• Users Online: 54
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
Year : 2015  |  Volume : 2  |  Issue : 3  |  Page : 167-176

56-year-old female with type 2 diabetes mellitus

1 Department of Integrative and Functional Medicine, Newtown, CT 06482, USA
2 The Ultra Wellness Center/Institute for Functional Medicine, Lenox, MA, 01240, USA
3 The Kripalu Center for Yoga and Health, Stockbridge, MA 01262, USA

Date of Submission03-Mar-2014
Date of Decision04-Apr-2015
Date of Acceptance08-Jun-2015
Date of Web Publication6-Aug-2015

Correspondence Address:
Kara N Fitzgerald
27 Glen Road, 4th Floor, Newtown, CT 06482
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2347-9906.162352

Rights and Permissions

A 56-year-old female presented with type 2 diabetes (DMII), obesity, hypertension, elevated cholesterol, and sleep apnea. She was taking atorvastatin (Lipitor ® ), glyburide (Micronase ® ), metformin (Glucophage ® ), metoprolol, amlodipine, benazepril (Lotrel ® ), aspirin, and one-a-day multivitamin, and mineral supplement. Lab tests to identify underlying imbalances and to direct treatment were ordered. Treatment included dietary, nutritional, and mind-body support. After nine months of therapy, laboratory data continued to reflect improvement, including a 30-pound weight loss, improvement in blood pressure and fasting blood sugar. A1C normalized as well as liver enzymes, lipids, Vitamins D and B, and mitochondrial markers. The patient's sleep apnea resolved, and she was able to reduce her metformin and eliminate the glyburide and metoprolol. She also began regular exercises. The mentioned comprehensive lifestyle management offered with detailed knowledge and professional skills attenuated DMII mellitus and its co-morbid conditions in this patient. The case report aptly illustrates and emphasis that today's medical fraternity often unduly depends on pharmacological therapy neglecting the nonpharmacological intervention for noncommunicable diseases.

Keywords: Diabetes, hypertension, hyperlipidemia, obesity, sleep apnea

How to cite this article:
Fitzgerald KN, Hyman M, Swift KM. 56-year-old female with type 2 diabetes mellitus. J Obes Metab Res 2015;2:167-76

How to cite this URL:
Fitzgerald KN, Hyman M, Swift KM. 56-year-old female with type 2 diabetes mellitus. J Obes Metab Res [serial online] 2015 [cited 2021 Apr 15];2:167-76. Available from: https://www.jomrjournal.org/text.asp?2015/2/3/167/162352

  Introduction Top

Adiabetic is diagnosed in the U.S. every 20 seconds [1] Diabetes mellitus (DM) is the seventh leading cause of death in the United States, with type II diabetes mellitus (DMII) accounting for 90-95% of all diabetes. Significant comorbidites include heart disease, hypertension, respiratory infection, kidney disease, stroke, retinopathy, neuropathy and dementia, of which all except the last three are among the top ten causes of death in the U.S. These co-morbidities are all linked by common underlying mechanisms. Treating the underlying causes and mechanisms can prevent or reverse most of these "co-morbidities". Pre-diabetes was found in more than 40% of the population between 1988 and 1994, and 7% of all adolescents have been diagnosed with impaired fasting glucose. The estimated annual cost to society of diabetes-related concerns in the U.S. is 218 billion dollars. Hypoglycemic medications, while very important in minimizing diabetic-associated sequelae, have long carried risks. Most recently rosiglitazone (Avandia ® ) was shown to increase risk of myocardial infarction by 43%, [2] which is concerning in any population, but particularly so in a group already vulnerable to cardiovascular (CV) events. Lifestyle intervention has been shown to reduce the incidence of diabetes by 71% in those 60 years of age and older, and by 58% in all adults. Such findings strongly suggest that diabetes, while subject to genetic influence, is primarily a disease of lifestyle choice and increasingly environmental toxicity. [3],[4]

  Case report Top

CK, a 56-year-old female presented to the clinic with type 2 diabetes (DMII), obesity, high blood pressure, elevated cholesterol, and sleep apnea. CK was diagnosed with diabetes in 1999 and was prescribed glyburide and metformin. She did not regularly test her blood sugar, although she did attempt to adhere to a healthy diet, including oatmeal for breakfast, chicken and other lean protein with salads for lunch and dinner. However, she craved sugary foods and consumed much candy and ice cream at night. She generally felt ravenous before lunch and dinner, and experienced nausea, and mood swings when she waited too long to eat. She also had wine with dinner most nights. These habits provided palliation for her high-stress job as a university professor and researcher. CK was diagnosed with hypertension in 1997, for which she took metoprolol and amlodipine/benazepril. She did not monitor her blood pressure levels regularly. She was diagnosed with hyperlipidemia in 2003 for which she took atorvastatin. CK had sleep apnea for years but did not use a CPAP machine. She experienced occasional constipation. She felt well in the mornings, and meditated daily for 15 min but was frequently sleepy after lunch and dinner.

CK's past medical history was unremarkable, with the exception of mononucleosis at age 16.

CK's father died at 55 years of age from a cerebrovascular accident, also had coronary artery disease. CK's father was adopted, and therefore extended paternal family history was unknown. CK's mother died at 70 years of age. She was diagnosed with DMII and heart disease. CK has no siblings. CK's maternal aunts have DMII.

CK did not smoke. She meditated for 15 min each morning. She took one-a-day multivitamin and mineral supplement. She traveled a great deal for work and went out 1-2 nights/week. CK generally did not exercise but did some limited walking during vacations.

