The Labs I Run

[cpeil2]

one can also go to www.bodylogicmd.com to find a friendly physician or lab to run the tests mentioned. The Life Extension Foundation also runs these tests.

Do I smell spam?

 

[daphne]

No spam, just mentionign a medical group affiliated with the A4M.

 

[marianco]

I am down in Latin America. I have never had labs done before. I have located a Blood lab in a town near hear. I want to go get my levels checked. My question is, what test do I have them run? Do I ask for a Hormone test (Testosterone, Estrogen Ect?) Or is there a specific named test? Down here you don't need a doctor for test referals and health care is cheap and very good. I just don't know what to ask for.

Look up sticky called TRT: A Recipe for Success for SWALE/Dr. Crisler's protocol including the initial labs.

The labs need to be customized to the individual. A comprehensive set of labs for my patiens would cost close to $5,000 or more. Not everyone can afford this, even with insurance, nor may it be necessary or practical in order to address the most important problems, so I customize the lab tests for the person.

A fairly comprehensive general initial lab work-up using standard blood and urine tests may include:

REPRODUCTIVE:
Free and Total Testosterone Panel (this includes Total Testosterone, Free Testosterone, Bioavailable Testosterone, and Sex Hormone Binding Globulin), Estradiol, Progesterone, Luteinizing Hormone, Follicle Stimulating Hormone, Prolactin, Prostate Specific Antigen (in men)

THYROID:
Free T4 (Free Thyroxine), Free T3 (Free Liothyronine), Thyroid Stimulating Hormone, antithyroglobulin antibody, antithyroid peroxidase antibody, thyroid stimulating immunoglobulin.

ADRENAL:
Cortisol AM, Cortisol PM, Cortisol-Binding Globulin, Adrenocorticotropic Hormone (ACTH), Dehydroepiandrosterone Sulfate (DHEA-s),

CARBOHYDRATE METABOLISM:
fasting glucose (included in comprehensive metabolic panel when fasting), Hemoglobin A1c, fasting insulin, 3-Hour Glucose Tolerance Test (samples of blood for measuring glucose and insulin are taken at 0, 60, 120, and 180 minutes after ingesting a 1.75 g/kg glucose solution).

GROWTH HORMONE:
IGF-1 (Insulin-like growth factor I / Somatomedin-C), Growth Hormone Stimulation Test using GHRH (growth hormone releasing hormone) plus Arginine (samples of blood for measuring growth hormone are taken at 0, 30, 60, 90, and 120 minutes).

GENERAL:
Comprehensive Metabolic Panel (glucose, urea nitrogen, creatinine, calcium, sodium, potassium, CO2, cholride, total protein, albumin, globulin, total bilirubin, alkaline phosphatase, AST, ALT)
CBC (complete blood count)
Lipid Profile (including total cholesterol, triglycerides, HDL cholesterol, VLDL cholesterol, calculated LDL cholesterol)
Urinalysis
Magnesium
Vitamin D, 1, 25-Dihydroxy
Vitamin B12
Folate
Heavy Metal Screen (blood)

The tests are done in the morning after fasting overnight (no food or drink after dinner except for water). The patient should drink 0.5 liters of water before the test to avoid dehydration. The patient should avoid strenuous activity the day before, avoid restaurant food and stimulants such as coffee, eat their regular meals, and avoid stressful situations for at least 2 days before the test.

Cortisol-PM is done in the afternoon between 4-6 PM on the same day as the morning test.

The 3-hour glucose tolerance test and growth hormone stimulation tests should be done on different days.

ADDITIONAL SPECIALIZED TESTS:

A comprehensive 24-hour urine hormone panel (including DHEA, Androsterone, Etiocholanolone, Pregnanetriol, Cortisone, Cortisol, Tetrahydrocortisone, Tetrahydrocortisol, Allo-tetrahydrocortisol, Aldosterone, Tetrahydrocorticosterone, Allo-tetrahydrocorticosterone, Estrone, Estradiol, Estriol, Pregnanediol, Testosterone, Androsterone, 2-hydroxyestrogens, 16a-hydroxyestrone, 4-hydroxyestrone, 2-methoxyestrone, 2-methoxyestradiol, 5a-androstanediol, 5b-androstanediol, 11b-hydroxyandrosterone, 11b-hydroxyetiocholanolone, Free T3, Free T4, Sodium, Potassium, Calcium, Phosphorus, Magnesium).

24-hour urine growth hormone

Saliva test for Cortisol (4 samples in a day), DHEA-s (2 samples in a day).

