L.S. is a 52-year-old Caucasian woman who was diagnosed with type 2 diabetes in 1988. She developed hypertriglyceridemia 3 years later and hypertension 9 years later. Other medical problems include obesity and diverticulosis. She presents now for screening to determine eligibility for a clinical research protocol using once-daily insulin.
Physical exam reveals a height of 64 inches, a weight of 181 lb, a body mass index of 31 kg/m2, and a waist circumference of 40 inches. Blood pressure, well controlled on 20 mg lisinopril (Prinivil) daily, is 104/70 mmHg.
Laboratory results reveal a fasting lipid panel as follows: total cholesterol 214 mg/dl, triglycerides 940 mg/dl, direct HDL cholesterol 24 mg/dl, an invalid LDL cholesterol unobtainable because of the hypertriglyceridemia, and a free fatty acid of 1.1 mEq/l (normal range 0.1–0.6 mEq/l). Hemoglobin A1c (A1C) is 9.5%, and fasting blood glucose (FBG) is 304 mg/dl. When called to discuss the finding of severe hypertriglyceridema, the patient commented that she had previously had fasting triglycerides as high as 3,000 mg/dl.
L.S. is currently taking metformin (Glucophage), 1,000 mg twice daily, and glipizide (Glucatrol XL), 10 mg twice daily, to control her blood glucose. She is also on gemfibrizol (Lopid), 600 mg twice daily, for hypertriglyceridemia and estradiol (Estraderm) for menopause (topical estrogen does not induce hypertriglyceridemia).
What nutritional modification would be effective in rapidly lowering serum triglycerides when the patient is at risk of pancreatitis?
What treatment strategies can be employed to lower triglycerides, and how effective are they?
How can nutritional modifications improve insulin resistance?
Type 2 diabetes carries a two- to fourfold excess risk of coronary heart disease. The most common pattern of dyslipidemia in patients with type 2 diabetes is elevated triglycerides and decreased HDL levels.1 Although coexistent increases in small, dense LDL cholesterol particles—not the triglycerides themselves—may be responsible for the increase in cardiovascular risk, hypertriglyceridemia poses a significant burden on society.2
In type 2 diabetes, characterized by insulin resistance and insulin deficiency, the pathophysiology of hypertriglyceridemia is an increased hepatic production of triglycerides as well as a decreased lipoprotein lipase activity leading to slower breakdown of VLDL cholesterol and chylomicrons.3 The American Diabetes Association (ADA) Clinical Practice Recommendations list serum triglycerides ≥400 mg/dl and an HDL level <45 mg/dl for women as indicative of high risk of coronary heart disease.1
By both ADA and National Cholesterol Education Program (NCEP III) guidelines, the first goal for this patient is to lower triglycerides to prevent pancreatitis, which not only can result in hospitalization, but also is potentially lethal.4 Although L.S. is already on the maximum dose of gemfibrozil, her triglycerides are still inadequately controlled.
With triglycerides in this range, she should be alerted immediately to the fact that any alcohol, even that found in over-the-counter cold remedies can trigger pancreatitis until her serum triglycerides are brought down to a safer range (<500 mg/dl). In addition, a single high-fat meal can also trigger pancreatitis.
A severely restricted fat intake (<10% of daily kcal) can effectively bring down serum triglycerides by 20% per day until triglycerides are <500 mg/dl. A diet in which fat is so severely restricted usually brings about weight loss as well. A loss of 2.5 kg body weight would bring an expected 15–20% decrease in serum triglycerides. In addition, aerobic exercise can help to lower serum triglycerides by 10–15%.2
Interventions to further decrease serum triglycerides to <200 mg/dl, increase HDL to 45 mg/dl, and decrease LDL to <100 mg/dl should be attempted to decrease the risk of coronary heart disease.
At the first clinic visit, L.S. was advised of the risk of pancreatitis and advised to forego any alcohol and to adhere to severe fat restriction until she has a fasting serum triglyceride level <400 mg/dl. She and her husband are both from the South, and their traditional Southern fare used quite a bit of salt pork, which deleteriously augmented the saturated as well as total fat in her diet. She had been advised to “watch her weight” when her triglycerides were in the 3,000 mg/dl range, but she had been unable to follow that recommendation.
