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November 2003

A Comprehensive Guide to Preventative Blood Testing
By Penny Baron

Vitamin B12 and folate deficiencies are most commonly due to problems of malabsorption (B12: gastrointestinal disorders, pancreatitis, tapeworm, and alcoholism; folate: drug interference and jejeunal mucosal disease) or inadequate dietary intake (B12 in rare cases of strict vegetarian diets and folate in general malnutrition or alcoholism),

Low levels of B12 are also seen in patients with multiple myeloma and iron deficiency, in those who smoke, and the elderly; in patients with cancer, aplastic anemia, and folate deficiency; in patients on hemodialysis; and in those who ingest high doses of vitamin C. High levels may be increased in acute and myelogenous leukemia, polycythemia vera, leukocytosis and liver disease.

Folic acid levels may be decreased in alcoholics; those with a chronic disease, undergoing hemodialysis, or having anorexia nervosa; and in premature infants and the elderly. Besides pregnancy, Increased doses of folic acid may be indicated in hyperthyroidism, neoplasia, hemolytic anemias, and psoriasis.


DHT (5a-Dihydrotestosterone)
DHT is synthesized from free (noncomplexed) testosterone by the enzyme cholestenone 5a-reductase, which is found in the prostate, various adrenal glands, and hair follicles. It is responsible for the development of the male genitals and prostate, the physical changes that accompany male maturation, and growth of muscle tissue. Only a small portion of DHT is found in the blood, primarily complexed to sex hormone-binding globulin (SHBG).

Low levels of DHT may be associated with decreased sex drive, erectile dysfunction, male pseudohermaphroditism, or pseudovaginal perineoscrotal hypospadias. Increased levels of DHT may be implicated in male-pattern baldness (alopecia), hirsutism (excessive hair growth in women), benign prostatic hyperplasia, and acne.

Drugs that block 5-alpha-reductase, such as Propecia (finasteride) for male-pattern baldness, interfere with the production of DHT with possible consequential erectile dysfunction and hindrance of muscle growth.

Fasting Insulin and HOMAIR
Fasting serum insulin is used as an index of insulin sensitivity and resistance. Insulin resistance, estimated by homeostasis model assessment (HOMAIR), has been shown to increase accuracy over the traditional test.62 HOMAIR is determined by multiplying fasting blood glucose level by fasting insulin level and then dividing by 22.5. The lower the number, the better.

Insulin resistance (where the body does not respond to the insulin that it produces) is a common finding in metabolic disorders, including glucose intolerance, dyslipidemia, hyperuricemia, and hypertention,62 and is associated with an increased risk of symptomatic coronary artery disease.63 Furthermore, approximately 25% of persons with insulin resistance will go on to develop diabetes Type II.

According to Bonora et al, the prevalence of insulin resistance estimated by HOMA is 65.9% in patients with impaired glucose tolerance, 83.9% in NIDDM (non-insulin-dependent diabetes mellitus) subjects, 53.5% in persons with hypercholesterolemia, 84.2% in hypertriglyceridemia patients, 88.1% in patients with low HDL cholesterol, 62.8% in patients with hyperuricemia, and 58% in hypertensive patients. In patients with a combination of glucose intolerance, dyslipidemia and/or hypertension, the prevalence of insulin resistance was 95.2%.62

Data also show that HOMA-estimated insulin resistance is an independent predictor of cardiovascular disease in patients with Type II diabetes.64

Insulin resistance may also be an indictor and likely cause of kidney disease in persons with diabetes Type I, according to a study at the University of Pittsburgh. Investigators also found that since insulin resistance predicts heart disease “it may explain the longstanding observation that in Type I diabetes, kidney disease predicts heart disease. In other words, insulin resistance may be the ‘common ground’ for both complications.”65

Early detection of insulin resistance may, therefore, help prevent potentially serious complications that may result from metabolic disorders, including diabetes type I and II, dyslipidemia, hyperuricemia, and hypertention.

Somatomedin-C (Insulin-like growth factor/IGF-1)
IGF-1 is the main effector of human growth hormone (HGH) activity and also affects glucose metabolism (insulin-like activity). Because it remains constant in the blood longer than HGH (which tends to fluctuate in response to various stimuli), it is a more accurate indicator of HGH deficiency, and is also more precise for monitoring HGH therapy than is testing HGH directly.

IGF-1 is critical in mediating the growth of muscle and other tissues, and normal levels steadily increase until 12-15 years of age, and then begin to decline. Up to one-third of skeletal muscle mass and strength is lost between the ages of 30 and 80.66 A study by Barton-Davis et al showed that IGF-1 overexpression in the muscle cells of mice can preserve the characteristics (morphological and functional) of the skeletal muscles of old mice such that they are equivalent to those of young adult muscles.66 Ruiz-Torres et al showed that when IGF-1 levels in older (>70 year-old) males were similar to levels in younger males (up to 39 years), the older males do not show age-dependent decreases in serum testosterone and lean body mass, nor increases in fat body mass.67

Low levels of IGF-1 have been implicated in the development of atherosclerosis. Van den Beld et al found that free IGF-1 concentrations appeared to be linearly inversely related to atherosclerosis, suggesting that IGF-1 (along with endogenous testosterone and estrone) may play a protective role in the development of atherosclerosis in aging men.68

A study by Carro et al suggests a role for IGF-1 as a neuroprotective hormone. Data show an inverse correlation between levels of IGF-1 (decreased) and amyloid-B (increased) accumulation in the brain of patients with Alzheimer’s disease. In studies of mutant mice, high amyloid-B levels are seen when serum IGF-1 levels are low. Conversely, the amyloid-B burden can be decreased by increasing levels of serum IGF-1. Investigators suggested that “circulating IGF-1 is a physiological regulator of brain amyloid levels with therapeutic potential.”69

Elevated levels of IGF-1 may be indicative of acromegaly (gigantism) and diabetic retinopathy. Although it has been suspected that high levels of IGF-1 are associated with increased risk of prostate cancer, recent data suggest that IGF-1 may be serving as a tumor marker rather than an etiologic factor for the disease.70 The IGF-1 test (decreased levels) may also be used to evaluate pituitary insufficiency and hypothalamic lesions in children (diagnosis of dwarfism and response to therapy). Low levels have also been found in patients with amyotrophic lateral sclerosis.71