CK's significant physical exam findings included a blood pressure of 160/104 (left arm seated) and a heart rate of 94 beats/min. She weighed 190 pounds and was 5'2" tall. Her body mass index (BMI) was 34.7, considered obese, and her waist-to-hip ratio (WHR) was slightly above optimal at 0.89. [Table 1] summarizes the patient data.
Table 1: Case overview

Click here to view

Laboratory tests ordered and rationale

  • Fasting insulin, hemoglobin A1 C , urinalysis*, metabolic panel*, thyroid panel, hs-CRP, and fibrinogen: Comprehensive, standard laboratory assessments for DMII and associated inflammation
  • Lipids, lipoprotein subclasses with lipoprotein (a): Lipid subclass assessment may be a more sensitive predictor of cardiovascular risk in metabolic syndrome than a standard lipid assay. Lp (a) is an independent risk marker for cardiovascular disease that is not responsive to statin therapy [5],[6],[7]
  • Vitamin D: Low levels are associated with increased inflammation and increased incidence of numerous diseases [8]
  • Multi-profile metabolic panel*: A comprehensive assessment including organic acids, fatty acids, amino acids, fat soluble vitamins, essential elements, and oxidative stress markers; assists in detecting individual etiopathogenic factors and in individualizing treatment plans
  • Stool test: Assessment of GI microbial status and GI function. Imbalances may be associated with glycemic regulation and obesity. [9]

Initial assessment

  • Type 2 diabetes
  • Obesity
  • Hypertension
  • Hyperlipidemia
  • Sleep apnea
  • Subclinical fatty liver disease
  • Subclinical hypothyroidism
  • Hypovitaminosis D
  • Mitochondriopathy
  • Oxidative stress
  • Initial plan.

Dietary intervention

Begin low carbohydrate/low glycemic diet. Have protein with each meal. Chew food adequately, eat slowly and allow digestion time. Protein-based snacks in afternoon.

Lifestyle intervention

Increase exercise - begin interval training:

  • Monitor fasting blood sugar and 2 h post prandial blood sugar qd
  • Sleep apnea: Recommend mandibular repositioning appliance and home sleep study.

Nutrient support

  • Nutrients for glucose metabolism (chromium, vanadium, alpha-lipoic acid (ALA), n-acetyl cysteine (NAC), biotin, banaba leaf extract, gymnema sylvestre): 1 packet PO bid
  • Fiber complex (Konjac Mannan, sodium alginate, xanthan gum): 4 capsules before meals with water
  • Medicinal food containing rice protein powder, medium chain triglycerides, vitamins, and minerals specific for hepatic function: 2 scoops QAM (mix/blend with ice, unsweetened soy milk and berries; add 2 TBSP ground flax)
  • Nutrients for mitochondrial support (including: magnesium, CoQ10, creatine, acetyl-carnitine): 1 tablet PO bid
  • Eicosapentaenoic acid/DHA 720 mg: 2 gelcaps PO bid
  • CoQ10 100 mg: 1 tablet PO bid
  • R-alpha lipoic acid (R-ALA) 100 mg: 1 capsule PO qd
  • Cinnamon (Cinnamomi burmannii) extract: 2 capsule PO bid
  • Biotin 8 mg: 1 capsule qd
  • Vitamin D3 10,000 IU daily.


  • One-a-day multivitamin mineral formula.


  • Niacin sustained release 500 mg: 1 tablet qhs.


  • Atorvastatin 10 mg 1 tablet qhs
  • Glyburide 5 mg 1 tablet qd
  • Metformin 500 mg 1 tablet tid
  • Metoprolol 25 mg 1 tablet qd
  • Lotrel 10 mg-20 mg 1 capsule qd
  • Aspirin 81 mg 1 tablet qd.

Follow-up laboratory tests ordered

  • Hemoglobin AIC
  • Fasting blood glucose
  • Urinary microalbumin.

Treatment plan rationale

Intensive dietary intervention was recommended to reduce glycemic load and increase phytonutrient density, in combination with addressing meal timing and frequency. A regular exercise program was initiative to improve insulin sensitivity and increase VO 2 max and mitochondrial number and efficiency. Supplementation of glucose metabolism-supportive nutrients was initiated, including a specifically-designed product with chromium, vanadium, alpha lipoic acid (ALA) and NAC, biotin and botanicals banaba leaf, and gymnema sylvestre. Extra biotin was also given, based on research using higher doses in insulin resistance (IR), and the significant biotin deficiency identified [Figure 1]. [11] All nutrients prescribed have shown efficacy in improving insulin sensitivity in human trials. [1],[11],[12],[13],[14],[15],[16] Additional lipoic acid was also given in the form of R-ALA, which may be more potent than ALA [17] and may therefore be more effective for IR. A fiber complex including Konjac-Mannan (KJM) was initiated. KJM has been shown to improve insulin sensitivity. [18] Fiber is also a demonstrated hypolipidemic agent. [19] KJM may have similar promise. A proprietary rice protein and nutrient-based medicinal food were given. Research suggests this medicinal food benefits hepatic function and was therefore prescribed for the suspected subclinical fatty liver. [20] The medicinal food contains B vitamins and essential elements, both found to be insufficient in this patient [Figure 1] and [Figure 2]. The anti-inflammatory fatty acids EPA and DHA have been shown to reduce the pro-inflammatory fatty acid arachidonic acid, which was found to be elevated [Figure 3]. Both fatty acids also have demonstrated benefit in hypertriglyceridemia. [21] Mitochondrial supportive nutrients, including CoQ10, creatine, carnitine, and magnesium were started based on the organic acid findings [Figure 4] and high lipid peroxide level [Figure 5], which suggested an oxidative stress picture and mitochondriopathy. Niacin has been shown to effectively reduce lipids, including Lp (a), which was found to be very high. Atorvastatin, which CK was taking, has not been shown effective at lowering Lp (a). [22] Vitamin D was given for the identified deficiency [Figure 6]. The multivitamin and mineral formula was stopped because it did not supply enough of the specific nutrients required.
Figure 1. Standard laboratory assessments. Numerous high markers of insulin resistance despite hypoglycemic therapies. Liver enzyme ALT elevation suggested early non-alcoholic fatty liver disease. Thyroid panel result was within normal limits, although the TSH may be suboptimal. Fibrinogen, microalbumin and kidney function test results were within normal limits

