Case Study - Metametrix Clinical Laboratory

History
1999 - FROM HYPO- TO HYPERTHYROID? When consultation with this patient began in February, 2003, as soon as she was asked to describe her problem she immediately responded: "On May 13, 1999, after 3 years on Armor thyroid for a low energy complaint, I was taken to the local EMS for tachycardia & flushing. They diagnosed hyperthyroid and started adjusting thyroid hormones which were I soon afterward discontinued because they seemed to make the symptoms worse."

2003 - SEVERE INSOMNIA - Since that incident in 1999 and until the testing in January, 2003, the patient had never slept for more than two hours a night. Both L-Trp and Ambien had been tried, but they gave no sleep improvement. In fact both agents caused a very ill feeling for the next 36 hours. In February, 2003, she still can't sleep & can't handle stress of any kind, nor can she walk around the block or lift her grandchildren off the floor.

2004 - By January 2004, she was sleeping normal hours every night, and had much more strength and endurance. She is doing Yoga, walking with no difficulty, and picking up her grandchildren. She continues to feel periods of mental confusion.

Description of Results

ION Profile Date ----> See
February, 2002 ----> Figures 1-7
January, 2003 ----> Figures 8-15
January, 2004 ----> Figures 16-21

FEBRUARY, 2002 - Difficulties with maintaining many areas of essential and conditionally essential nutrients are found along with multiple urinary markers of intestinal dysbiosis. High body burdens of toxic metals are indicated by the elevated erythrocyte lead and mercury.

JANUARY, 2003 - Fortunately, the toxic metals have returned to normal ranges over the course of the past year, so we conclude no ongoing toxic exposure is present. The key feature at this time was elevated urinary quinolinate because of her adverse responses to L-Trp supplementation and to Ambien. The responses are consistent with an up-regulated macrophage kynurenin pathway where tryptophan is converted to quinolinic acid. Quinolinate is a powerful agonist of NMDA receptors for glutamate and aspartate in the hipocampus.

Two previously unreported markers for deficiencies of vitamin B6 (Xanthurenate) and folic acid (Formiminoglutamate) were positive (elevated). Also her fatty acids show a low AA/EPA ratio . This means the eicosanoid cell regulation signals are dominated by the series 3 members. There is a need to raise the n-6 family of essential fatty acids. These factors may be producing poor immune responsiveness to microbial antigens. Microbial overgrowth is indicated by the elevated urinary microbial metabolic markers. Intestinal dysbiosis is an area of chronic difficulty over the two reports now available.

JANUARY, 2004 - Her data shows improvements in many areas, including almost complete normalization of amino acids, minerals, and fatty acids. The quinolinate has dropped by 50% to a level well under the high limit. (see Organix p.1) However, at this point another new marker has been added that may shed much light on the entire previous history. The marker of invasive candidiasis, D-arabinitol, is greatly elevated. At the same time, high orotate shows difficulty with hepatic ammonia clearance. It is likely that the combination of transient ammonemia and yeast toxins are a prime block to full restoration of mental function. (see Organix p.2)

Simultaneous elevation of the three keto acids and xanthurenate shows a need for B-complex vitamins to be started again. We now know that gut healing is a key part of her full normalization, and one might consider the use of 3-6gm/day L-glutamine. However, the ammonia difficulty means that caution is needed for the use of L-glutamine until the urea cycle can be up-regulated. Supplemental L-arginine will be recommended for this purpose.

Recommendations
Because of the hypersensitive responses in this patient, all nutrient additions are to be done with gradual increases to the doses specified. Also, the general rule of sustaining supplementation for 90 days and then decreasing is well-embraced by this patient who is leery of any additions that might upset her delicate balance.

January, 2003: Start a high fiber diet. Vitamin B6 50 mg, Folate 400 mcg, beta Carotene 20,000 IU, Se 250 mcg, Vit E 800 IU, NAC 300 mg, L-Arg 2 gm bid, Black currant oil 2 gm bid

January, 2004: Use L-arginine to stimulate urea cycle clearance of ammonia. Start at 1gm/day and increase to 2gm/day. Start a low carbohydrate diet to bring yeast growth down. Use the Specific Carbohydrate Diet (SCD) of Gottschall for this purpose. Add zinc at 20 mg and a 50mg B-complex product. After the nutrient additions and SCD have been in place for 3-4 weeks, carefully add L-glutamine to assist gut restoration.

Other Comments
JANUARY, 2003: The most outstanding finding is the elevated QUIN on the recent report. Many favorable changes are indicated from the previous data where QUIN was not reported. The hyper-stimulation of NMDA receptors may explain the insomnia and resulting fatigue in this case. Quinolinate is produced from tryptophan, explaining the adverse reactions to this nutrient and to Ambien.

The question raised at this point is regarding the origin of the stimulation. We know that viral infections or other events that produce chronic inflammatory response can initiate macrophage quinolinate production via the cytokine, interferon gamma. Since we see evidence of intestinal bacterial overgrowth, we can recommend corrections of gut microbial populations to reduce inflammatory signals from the gut. A part of this correction is to increase dietary fiber.

For the high fiber diet instruction, she started eating cabbage soup every day. Within four weeks, she noticed that she had slept almost five hours for the first time in over three years. She had very good compliance with the rest of the nutrient instructions.

JANUARY 2004: This case illustrates several principles of molecular medicine. First, the correction of nutrient insufficiencies is a powerful alternative to the administration of thyroid hormone to patients who report low energy and fatigue. Second, the combination of markers that allow discrimination of subtle nutrient, toxicant, cell-regulator, and intestinal dysbiotic events allow focused interventions that change over the course of the restoration of wellness. Finally, the progress from disease to wellness is faithfully reflected in the correction of nutrient and metabolic markers measured in the laboratory.

At this time the patient is very pleased and ready to take on the dietary restriction to overcome yeast overgrowth. She has become well-acquainted with the way her body responds to stimulation, so she is able to self adjust nutrient additions for optimal results without upsetting her hormonal balance. The evidence points to a greatly improved prognosis for energetic senior years.

At this point, effort needs to be focused on healing the gut and controlling populations of intestinal yeast while stimulating urea cycle ammonia clearance. Stress on B-complex vitamin status continues to call for supplementation of this group of essential nutrients.

Lab Data

Figure . -Hypo-hyperthyroid-020201p1.gif