucose control than a medium carbohydrate, low fat, calorie-restricted, carbohydrate counting diet that remains the standard for most diabetes education efforts.