Effects of Almond Intake on Atherogenic Dyslipidemia of the Metabolic Syndrome
Status: | Completed |
---|---|
Conditions: | High Cholesterol, Endocrine, Metabolic |
Therapuetic Areas: | Cardiology / Vascular Diseases, Endocrinology, Pharmacology / Toxicology |
Healthy: | No |
Age Range: | 20 - Any |
Updated: | 8/3/2016 |
Start Date: | April 2013 |
End Date: | April 2016 |
Metabolic syndrome includes a cluster of cardiovascular disease (CVD) risk factors including
insulin resistance, abdominal obesity, high blood pressure and an atherogenic lipoprotein
phenotype characterized by increased plasma triglycerides, low HDL-C, and increased levels
of small LDL particles. While lifestyle intervention remains the cornerstone for its
management, the optimal dietary macronutrient distribution for improving blood lipids and
CVD risk remains a topic of controversy. While both low carbohydrate diets and weight
reduction are effective for managing atherogenic dyslipidemia, long-term compliance is low,
and it becomes imperative to identify alternative dietary approaches.
Increased consumption of almonds has been shown to lower LDL-C, an effect that exceeds that
predicted from changes in fatty acid intake. However, although LDL-C lowering by almonds has
been demonstrated in patients with diabetes, there have been no trials in non-diabetic
patients with metabolic syndrome. Moreover, there is limited information of the effects of
almond intake on LDL particle subclasses.
The overall objective of the present study is to determine whether lipoprotein measures of
CVD risk in individuals with the metabolic syndrome are reduced by almond supplementation in
a diet with overall macronutrient content that conforms to current guidelines. Our main
hypothesis is that in these individuals, almond consumption can reduce levels of small and
medium LDL particles without the need to restrict dietary carbohydrates to levels below
those currently recommended.
This hypothesis will be tested by comparing the lipoprotein effects of an
almond-supplemented diet (20%E) with those of two reference diets that do not contain almond
products: one with similar content of carbohydrate, protein, and fat (standard reference),
and the other in which carbohydrate content is reduced by substitution of protein and
monounsaturated fat (low-carbohydrate reference).
We will provide the diets for 3 weeks each in a randomized 3-period crossover design to 40
individuals with atherogenic dyslipidemia of the metabolic syndrome. We will test whether
the almond supplemented diet will result in lower levels of lipoprotein measures of CVD
risk, specifically LDL-C and small and medium LDL particles, compared to either the standard
or low-carbohydrate reference diets.
insulin resistance, abdominal obesity, high blood pressure and an atherogenic lipoprotein
phenotype characterized by increased plasma triglycerides, low HDL-C, and increased levels
of small LDL particles. While lifestyle intervention remains the cornerstone for its
management, the optimal dietary macronutrient distribution for improving blood lipids and
CVD risk remains a topic of controversy. While both low carbohydrate diets and weight
reduction are effective for managing atherogenic dyslipidemia, long-term compliance is low,
and it becomes imperative to identify alternative dietary approaches.
Increased consumption of almonds has been shown to lower LDL-C, an effect that exceeds that
predicted from changes in fatty acid intake. However, although LDL-C lowering by almonds has
been demonstrated in patients with diabetes, there have been no trials in non-diabetic
patients with metabolic syndrome. Moreover, there is limited information of the effects of
almond intake on LDL particle subclasses.
The overall objective of the present study is to determine whether lipoprotein measures of
CVD risk in individuals with the metabolic syndrome are reduced by almond supplementation in
a diet with overall macronutrient content that conforms to current guidelines. Our main
hypothesis is that in these individuals, almond consumption can reduce levels of small and
medium LDL particles without the need to restrict dietary carbohydrates to levels below
those currently recommended.
This hypothesis will be tested by comparing the lipoprotein effects of an
almond-supplemented diet (20%E) with those of two reference diets that do not contain almond
products: one with similar content of carbohydrate, protein, and fat (standard reference),
and the other in which carbohydrate content is reduced by substitution of protein and
monounsaturated fat (low-carbohydrate reference).
We will provide the diets for 3 weeks each in a randomized 3-period crossover design to 40
individuals with atherogenic dyslipidemia of the metabolic syndrome. We will test whether
the almond supplemented diet will result in lower levels of lipoprotein measures of CVD
risk, specifically LDL-C and small and medium LDL particles, compared to either the standard
or low-carbohydrate reference diets.
Inclusion Criteria:
- Age 20 or older
- Plasma triglycerides ≥ 150mg/dL and plasma HDL-C < 40 mg/dL (men) or < 50 mg/dL
(women) and at least one additional metabolic syndrome criteria: waist circumference
> 102 cm (men) or > 88 cm (women), blood pressure ≥ 130/≥ 85 mmHg, or fasting glucose
≥ 110mg/dL.
- Fasting blood sugar (FBS) < 126 mg/dl
- Weight stable for > 3 months.
Exclusion Criteria:
- History of coronary heart disease, cerebrovascular disease, peripheral vascular
disease, bleeding disorder, liver or renal disease, diabetes, lung disease, HIV, or
cancer (other than skin cancer) in the last 5 years.
- Taking hormones or drugs known to affect lipid metabolism or blood pressure.
- Systolic blood pressure > 160 mm Hg and diastolic blood pressure > 95 mm Hg.
- Body mass index (BMI) > 35 kg/m2
- User of nicotine products or recreational drugs
- Refusal to abstain from alcohol or dietary supplements during the study.
- Total- and LDL-C > 95th percentile for sex and age.
- Fasting triglycerides > 500 mg/dl
- Abnormal thyroid stimulating hormone (TSH) levels.
- Pregnant or breast-feeding
We found this trial at
1
site
Berkeley, California 94705
Principal Investigator: Ronald M Krauss, MD
Phone: 510-665-0500
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