Click here to view
Figure 2. Lipid panel with lipoprotein subclasses with Lp (a). Despite a normal lipid panel (on statin), the elevated Lp (a), small particle size of HDL and LDL and increased quantity of LDL particles suggested metabolic syndrome.

Click here to view
Figure 3. Serum vitamin D. Results demonstrated insufficiency

Click here to view
Figure 4. Urinary Organic Acid B vitamin Markers. Beta-Hydroxyiosvalerate is a sensitive and specific biomarker for biotin insufficiency.[10] The two alpha-keto acid elevations have been associated with increased need for thiamin and may also suggest a need for niacin, pantothenic acid, riboflavin and alpha lipoic acid. Methylmalonate, a biomarker for intracellular B12 status, was shown to be within normal limits

Click here to view
Figure 5. Urinary Organic Acid Mitochondrial Markers. Elevated lactate, B-hydroxybutryrate, hydroxymethylglutarate and normal pyruvate were found. The latter finding may be associated with insulin resistance, and the former with and statin use. Together, they suggest mitochondropathy

Click here to view
Figure 6. Omega 3 and 6 fatty acids. Normal omega 3 fatty acids EPA and DHA with high-normal omega 6 fatty acid AA were found

Click here to view

Four-month follow-up

After making dietary changes and taking supplements, CK reported improvement in energy, particularly in the mid-afternoon and evening. Her morning blood sugar average was 90. She noted that her skin was clearer. Protein-based afternoon snacks were very helpful in improving mood, energy, and reducing cravings. The fiber was helping with bowel movements. She was exercising on treadmill 30 min/day on most days. Her weight loss was at 20 lbs. Her sleep apnea resolved without any interventions. She was very pleased with her progress.

CK's diet consisted primarily of organic or cleaner sources of protein (lean meats, fish, eggs, and protein powder), low glycemic snack bars, nuts, seeds, legumes, fresh fruit, vegetables, and some whole grains. When she started the program, she was inspired to clean out her kitchen cabinets of all unhealthy foods. She then stocked up at the natural foods market, buying a greater variety of foods. CK admitted that she followed the diet perfectly for 1-week, and then began to cheat. When she did so, she noticed that certain foods caused symptoms. In particular, she thought that dairy and sugary foods significantly worsened her afternoon fatigue.

She reported that it was difficult to maintain dietary changes when traveling, and noticed that her blood sugar was significantly higher after flying, reaching 180 on a recent trip. CK also confessed to being addicted to buffet foods, and decided to limit eating out.

CK's physical exam findings showed great improvement: Blood pressure: 127/79, left arm seated (previous reading: 160/104); heart rate: 79 beats/min (previous rate: 94); weight 170 lbs (previous weight: 190 lbs); BMI: 32.66 (previously: 34.7); waist-to-hip ratio: 0.86 (previous ratio: 0.89).

  Four-Month follow-up Laboratory Testing Top

  • H Fasting blood glucose 124 mg/dL (RR 65-99; OR ≤ 87 [23] ) (previous level: 312)
  • H Hemoglobin A1 C : 6.4% (0.0-5.9% nondiabetic range) (previous level: 9.9%).

Four-month follow-up plan

Dietary intervention

  • Keep daily food journal included Brassica vegetables at least 3 times/week; daily is best. Examples: Arugula, watercress, cabbage, radish, broccoli sprouts, broccoli, and brussel sprouts
  • 15 min walking if you overeat in a restaurant, followed by blood sugar check

Travel food suggestions:

  • Dehydrated bean hexachlorobenzene, and soups
  • Canned wild salmon (www.vitalchoice.com)
  • Fresh fruit
  • Nuts/Seeds
  • Organic fiber bars
  • Medicinal food: Store individual servings in plastic bags for easy access.

Medications and nutrient therapy:

  • Continue supplements as directed
  • Reduce metformin dosage to 500 mg bid
  • Discontinue glyburide
  • Discontinue metoprolol (has been shown to raise blood glucose [24] )
  • Continue to monitor blood sugar.