Urine test for neurotransmitters (including sertonin, norepinephrine, dopamine, GABA, glutamate, epinephrine)

MRI of Brain

Chest X-Ray

EKG

The follow up tests include a subset of these tests as well as other tests depending on the situation.

 

[JackBauer]

Here is the standard order for my over 40 patients:

"Even though you will be fasting for 12 hours, please remember to drink lots of water. .

I just had labs done yesterday, and drank plenty the night before, but none before my blood work in the morning. (Fasting)

I chose not to drink because there seemed to be conflicting information online about it, I did not see this thread until today.

How substantial of an impact could me not drinking the morning of the lab test, have on results?

Thanks

 

[marianco]

I just had labs done yesterday, and drank plenty the night before, but none before my blood work in the morning. (Fasting)

I chose not to drink because there seemed to be conflicting information online about it, I did not see this thread until today.

How substantial of an impact could me not drinking the morning of the lab test, have on results?

Thanks

Overnight, one can become dehydrated.

Dehydration will artificially raise levels on blood tests.

This will cause low test levels to artifically appear in the "normal" range when they may actually be low. Thus, one risks not finding deficiencies by not drinking water before the lab test.

The amount to drink is about 0.5 to 1.0 liter.

The albumin level is one indication of the amount of dehydration that is occurring.

 

[theman24]

swale can you test me if i senfd my blood through mail,im in england.

 

[pmgamer18]

swale can you test me if i senfd my blood through mail,im in england.

SWALE aka Dr. John is not posting here anymore but you can reach him at www.allthingsmail.com he will work with your Dr. over the phone if you can get your Dr. to do this.

 

[Andrew Androgen]

Overnight, one can become dehydrated.

Dehydration will artificially raise levels on blood tests.

This will cause low test levels to artifically appear in the "normal" range when they may actually be low. Thus, one risks not finding deficiencies by not drinking water before the lab test.

The amount to drink is about 0.5 to 1.0 liter.

The albumin level is one indication of the amount of dehydration that is occurring.

Marianco, does dehydration before a blood test artificially raise testosterone levels as well?
Thanks.

 

[RussianRocket]

Any luck for people in the province of Qubec, Canada???? (Montreal)

I'm going to bring the list to my doc tomorrow and see if he can help me.

 

[pmgamer18]

Any luck for people in the province of Qubec, Canada???? (Montreal)

I'm going to bring the list to my doc tomorrow and see if he can help me.

In this thread SWALE aka Dr. John says.
Yes, contact my good friend and coleague Dr. Larry Komer at:

info@mastersmensclinic.com
I think this Dr. is in your area.

 

[WillBrink]

Total Testosterone
Bioavailable Testosterone (sometimes called Free and Loosely Bound)
Free Testosterone (if Bio T is not available)
SHBG
DHT
Estradiol (specify by the Extraction Method or Ultra-Sensitive)
Total Estrogens
LH
FSH
Prolactin
Cortisol
Thyroid Panel (TSH, FT3, FT4)
CBC
Comprehensive Metabolic Panel
Lipid Panel
Homocysteine
PSA (if over 40)
IGF-1 (if HGH therapy is desired)
Fasting Insulin


At the one month point, I follow-up with these assays:
Total Testosterone
Bioavailable Testosterone
Free T and SHBG (if Bio T is not available)
Estradiol (specify by the Extraction Method or Sensitive)
DHT (if patient is using a transdermal delivery system)
SHBG
FSH (3rd gen "sensitive" assay)
CBC
Lipid Panel
Comprehensive Metabolic Panel
(if ALT/AST from above are elevated, then get a GGT)

...I hope this helps!


__________________

Have you looked at the correlation between low IGF-1 and CHD? There is a lot of data that finds clear correlations between low IGF-1 and increased risk of CHD. I have had a hell of a time convincing a single endo of this relationship even when I dump a pile of studies on them. Some, but not all endos acknowledge the fact that low T is a risk factor for CHD, but none I have talked to will even look at the IGF-1 relationship. The real kicker to me is the data appears more robust and extensive with IGF-1 then it does for T regarding low IGF-1 as a risk factor for CHD. I have always had very low IGF-1 myself. I know increasing T can have effects on IGF-1, but not to the same degree, as GH will. IGF-1 was made the boogieman hormone some years ago via its association to prostate cancer, and from that day on appears to have been ignored for its other potential benefits. Just some of the data:

_________________

J Endocrinol Invest. 2005 May;28(5):440-8.

