Sherman 1

Alana Sherman
Dr. Davidson
NTD 615 Case #1

Introduction: Ms. R has been diagnosed with metabolic syndrome as well as

prediabetes. Metabolic syndrome is defined as a group of cardiometabolic risk factors
that predisposes an individual to developing coronary heart disease (CHD),
cardiovascular disease (CVD), or diabetes. In 2012, 34.7% of individuals ages 20 years
and older in the United States met diagnostic criteria for metabolic syndrome (National
Institutes of Health [NIH], 2016).
Prediabetes affects 79 million people worldwide and half of adults 65 years and
older. 11% of individuals with prediabetes will develop Type 2 Diabetes Mellitus
(T2DM) if no treatment is sought (Bergman, 2013). The diagnostic criteria for
prediabetes includes: impaired fasting glucose, impaired glucose tolerance, and elevated
HbA1c levels (Parker, Byham-Gray, Denmark, & Winkle, 2014). Impaired fasting
glucose and/or impaired glucose tolerance will be seen in patients with prediabetes. In
impaired glucose tolerance (IGT), there is a deficit in late phase insulin and delayed first
phase insulin. In other words, when glucose levels begin to rise, insulin production is
lagging behind. In IGT, moderate to severe muscle insulin resistance occurs, but
individuals will have normal hepatic insulin sensitivity. Therefore, the liver does not
overproduce insulin from gluconeogenesis. In comparison, impaired fasting glucose
(IFG) involves delayed first phase insulin but muscle insulin resistance is not seen.
However, hepatic insulin resistance occurs where the liver overproduces glucose during
sleep (Davidson, 2016).
Metabolic syndrome and prediabetes overlap in that they have similar
pathogeneses. Both conditions lead to oxidative stress, inflammation, and vascular
changes. Dyslipidemia and insulin resistance subsequently occur in both metabolic
syndrome and prediabetes (Ross, Caballero, Cousins, Tucker, & Ziegler, 2014). Similar
to prediabetes, the pathogenesis of metabolic syndrome also involves impaired utilization
of insulin. This impaired utilization leads to vascular changes, oxidative stress, and
metabolic abnormalities seen prior to the development of diabetes and other
cardiometabolic complications (Davidson, 2016).
Ms. R’s strong family history of diabetes and poor glucose control, her sedentary
lifestyle, as well as her ethnic background, all are contributing factors to her current
diagnosis. Metabolic syndrome affects 37.4% of non-Hispanic Whites and 34% of
individuals between the ages of 40 and 59, further increasing her risk of developing the
conditions she is experiencing (Aguilar, Bhuket, Torres, Liu, & Wong, 2015).
Furthermore, her recent abdominal weight gain, diet high in refined carbohydrates, and
increased cravings for sweets, all indicate the presence of insulin resistance which
underlies both prediabetes and metabolic syndrome.

Symptoms/Problems/Diagnosis:. Ms. R has hypertension with BP at 150/88 Hg/mm;

abdominal obesity with a high waist circumference at 42 inches and BMI of 34;
dyslipidemia with elevated TG at 350mg/dL; low HDL at 30 mg/dL; and total cholesterol
of 300 mg/dL. Ms. R also has elevated blood glucose (135mg/dL) indicative of possible
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progression to T2DM. Her complaints of increased appetite, fatigue, and craving for
sweets all suggest impaired glucose utilization, insulin resistance, and potential T2DM.
Ms. R also meets the diagnostic criteria for metabolic syndrome presenting all five of the
risk factors associated with the disease.

Evidence Based Treatment Plan: The Registered Dietitian Nutritionist (RDN)