Laboratory tests ordered (to be completed prior to next office visit)

  • Hemoglobin A1 C , metabolic panel, thyroid panel
  • Lipids, lipoprotein subclasses, and lipoprotein (a)
  • Vitamin D
  • Organic acids.
Treatment plan rationale: Dietary suggestions for travel were given. Hypoglycemic medications were reduced based on laboratory findings that demonstrated significant improvement in glucose control. Metoprolol was stopped because it has been shown to elevate blood glucose, and CK's blood pressure was significantly improved. [24]

Nine-month follow-up

CK reported a 30 lb weight loss and stated that her average fasting blood sugar was 91. Her cravings were minimal. She reported no sleep apnea and no colds or other health problems since the start of treatment. She wanted to lose another 15 lbs, after which she would completely discontinue glyburide and metformin. She started working with a trainer on interval and strength training two times a week. CK complained of being very busy with work-related travel though in general she felt empowered in life and health. She described herself as being at a magical point, happy and enjoying her life.

Nine-month follow-up laboratory testing

Nine-month follow-up plan

  • Increase exercise as planned
  • Continue interventions as directed.

  Discussion Top

Diabetes, epidemic in the West, is a disorder of glucose homeostatis, excess of which is damaging to every tissue in the body. As such, diabetes is a gateway disease, being associated with cardiovascular and kidney disease, dementia, retinopathy and numerous other conditions. Not surprisingly, morbidity, mortality and cost to society of this preventable illness are extremely high.

As with most complex, chronic conditions, the development of DMII involves environmental exposure coupled with genetic predisposition. It is clear that DMII is strongly associated with physical inactivity, obesity, low high-density lipoprotein (HDL) levels, excessive alcohol intake, [25] stress, [26] and poor dietary choices. Organotoxin exposures, including persistent organic pollutants (POPs), polychlorinated biphenyls (PCBs) and bisphenol A, among others, have also been associated with DMII, and individuals eating a typical diabetogenic diet of highly refined, processed foods are at particular risk for exposure. [27] Identifying genetics has been a more elusive path; however, variants in the transcription factor 7-like 2 (TCF7L2) gene, involved in insulin exocytosis, have been shown to be associated with almost a 30% increased risk of DMII in certain populations. [28],[29],[30]

As shown in her family history, CK demonstrated a strong genetic predisposition toward heart disease and diabetes. Environmental risk factors antecedent to her diagnoses included a high-stress, sedentary lifestyle with excessive sugar and alcohol intake. Further, her waist-hip ratio, considered to be a more sensitive marker of cardiovascular risk than BMI, was mildly elevated at 0.89. [31]

As shown in [Figure 7], hemoglobin A1 C , blood, and urinary glucose were all markedly elevated despite being on glyburide and metformin. Looking at the high-normal insulin level in relation to the pronounced elevation of blood and urinary glucose suggested that the pancreas was unable to produce enough insulin to overcome resistance. Allowed to continue, CK would likely have required exogenous insulin at some point in the future. CK's use of the beta-blocker metoprolol could also have been contributing to the dysglycemia. [32] BUN, creatinine, and urinary microalbumin were within normal limits, demonstrating intact kidney function.
Figure 7. Red blood cell essential elements. All found at low-normal levels

Click here to view

An elevated alanine transaminase (ALT) and an ALT: Aspartate transaminase ratio of >1 as shown in [Figure 7], may be early indication of non-alcoholic fatty liver disease (NASH) and is associated with DMII. [33],[34] Medications including atorvastatin also may increase liver enzymes. While the thyroid panel findings were within normal limits, a thyroid stimulating hormone (TSH) >2.5 has been considered indicative of subclinical hypothyroidism. [35] Subclinical hypothyroidism occurs with significantly greater frequency in type 2 diabetics and may contribute to dyslipidemia. [36]

The lipid panel [Figure 8] including low-density lipoprotein (LDL), HDL, and triglycerides was within normal limits. However, a closer inspection of cholesterol particle quantity and size demonstrated a significantly different risk picture. Elevated total LDL particle quantity, despite normal LDL-C, is associated with increased risk for cardiovascular disease in type 2 diabetics. [5] The small size of LDL and HDL particles is associated with atherosclerosis in type 2 diabetics. [6] The markedly elevated lipoprotein (a) is indicative of increased risk for vascular disease, particularly in diabetics. [7] Further, Lp (a) is not controlled by statin therapy. [22] Thus, individuals with DMII with pharmaceutically controlled levels of total cholesterol may continue to have an increased risk of cardiac and cerebrovascular events based on size, quantity and type of lipoproteins present. [5]
Figure 8. Serum lipid peroxides. Elevated level demonstrated increased oxidative stress

Click here to view

[Figure 6] demonstrates hypovitaminosis D. Vitamin D has been found lower in type 2 diabetics as compared to type 1, and inversely correlated with BMI. [37]

[Figure 1] demonstrates functional evidence of biotin deficiency (elevated beta-hydroxyisovalerate). Biotin deficiency is associated with impaired glucose tolerance and utilization of glucose. Biotin upregulates genes involved in lowering blood sugar, including pancreatic, and hepatic glucokinase enzymes. [11] CK also demonstrated significant elevation of two alpha-keto acids, both of which have been shown to normalize in some cases with high-dose thiamine and may be lowered with pantothenic acid, niacin, riboflavin, and alpha lipoic acid. Finally, while the level of the B12 functional marker, methylmalonic acid, was normal, B12 should be periodically monitored because CK was taking Metformin, which has been shown to deplete this nutrient in certain individuals. [38]

There are some possible reasons for CK's lactate elevation. An elevated blood lactate: Pyruvate ratio was shown to occur in individuals on statin therapy, demonstrating a mitochondriopathy and compromised cellular respiration. [39] It is hypothesized that urinary lactate is likely elevated in diabetic patients, as plasma lactate has been shown to be. [40] Furthermore, Metformin has been shown to increase serum lactate levels [Figure 4]. [41]

