Groundbreaking new research has revealed that substituting carbohydrates with protein and fat in the diet can enhance cholesterol profiles for individuals with type 2 diabetes, and this positive impact occurs irrespective of whether weight loss is achieved.
Managing type 2 diabetes (T2D) hinges on adopting a healthier lifestyle, with weight loss often being a central focus. Traditionally, dietary guidelines have leaned towards low-fat, high-carbohydrate regimens. However, emerging data indicates that cutting back on carbohydrate intake might be more beneficial, potentially improving glycemic control and combating diabetic dyslipidemia.
Carbohydrate restriction has shown the ability to normalize levels of triacylglycerol (TAG) and High-density lipoprotein (HDL) cholesterol, though its effect on Low-density lipoprotein (LDL) cholesterol has been inconsistent. It also holds promise in reducing metabolic dysfunction-associated steatotic liver disease (MASLD), yet conclusive evidence has been elusive due to factors like poor adherence and confounding elements such as concurrent weight loss or exercise regimens. Hence, further in-depth research is imperative to delineate the stand-alone effects of carbohydrate curtailment on lipid metabolism.
Two studies, designed as open-label, prospective, randomized controlled trials (RCTs), were carried out at Copenhagen University Hospital Bispebjerg. Their objective was to assess the impact of a carbohydrate-reduced high-protein (CRHP) diet against a conventional diabetes (CD) diet over a six-week period.
The Iso study incorporated a cross-over design, involving 30 participants who maintained a stable weight. In contrast, the Hypo study utilized a parallel-group design with 72 participants aiming for a 6% weight reduction. Both trials received the green light from the local ethics committee and adhered stringently to eligibility benchmarks.
Individuals with T2D, with Hemoglobin A1c (HbA1c) levels ranging from 48 to 97 mmol/mol (6.5–11%), were included. Exclusions were made for those with severe renal disease, anemia, critical illness, or taking certain medications.
The dietary intervention was meticulously planned. The CRHP diet provided meals with 30% of energy (E%) sourced from carbohydrates, 30 E% from protein, and 40 E% from fat. Comparatively, the CD diet had a breakdown of 50 E% carbohydrates, 17 E% protein, and 33 E% fat. All meals were prepared and distributed by the research team to ensure compliance, and participants were instructed to consume only the provided fare. Weight maintenance or loss was overseen according to the study blueprints, while physical activity was kept at habitual levels.
Pre- and post-intervention, blood samples were drawn and lipoprotein profiling was conducted, analyzing parameters like HbA1c, lipid concentrations, and insulin resistance. Intrahepatic triglyceride (IHTG) content was gauged via magnetic resonance spectroscopy. Sophisticated statistical analyses, including linear mixed models, were employed to evaluate diet effects while accounting for body weight fluctuations. Pearson’s analysis was used to explore correlations between changes in IHTG and lipid profiles.
In both investigations, participant retention was remarkably high, with a mere 7% dropping out post-randomization for reasons unrelated to trial outcomes or adverse events. The baseline characteristics of participants in the Iso and Hypo studies were largely comparable, although those in the Hypo study were more obese, had higher fasting insulin concentrations, and exhibited greater insulin resistance. In the Hypo study, baseline traits between dietary groups were balanced, barring a higher proportion of men and participants using dipeptidyl peptidase-4 (DPP-4) inhibitors in the CRHP cohort.
Most participants had well-controlled dyslipidemia, with group mean concentrations of TAG, LDL cholesterol, and HDL cholesterol falling within normal parameters.
In the Iso study, where weight was successfully maintained across both diet groups, the CRHP diet markedly improved lipoprotein profiles compared to the CD diet. It reduced the atherogenic subfractions of TAG-rich lipoproteins (TRL) and LDL5, while augmenting the HDL2/HDL3 ratio – a clear shift towards a less atherogenic lipoprotein makeup.
In the Hypo study, where both groups achieved comparable weight loss, the CRHP diet demonstrated a propensity to reduce TRL. It significantly slashed LDL5, increased the HDL2/HDL3 ratio, and showed a more pronounced improvement in IHTG compared to the CD diet.
Glucometabolic enhancements were noted in both studies. In the Iso study, the CRHP diet outperformed the CD diet in reducing HbA1c, fasting TAG, and IHTG. In the Hypo study, while weight loss alone improved these markers, the CRHP diet amplified the benefits, more effectively reducing HbA1c and circulating TAG. Across both studies, the CRHP diet proved superior in reducing IHTG compared to the CD diet.
Correlations between changes in IHTG and lipid parameters were consistent. In the Iso study, reductions in IHTG were significantly linked to improvements in TAG, TRL, LDL5, and the HDL2/HDL3 ratio. Similar patterns emerged in the Hypo study, where changes in IHTG correlated with reductions in TAG, TRL, and LDL5.
To sum it up, the six-week study established that a CRHP diet could enhance plasma lipoprotein density profiles in T2D patients. Notable changes encompassed reductions in fasting TAG and small-dense LDL5 particles, along with an elevated HDL2/HDL3 ratio when contrasted with a CD diet. These effects were evident during both weight maintenance and loss phases.
Moreover, in the weight-maintenance scenario, the CRHP diet lowered total cholesterol, non-HDL cholesterol, and Apolipoprotein B (ApoB) levels. The improvements were strongly tied to reductions in IHTG, underlining the crucial role of liver fat depletion.
While weight loss in both diet groups bolstered lipid profiles, the CRHP diet proffered additional atheroprotective advantages. This lends credence to its potential as a targeted dietary approach for managing T2D-associated dyslipidemia and metabolic dysfunction.
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