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Published on: September 9, 2012
The Type and Amount of Dietary Fat Affect Plasma Factor VIIc, Fibrinogen, and PAI-1 in Healthy Individuals and
Penny M Kris-Etherton1, Paul W Stewart2, Henry N Ginsberg3
1Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA, USA.
Insights
Replacing saturated fats with carbohydrates or monounsaturated fats (MUFAs) had mixed effects on cardiovascular disease (CVD) risk factors like factor VIIc and fibrinogen. The impact on plasminogen activator inhibitor 1 (PAI-1) varied, suggesting uncertain cardiometabolic risk reduction.
Area of Science:
- Cardiovascular disease research
- Nutritional science
- Thrombosis and hemostasis
Background:
- Factor VIIc, fibrinogen, and PAI-1 are key cardiovascular disease (CVD) risk factors.
- Dietary fat type and amount influence these hemostatic factors.
- Understanding these modulations is crucial for CVD risk assessment.
Purpose of the Study:
- To evaluate the effects of substituting saturated fatty acids (SFAs) with carbohydrates or monounsaturated fatty acids (MUFAs) on CVD risk factors.
- Primary outcomes included changes in factor VIIc, fibrinogen, and plasminogen activator inhibitor 1 (PAI-1).
Main Methods:
- Two controlled crossover feeding studies (DELTA Trial) were conducted.
- Study 1: Healthy participants (n=103) consumed diets varying in SFA content.
- Study 2: Participants at risk for CVD/metabolic syndrome (n=85) consumed diets varying in SFA and MUFA content.
Main Results:
- Replacing SFAs with carbohydrates or MUFAs decreased factor VIIc and increased fibrinogen in both healthy and metabolically unhealthy individuals.
- PAI-1 increased in healthy subjects on carbohydrate-rich diets but showed less consistent changes in Study 2.
- Overall, observed changes in hemostatic factors were small, with differing responses.
Conclusions:
- Replacing SFAs with carbohydrates or MUFAs yields uncertain effects on cardiometabolic risk due to modest changes in hemostatic factors.
- Dietary fat modification strategies require careful consideration of individual responses and overall health impact.
- Further research is needed to clarify the long-term implications of these dietary changes on CVD risk.
Background:
Factor VIIc, fibrinogen, and plasminogen activator inhibitor 1 (PAI-1) are cardiovascular disease (CVD) risk factors and are modulated, in part, by fat type and amount.
Objective:
We evaluated fat type and amount on the primary outcomes: factor VIIc, fibrinogen, and PAI-1.
Methods:
In the Dietary Effects on Lipoproteins and Thrombogenic Activity (DELTA) Trial, 2 controlled crossover feeding studies evaluated substituting carbohydrate or MUFAs for SFAs. Study 1: healthy participants (n = 103) were provided with (8 wk) an average American diet [AAD; designed to provide 37% of energy (%E) as fat, 16% SFA], a Step 1 diet (30%E fat, 9% SFA), and a diet low in SFA (Low-Sat; 26%E fat, 5% SFA). Study 2: participants (n = 85) at risk for CVD and metabolic syndrome (MetSyn) were provided with (7 wk) an AAD, a step 1 diet, and a high-MUFA diet (designed to provide 37%E fat, 8% SFA, 22% MUFA).
Results:
Study 1: compared with AAD, the Step 1 and Low-Sat diets decreased mean factor VIIc by 1.8% and 2.6% (overall P = 0.0001), increased mean fibrinogen by 1.2% and 2.8% (P = 0.0141), and increased mean square root PAI-1 by 0.0% and 6.0% (P = 0.0037), respectively. Study 2: compared with AAD, the Step 1 and high-MUFA diets decreased mean factor VIIc by 4.1% and 3.2% (overall P < 0.0001), increased mean fibrinogen by 3.9% and 1.5% (P = 0.0083), and increased mean square-root PAI-1 by 2.0% and 5.8% (P = 0.1319), respectively.
Conclusions:
Replacing SFA with carbohydrate decreased factor VIIc and increased fibrinogen in healthy and metabolically unhealthy individuals and also increased PAI-1 in healthy subjects. Replacing SFA with MUFA decreased factor VIIc and increased fibrinogen but less than carbohydrate. Our results indicate an uncertain effect of replacing SFA with carbohydrate or MUFA on cardiometabolic risk because of small changes in hemostatic factors and directionally different responses to decreasing SFA. This trial was registered at https://clinicaltrials.gov/ct2/show/NCT00000538?term=NCT00000538&rank=1 as NCT00000538.
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