Also as shown in [Figure 4], they were high urinary ketones (β-hydroxybutyrate), evidence for increased fatty acid beta oxidation due to insulin resistance. HMG was also mildly elevated, suggesting inhibition of HMG-CoA reductase enzyme, which was expected given CK's use of the pharmaceutical inhibitor, atorvastatin. HMG-CoA reductase is the rate-limiting enzyme in cholesterol and CoQ10 synthesis. CoQ10 deficiency has been shown to occur in statin users. [39],[42] In cell studies, statin exposure causes increased oxidative DNA damage, early cell death, decreased ATP production and CoQ10 deficiency. [43] Taken together, the elevated lactate along with the HMG elevation may have been associated with inadequate CoQ10 availability compromising cellular respiration, causing subclinical mitochondriopathy. As discussed below [Figure 5], the high level of lipid peroxidation is further evidence for mitochondrial dysfunction.

Omega 3 fatty acids EPA and DHA were within normal limits, but the omega 6 fatty acid AA was elevated, providing the substrate for eicosanoid inflammatory compounds. Insulin stimulates the production of AA [44] through up-regulation of delta-5-desaturase. AA elevation has been associated with insulin resistance [Figure 3]. [45],[46]

The element insufficiencies as shown in [Figure 2] may have been contributing to the pathogenesis of CK's complaints. In brief, chromium is involved in cellular glucose uptake via potentiating insulin receptor tyrosine kinase. Indeed, elevated blood sugar itself has been proposed as a surrogate marker for chromium deficiency. [47] Vanadium is believed to be involved in lipid and glucose metabolism. [47] Selenium is a cofactor in multiple enzymes involved in glutathione and thyroid metabolism, and thus low selenium status may be contributing to increased oxidative stress [Figure 3] as well as the mild thyroid dysfunction. Magnesium is a cofactor for some 375 enzymes, including those involved in glucose and insulin regulation. It also plays a role in modulating blood pressure by means of supporting smooth muscle relaxation. [47] Magnesium is frequently found to be low in diabetics. [48] Multiple essential element deficiencies also suggest compromised digestion and absorption, in addition to poor dietary intake.

The elevated lipid peroxidation [Figure 5] was indicative of oxidative damage to cell membranes, which occurs with greater frequency in diabetic individuals. An association between glycemic control, A1C, and lipid peroxides has been demonstrated in individuals with DMII. [49] Mitochondriopathy as poor cellular respiration has also been associated with increased reactive oxidative species and CoQ10 deficiency. [50],[51]

As discussed above in Treatment plan rationale, the plan for CK was based on the laboratory findings and included aggressive nutrient intervention with attention to glucose metabolism, oxidative stress, lipid abnormalities, nutrient deficiencies and subclinical mitochondriopathy. Diet and exercise were important components of the plan.

On follow-up, CK presented with improved energy, reduced sugar cravings, decreased blood pressure, and a 20-pound weight-loss. She was inspired by her progress to continue exercising consistently and to focus on a healthy diet. Her follow-up laboratory data [Figure 9] reflected her commitment: Glucose and A1C were both significantly improved. Though not yet in the normal range, A1C did meet guidelines for those with DMII. Her follow-up plan included stopping glyburide, metoprolol (which has been shown to contribute to dysglycemia [24] ) and reducing metaformin.
Figure 9. Follow-up glucose and A1C. Significant improvements in blood glucose and A1C values were demonstrated

Click here to view

At her 9-month follow-up visit, CK reported her average blood sugar to be 91 and total weight loss of 30 pounds. Her sleep apnea was resolved. She was pleased with her progress and inspired to lose 15 additional pounds, which she intended to do by increasing her exercise routine with a personal trainer. She would continue to work with the clinician to achieve her goals.

It is important to note that CK's weight loss may have been assisted by the resolution of her sleep apnea, as poor sleep quality is associated with weight gain or difficulty in losing weight. [52],[53] Also, the relatively slow rate of weight loss (30 pounds over nine months) by CK may have minimized exposure to stored organotoxins liberated from adipose, making the process of weight reduction safer. [54],[55] Recent research has demonstrated a highly significant increase in the blood level of key fat-soluble toxins normally stored in adipose during weight loss. The rate of release parallels the rate of weight loss, suggesting that a slower pace of weight loss may reduce toxic exposure. [54] These toxins, including PCBs, hexachlorobenzene, and p,p'-dichlorophenyldichloroethylene are ubiquitous microcontaminants that are lipid soluble and accumulate in stored fat. Assessment of organotoxin status may be indicated prior to and during weight reduction programs.