Between clinic visits, L.S. was given written information about a low-fat (10% of kcal) diet, including lists of foods to restrict and foods to encourage until a more thorough meal plan could be developed based on an assessment of her previous dietary patterns. She was advised that this was a short-term, severe dietary change. She had already instituted an exercise program, walking for 1 hour, five times a week regularly.
Two weeks later, when L.S. returned to clinic after following the suggested fat restriction, her lab results showed the following lipid profile: serum total cholesterol 193 mg/dl, serum triglycerides 355 mg/dl, direct HDL cholesterol 32 mg/dl, and LDL cholesterol 90 mg/dl. Her A1C had dropped to 8.8% with no change in therapy for her diabetes, and her FBG was 158 mg/dl. Her fasting free fatty acid level was 0.7 mEq/l. Her weight had dropped by 3 lb.
At this visit, medical nutrition therapy (MNT) was initiated, and the patient was put on 10 units of 75/25 insulin before dinner.
Six weeks later, her A1C had dropped further, to 7%, her FBG was 110 mg/dl, and her weight was down another 2 lb. Her lipid profile was as follows: total cholesterol 181 mg/dl, triglycerides 299 mg/dl, direct HDL cholesterol 32 mg/dl, and LDL cholesterol 89 mg/dl. Her fasting free fatty acid level was now 0.6 mEq/l, the upper level of normal. Meal plan records showed that she was consuming ∼1,500 kcal/day and getting ∼25% of daily kcal from fat.
Commonly, controlling hyperglycemia leads to a decrease in triglycerides.1 However, in this patient, the clearing of serum triglycerides, the restricted saturated fat, and the weight loss had a substantial impact on improving glucose tolerance without adding further diabetes oral agents. Studies have shown that dietary fat, primarily saturated fat, has adverse effects on insulin sensitivity.5 Restricting fat intake, especially saturated fat, resulted in a better metabolic profile in regard to both glucose tolerance and fasting serum triglycerides.
Lifestyle changes had been recommended previously; why was L.S. successful this time when she hadn’t been before? The patient offered the following comments when asked this question.
“I was handed written information, but concern about the numbers (hypertriglyceridemia) was never conveyed.”
“They tell you what you need to do, but not how or why to do it.”
“No one sat down and talked with me. I never received individualized attention.”
“If my triglycerides were potentially harmful, why did they not see me sooner than 3 months? Three months was the usual time between visits and again they conveyed no concern.”
In previous attempts to encourage this patient make lifestyle changes, the compliance approach was used, but the benefits of self-care, the costs of not complying, the susceptibility to pancreatitis and cardiovascular disease, and the severity of such elevated triglycerides were not conveyed. A referral to an educator, time spent in assessing eating patterns and teaching alternatives, and more frequent visits or follow-up serve to convey the importance of recommended lifestyle changes. MNT coupled with an empowerment approach through which patients are the primary decision makers is important.
Although lifestyle changes are always recommended as first-line therapy, the approach to helping patients achieve these lifestyle changes in busy office practices is too often insufficient. A new Medicare benefit effective January 2002 allows patients with diabetes access to insurance coverage for MNT. Evidence-based research shows that MNT provided by a registered dietitian experienced in the management of diabetes is clinically effective.6
Reducing dietary fat improves body weight, which in turn improves glucose tolerance and hypertriglyceridemia.7–9
There is evidence that saturated fat may elevate plasma glucose by way of increasing insulin resistance.
MNT for hypertriglyceridemia may be divided into three parts:
1. When fasting triglycerides are ≥1,000 mg/dl, restrict dietary fat to 10% of kcal until fasting triglycerides fall to <500 mg/dl.
2. For fasting triglycerides between 1,000 and 500 mg/dl, a) reduce saturated fat to <7% of energy and dietary cholesterol to 200 mg/day; b) increase viscous (soluble) fiber to 10–25 mg/day; c) encourage modest weight loss (5–7% of body weight); and d) increase physical activity.10 Monounsaturated fats or carbohydrates can be used to substitute for the decrease in saturated fats.
3. For fasting triglycerides <500 mg/dl, encourage weight loss and a decrease in simple sugars in addition to the above reduction in saturated fat.
Deborah Thomas-Dobersen, RD, MS, CDE, is a professional research assistant and certified diabetes educator in the Endocrinology Department of the University of Colorado Health Sciences Center in Aurora.