recommended that Ms. R follow a calorie-restricted diet of around 1,000kcals per day.
She also recommended that Ms. R increase her physical activity through daily walking
and lose weight to manage her symptoms and prevent future need for medication. The
dietitian’s caloric recommendations are extremely low. Obese adults should consume 16-
20kcals/kg (Nahikian-Nelms, 2011). Ms. R should therefore consume between 1,527-
1,909 kcals/day. Her current caloric recommendations are too low and not feasible to
follow, especially when Ms. R is experiencing difficulty controlling her hunger and
increased appetite.
Ms. R should instead follow a moderate fat diet, rich in monounsaturated fatty
acids (MUFAs). Moderate fat diets have been found to increase HDL-C levels and
decrease triacylglycerol (TAG) levels in patients with metabolic syndrome and diabetes
mellitus (DM) (Gillingham, Harris-Janz, & Jones, 2011). Ms. R can incorporate MUFA
rich foods into her diet such as: extra-virgin olive oil, mixed nuts and seeds (especially
walnuts), avocados and olives. Gillingham et al. found that diets rich in MUFA improve
lipid profiles, regulate blood pressure, and have a favorable effect on insulin sensitivity
and blood glucose levels. In addition, their research revealed that isocalorically replacing
saturated fatty acids with MUFAs decreased LDL-C levels while maintaining HDL-C
levels. In comparison to high carbohydrate diets, which have been shown to decrease
HDL-C levels, moderate fat/ MUFA rich diets increased HDL-C levels and decreased
TAG levels, as well as worked to prevent central adiposity through increasing fat
oxidation rates (Gillingham et al., 2011). As a result, it is recommended that Ms. R
consume a moderate fat diet with an emphasis on consuming foods with high content of
MUFAs.
Secondly, Ms. R should increase her fiber intake to around 30g per day. Ning,
Van Horn, Shay, and Lloyd-Jones (2014) found that increased dietary fiber consumption
is related to favorable cardiometabolic outcomes including improved waist
circumference, dyslipidemia, hypertension, reduced inflammation, and improved insulin
utilization (Ning et al., 2014). These positive outcomes occur due to the nature and
mechanisms of soluble and insoluble fiber. Soluble fiber binds to bile acids, and once
bonded, can be removed by the body. The body then compensates by utilizing more
cholesterol in order to synthesize bile acids, therefore decreasing the serum cholesterol
levels (Ning et al., 2014). Ms. R can increase her dietary intake of fiber by consuming:
brown rice instead of white rice, split peas, lentils, and black beans, vegetables such as
artichokes, green peas, broccoli, carrots, and baked potatoes with the skin (rather than
fried potatoes). She can also add raspberries or apples to her daily smoothie for additional
added fiber. By following these recommendations, Ms. R can improve the metabolic
abnormalities that identify with her diagnosis of metabolic syndrome and prediabetes to
reduce her risk of developing CVD, CHD, T2DM, and other related complications.
 Sherman 3

References

Aguilar, M., Bhuket, T., Torres, S., Liu, B., & Wong, R. J. (2015). Prevalence of the
metabolic syndrome in the United States, 2003-2012. JAMA, 313(19), 1973-1974.
doi:10.1001/jama.2015.4260

Bergman, M. (2013). Inadequacies of current approaches to prediabetes and diabetes

prevention. Endocrine, 44(3), 623-633. doi:10.1007/s12020-013-0017-9

Davidson, P. (n.d.). Prediabetes and Metabolic Syndrome. Lecture. Retrieved October 14,
2016, from https://d2l.wcupa.edu/d2l/le/content/2106503/viewContent/13003345/View

Gillingham, L. G., Harris-Janz, S., & Jones, P. J. (2011). Dietary Monounsaturated Fatty
Acids Are Protective Against Metabolic Syndrome and Cardiovascular Disease Risk
Factors. Lipids, 46(3), 209-228. doi:10.1007/s11745-010-3524-y

Nahikian-Nelms, M. (2011). Nutrition therapy and pathophysiology (2nd ed.). Belmont,

CA: Wadsworth, Cengage Learning.

Ning, H., Horn, L. V., Shay, C. M., & Lloyd-Jones, D. M. (2014). Associations of
Dietary Fiber Intake With Long-Term Predicted Cardiovascular Disease Risk and C-
Reactive Protein Levels (from the National Health and Nutrition Examination Survey
Data [2005–2010]). The American Journal of Cardiology, 113(2), 287-291.
doi:10.1016/j.amjcard.2013.09.020

Parker, A. R., Byham-Gray, L., Denmark, R., & Winkle, P. J. (2014). The Effect of
Medical Nutrition Therapy by a Registered Dietitian Nutritionist in Patients with
Prediabetes Participating in a Randomized Controlled Clinical Research Trial. Journal of
the Academy of Nutrition and Dietetics, 114(11), 1739-1748.
doi:10.1016/j.jand.2014.07.020

Ross, A. C., Caballero, B., Cousins, R. J., Tucker, K. L., & Ziegler, T. R. (2014). Modern
nutrition in health and disease / editors, A. Catharine Ross ... (11th ed.). Philadelphia:
Wolters Kluwer Health/Lippincott Williams & Wilkins.

What Is Metabolic Syndrome? - NHLBI, NIH. (2016, June 22). Retrieved October 01,
2016, from http://www.nhlbi.nih.gov/health/health-topics/topics/ms