CK's 9-month follow-up laboratory data continued to reflect improvement [Figure 10]. Blood sugar was at 111, down from an original 312. Liver enzymes were at normal levels, and her TSH was also improved at 1.6. [Figure 11] shows significant improvement in lipids, with HDL at a robust 68. While still elevated at 288, Lp (a) had dropped considerably from the original measurement of 423. Vitamin D was sufficient, as shown in [Figure 12]. Urinary organic acids in [Figure 13] also shows improvement, although beta-Hydroxyiosvalerate continued to be elevated, despite aggressive supplementation. Biotin is primarily produced by bacteria in the GI tract. Ongoing deficiency despite supplementation suggested possible GI imbalance. Lactate and β-Hydroxybutyrate were both within normal ranges [Figure 14], suggesting improved insulin sensitivity and mitochondrial function.
Figure 10. Metabolic panel, A1C and thyroid panel. Blood glucose and A1C continued to improve. ALT and AST were within normal limits. TSH had improved, although free T3 was lower than previously

Click here to view
Figure 11. Lipids, Lipoprotein Subclasses and Lp(a). Lipid analytes had greatly improved, although Lp(a), despite a significant reduction, was still quite elevated

Click here to view
Figure 12. Serum vitamin D. Follow-up results demonstrated sufficiency

Click here to view
Figure 13. Organic acid B vitamin markers. Beta-Hydroxyisovalerate continued to be elevated, despite high-dose supplementation. The alpha-keto acid levels were within normal limits

Click here to view
Figure 14. Organic acid mitochondrial markers. Lactate and ß-Hydroxybutyrate were both within normal range, suggesting improved insulin sensitivity and mitochondrial function

Click here to view

  Conclusion Top

It is difficult to overstate the diabetic epidemic and its associated ramifications. Diabetes is one of the top seven causes of death in the US and is associated with six of the top ten causes of death. In 2007, one of every five US. healthcare dollars was spent caring for someone diagnosed with diabetes. According to the World Health Organization, over 220 million people worldwide now have diabetes, and deaths from diabetes are expected to double by the year 2030. However, 90% of DMII is likely preventable through lifestyle changes alone. [1],[56],[57],[58]

Excess body weight is a strong independent risk factor in diabetes, and someone in three Americans (including children) is obese or overweight. [1] Obesity and DMII have been closely linked to organotoxins, exposure to which is greatly increased in those who follow the typical Standard American Diet. [27] Successful pharmacological control of DMII is achieved in fewer than 50% of all patients. [1] Alternatives in combating this disease are thus urgently needed.

It is well-established that lifestyle intervention can significantly reduce the incidence of DMII. As evidenced by the above statistics; however, these interventions go largely untried. DMII might be considered a socio-political disease, since the advent of government-subsidized foods such as wheat, soy, and high-fructose corn syrup has led to increased consumption of processed foods and simple carbohydrates, resulting in the twin epidemics of obesity and DMII. [59] This suggests that the solution to the epidemic will require government involvement not dissimilar to that which occurred with the tobacco industry. Moreover, the technological revolution has contributed to the onset of a more sedentary lifestyle, also contributing to the disease incidence. [60]

As in the case of CK, patient education, inspiration, and self-awareness are essential factors needed to alter the diabetic epidemic. Laboratory assessment of disease risk and nutrient status guided the development of safe interventions that involved individualized diet, nutrient, and lifestyle changes. Individualized therapies, education, and empowerment may be the key inspirational tools required to turn around the epidemic of DMII. Innovations in group treatment and sustainable behavior change are critical to help stem the rising tide of cost and suffering attributable to DMII.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Campbell RK, Martin TM. The chronic burden of diabetes. Am J Manag Care 2009;15:S248-54.  Back to cited text no. 1
Nissen SE, Wolski K. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med 2007;356:2457-71.  Back to cited text no. 2
Diabetes Statistics; 2010. Available from: http://www.diabetes.org/diabetes-basics/diabetes-statistics/. [Last accessed on 2010 Sep 16].  Back to cited text no. 3
Diabetes Public Health Resource-2007 National Diabetes Fact Sheet; 2010. Available from: http://www.cdc.gov/diabetes/pubs/general07.htm#gen_a. [Last accessed on 2010 Feb].   Back to cited text no. 4
Cromwell WC, Otvos JD. Heterogeneity of low-density lipoprotein particle number in patients with type 2 diabetes mellitus and low-density lipoprotein cholesterol<100 mg/dl. Am J Cardiol 2006;98:1599-602.  Back to cited text no. 5
Hayashi Y, Okumura K, Matsui H, Imamura A, Miura M, Takahashi R, et al. Impact of low-density lipoprotein particle size on carotid intima-media thickness in patients with type 2 diabetes mellitus. Metabolism 2007;56:608-13.  Back to cited text no. 6
Kubo M, Takami S, Matsuzawa Y. Contribution of Lp(a) to the occurrence of vascular diseases: Correlation of several risk factors including diabetes mellitus. J Atheroscler Thromb 1995;2 Suppl 1:S22-5.  Back to cited text no. 7
Holick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81.  Back to cited text no. 8
Membrez M, Blancher F, Jaquet M, Bibiloni R, Cani PD, Burcelin RG, et al. Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice. FASEB J 2008;22:2416-26.  Back to cited text no. 9
Mock DM, Henrich CL, Carnell N, Mock NI. Indicators of marginal biotin deficiency and repletion in humans: Validation of 3-hydroxyisovaleric acid excretion and a leucine challenge. Am J Clin Nutr 2002;76:1061-8.  Back to cited text no. 10
Fernandez-Mejia C. Pharmacological effects of biotin. J Nutr Biochem 2005;16:424-7.  Back to cited text no. 11
Wang ZQ, Cefalu WT. Current concepts about chromium supplementation in type 2 diabetes and insulin resistance. Curr Diab Rep 2010;10:145-51.  Back to cited text no. 12
Muramatsu T, Yatsuya H, Toyoshima H, Sasaki S, Li Y, Otsuka R, et al. Higher dietary intake of alpha-linolenic acid is associated with lower insulin resistance in middle-aged Japanese. Prev Med 2010;50:272-6.  Back to cited text no. 13
Klein G, Kim J, Himmeldirk K, Cao Y, Chen X. Antidiabetes and anti-obesity activity of Lagerstroemia speciosa. Evid Based Complement Alternat Med 2007;4:401-7.  Back to cited text no. 14
Al-Romaiyan A, Liu B, Asare-Anane H, Maity CR, Chatterjee SK, Koley N, et al. A novel Gymnema sylvestre extract stimulates insulin secretion from human islets in vivo and in vitro. Phytother Res 2010;24:1370-6.  Back to cited text no. 15
Martina V, Masha A, Gigliardi VR, Brocato L, Manzato E, Berchio A, et al. Long-term N-acetylcysteine and L-arginine administration reduces endothelial activation and systolic blood pressure in hypertensive patients with type 2 diabetes. Diabetes Care 2008;31:940-4.  Back to cited text no. 16
Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ. Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. Am J Physiol 1997;273:E185-91.  Back to cited text no. 17
Vuksan V, Sievenpiper JL, Xu Z, Wong EY, Jenkins AL, Beljan-Zdravkovic U, et al. Konjac-Mannan and American ginsing: Emerging alternative therapies for type 2 diabetes mellitus. J Am Coll Nutr 2001;20:370S-80.  Back to cited text no. 18
Anderson JW, Allgood LD, Lawrence A, Altringer LA, Jerdack GR, Hengehold DA, et al. Cholesterol-lowering effects of psyllium intake adjunctive to diet therapy in men and women with hypercholesterolemia: Meta-analysis of 8 controlled trials. Am J Clin Nutr 2000;71:472-9.  Back to cited text no. 19
Bland JS, Barrager E, Reedy RG, Bland K. A medical food-supplemented detoxification program in the management of chronic health problems. Altern Ther Health Med 1995;1:62-71.  Back to cited text no. 20
Fedor D, Kelley DS. Prevention of insulin resistance by n-3 polyunsaturated fatty acids. Curr Opin Clin Nutr Metab Care 2009;12:138-46.  Back to cited text no. 21
Scanu AM, Hinman J. Issues concerning the monitoring of statin therapy in hypercholesterolemic subjects with high plasma lipoprotein(a) levels. Lipids 2002;37:439-44.  Back to cited text no. 22
Hoogwerf BJ, Sprecher DL, Pearce GL, Acevedo M, Frolkis JP, Foody JM, et al. Blood glucose concentrations < or=125 mg/dl and coronary heart disease risk. Am J Cardiol 2002;89:596-9.  Back to cited text no. 23
Fonseca VA. Effects of beta-blockers on glucose and lipid metabolism. Curr Med Res Opin 2010;26:615-29.  Back to cited text no. 24
van de Wiel A. Diabetes mellitus and alcohol. Diabetes Metab Res Rev 2004;20:263-7.  Back to cited text no. 25
Wellen KE, Hotamisligil GS. Inflammation, stress, and diabetes. J Clin Invest 2005;115:1111-9.  Back to cited text no. 26
Porta M. Persistent organic pollutants and the burden of diabetes. Lancet 2006;368:558-9.  Back to cited text no. 27
da Silva Xavier G, Loder MK, McDonald A, Tarasov AI, Carzaniga R, Kronenberger K, et al. TCF7L2 regulates late events in insulin secretion from pancreatic islet beta-cells. Diabetes 2009;58:894-905.  Back to cited text no. 28
Owen KR, McCarthy MI. Genetics of type 2 diabetes. Curr Opin Genet Dev 2007;17:239-44.  Back to cited text no. 29
Yan Y, North KE, Ballantyne CM, Brancati FL, Chambless LE, Franceschini N, et al. Transcription factor 7-like 2 (TCF7L2) polymorphism and context-specific risk of type 2 diabetes in African American and Caucasian adults: The atherosclerosis risk in communities study. Diabetes 2009;58:285-9.  Back to cited text no. 30
Dobbelsteyn CJ, Joffres MR, MacLean DR, Flowerdew G. A comparative evaluation of waist circumference, waist-to-hip ratio and body mass index as indicators of cardiovascular risk factors. The Canadian heart health surveys. Int J Obes Relat Metab Disord 2001;25:652-61.  Back to cited text no. 31
Fonseca V, Bakris GL, Bell DS, McGill JB, Raskin P, Messerli FH, et al. Differential effect of beta-blocker therapy on insulin resistance as a function of insulin sensitizer use: Results from GEMINI. Diabet Med 2007;24:759-63.  Back to cited text no. 32
Schindhelm RK, Diamant M, Dekker JM, Tushuizen ME, Teerlink T, Heine RJ. Alanine aminotransferase as a marker of non-alcoholic fatty liver disease in relation to type 2 diabetes mellitus and cardiovascular disease. Diabetes Metab Res Rev 2006;22:437-43.  Back to cited text no. 33
Clark JM. The epidemiology of nonalcoholic fatty liver disease in adults. J Clin Gastroenterol 2006;40 Suppl 1:S5-10.  Back to cited text no. 34
Wartofsky L, Dickey RA. The evidence for a narrower thyrotropin reference range is compelling. J Clin Endocrinol Metab 2005;90:5483-8.  Back to cited text no. 35
Wu P. Thyroid disorders and diabetes. It is common for a person to be affected by both thyroid disease and diabetes. Diabetes Self Manag 2007;24:80-2, 85-7.  Back to cited text no. 36
Di Cesar DJ, Ploutz-Snyder R, Weinstock RS, Moses AM. Vitamin D deficiency is more common in type 2 than in type 1 diabetes. Diabetes Care 2006;29:174.  Back to cited text no. 37
Buvat DR. Use of metformin is a cause of vitamin B12 deficiency. Am Fam Physician 2004;69:264.  Back to cited text no. 38
De Pinieux G, Chariot P, Ammi-Saïd M, Louarn F, Lejonc JL, Astier A, et al. Lipid-lowering drugs and mitochondrial function: Effects of HMG-CoA reductase inhibitors on serum ubiquinone and blood lactate/pyruvate ratio. Br J Clin Pharmacol 1996;42:333-7.  Back to cited text no. 39
Cameron MA, Maalouf NM, Adams-Huet B, Moe OW, Sakhaee K. Urine composition in type 2 diabetes: Predisposition to uric acid nephrolithiasis. J Am Soc Nephrol 2006;17:1422-8.  Back to cited text no. 40
Davis TM, Jackson D, Davis WA, Bruce DG, Chubb P. The relationship between metformin therapy and the fasting plasma lactate in type 2 diabetes: The fremantle diabetes study. Br J Clin Pharmacol 2001;52:137-44.  Back to cited text no. 41
Rundek T, Naini A, Sacco R, Coates K, DiMauro S. Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke. Arch Neurol 2004;61:889-92.  Back to cited text no. 42
Tavintharan S, Ong CN, Jeyaseelan K, Sivakumar M, Lim SC, Sum CF. Reduced mitochondrial coenzyme Q10 levels in HepG2 cells treated with high-dose simvastatin: A possible role in statin-induced hepatotoxicity? Toxicol Appl Pharmacol 2007;223:173-9.  Back to cited text no. 43
Das UN. Is obesity an inflammatory condition? Nutrition 2001;17:953-66.  Back to cited text no. 44
Aldámiz-Echevarría L, Prieto JA, Andrade F, Elorz J, Sanjurjo P, Rodríguez Soriano J. Arachidonic acid content in adipose tissue is associated with insulin resistance in healthy children. J Pediatr Gastroenterol Nutr 2007;44:77-83.  Back to cited text no. 45
Galgani JE, Aguirre CA, Uauy RD, Díaz EO. Plasma arachidonic acid influences insulin-stimulated glucose uptake in healthy adult women. Ann Nutr Metab 2007;51:482-9.  Back to cited text no. 46
Bralley JA, Lord RS, editors. Laboratory Evaluations for Integrative and Functional Medicine. 2 nd ed. Atlanta: Metametrix Institute; 2008.  Back to cited text no. 47
Sales CH, Pedrosa Lde F. Magnesium and diabetes mellitus: Their relation. Clin Nutr 2006;25:554-62.  Back to cited text no. 48
Lawrence JR, Campbell GR, Barrington H, Malcolm EA, Brennan G, Wiles DH, et al. Clinical and biochemical determinants of plasma lipid peroxide levels in type 2 diabetes. Ann Clin Biochem 1998;35 (Pt 3):387-92.  Back to cited text no. 49
Addabbo F, Montagnani M, Goligorsky MS. Mitochondria and reactive oxygen species. Hypertension 2009;53:885-92.  Back to cited text no. 50
Quinzii CM, López LC, Gilkerson RW, Dorado B, Coku J, Naini AB, et al. Reactive oxygen species, oxidative stress, and cell death correlate with level of CoQ10 deficiency. FASEB J 2010;24:3733-43.  Back to cited text no. 51
Carter R 3 rd , Watenpaugh DE. Obesity and obstructive sleep apnea: Or is it OSA and obesity? Pathophysiology 2008;15:71-7.  Back to cited text no. 52
Patel SR. Reduced sleep as an obesity risk factor. Obes Rev 2009;10 Suppl 2:61-8.  Back to cited text no. 53
Chevrier J, Dewailly E, Ayotte P, Mauriège P, Després JP, Tremblay A. Body weight loss increases plasma and adipose tissue concentrations of potentially toxic pollutants in obese individuals. Int J Obes Relat Metab Disord 2000;24:1272-8.  Back to cited text no. 54
Hue O, Marcotte J, Berrigan F, Simoneau M, Doré J, Marceau P, et al. Increased plasma levels of toxic pollutants accompanying weight loss induced by hypocaloric diet or by bariatric surgery. Obes Surg 2006;16:1145-54.  Back to cited text no. 55
Pradhan A. Obesity, metabolic syndrome, and type 2 diabetes: Inflammatory basis of glucose metabolic disorders. Nutr Rev 2007;65:S152-6.  Back to cited text no. 56
WHO. Diabetes Key Facts; 2010. Available from: http://www.who.int/mediacentre/factsheets/fs312/en/.[Last accessed on 2010 Sep 20].  Back to cited text no. 57
Willett WC. Balancing life-style and genomics research for disease prevention. Science 2002;296:695-8.  Back to cited text no. 58
Muller M, Schoonover H, Wallinga D. Considering the contribution of U.S. Food and agricultural policy to the obesity epidemic: Overview and opportunities. Minneapolis: Institute for Agriculture and Trade Policy; 2007.  Back to cited text no. 59
Hu FB. Sedentary lifestyle and risk of obesity and type 2 diabetes. Lipids 2003;38:103-8.  Back to cited text no. 60


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14]

  [Table 1]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Case report
Four-Month follo...
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded53    
    Comments [Add]    

Recommend this journal