Circulating insulin-like growth factor-I levels are correlated with the atherosclerotic profile in healthy subjects independently of age.
Colao A, Spiezia S, Di Somma C, Pivonello R, Marzullo P, Rota F, Musella T, Auriemma RS, De Martino MC, Lombardi G.

Department of Molecular and Clinical Endocrinology and Oncology, "Federico II" University, Naples, Italy. colao@unina.it
To investigate the relationships between the GH-IGF-I axis and the atherosclerotic profile, we designed this open, observational, prospective study. Peak GH after GHRH+arginine (ARG) test, serum IGF-I and IGF binding protein-3 (IGFBP-3), lipid profile, homeostasis model assessment (HOMA) index and intima-media thickness (IMT) at common carotid arteries were measured in 174 healthy individuals (92 women, 82 men, aged 18-80 yr). Exclusion criteria for this study were: 1) body mass index (BMI) > or = 30 kg/m2; 2) personal history of cardiovascular diseases; 3) previous or current treatments of diabetes or hypertension; 4) previous corticosteroids treatment for longer than 2 weeks or estrogens for longer than 3 months; 5) smoking of more than 15 cigarettes/day and alcohol abuse. Subjects were divided according to age in decade groups from < 20 to > 70 yr. BMI increased with age, as did systolic and diastolic blood pressures, although they remained in the normal range. The GH peak after GHRH+ARG test was significantly higher in the subjects aged < 20 yr than in all the other groups (p < 0.01), but was similar in the remaining groups. An inverse correlation was found between the IGF-I z-score and total/HDL-cholesterol ratio (p = 0.02) and mean IMT (p = 0.0009); IGFBP-3 z-score and mean IMT (p = 0.043); IGF: IGFBP-3 molar ratio and total/HDL-cholesterol ratio (p < 0.0001) and mean IMT (p < 0.0001). Atherosclerotic plaques were found in 7 out of 12 subjects (53.8%) with a z-IGF-I score from < or = -2 to -1, in 4 out of 63 (6.3%) with a z-IGF-I score from -0.99 to 0.1 out of 66 (1.5%) with a z-IGF-I score from 0.1 to 1 and none of the 33 subjects with an IGF-I z-score >1 (p = 0.006). At multi-step regression analysis, age was the best predictor of HDL-cholesterol levels and mean IMT, IGF-I level was the best predictor of total cholesterol and total/HDL-cholesterol ratio, the IGF-I/IGFBP-3 molar ratio was the best predictor of triglycerides levels. The z-scores of IGF-I and IGFBP-3 were the second best predictors of mean IMT after age. In conclusion, IGF-I and IGFBP-3 were negatively correlated with common cardiovascular risk factors, studied as total/HDL-cholesterol ratio, and/or early atherosclerosis, studied as IMT at common carotid arteries. The prevalence of atherosclerotic plaques, though not hemodinamically significant, was higher in the subjects having a z-score of IGF-I of < or = -2 to -1. Our results support a role of the IGF/IGFBP-3 axis in the pathogenesis of atherosclerosis.
_______________________

Clin Endocrinol (Oxf). 2004 Sep;61(3):360-6.

Insulin-like growth factor-1 deficiency determines increased intima-media thickness at common carotid arteries in adult patients with growth hormone deficiency.
Colao A, Di Somma C, Filippella M, Rota F, Pivonello R, Orio F, Vitale G, Lombardi G.
Department of Molecular and Clinical Endocrinology and Oncology, Federico II University of Naples, Italy. colao@unina.it

OBJECTIVE: To investigate the role of IGF-1 on intima-media thickness (IMT) at common carotid arteries by Doppler ultrasonography. SUBJECTS: Thirty-nine patients (17 women, 22 men, aged 25-70 years) with severe GH deficiency (GHD), 19 with normal and 20 with low IGF-1 levels, and 39 sex-, age- and body mass index (BMI)-matched healthy controls. RESULTS: Patients with GHD showed abnormalities in lipid profile, and increased fibrinogen levels, mean IMT (0.88 +/- 0.26 vs. 0.69 +/- 0.14 mm, P < 0.001), and systolic and diastolic peak velocity (P < 0.001) compared to controls. Eight patients (18%) and one control (2.1%, P = 0.04) had well-defined plaques. In controls, but not in patients with GHD, mean carotid IMT was correlated with age (r = 0.78, P < 0.001). In both controls (r = -0.82; P < 0.0001) and patients with GHD (r = -0.84, P < 0.0001), serum IGF-1 levels were inversely correlated with mean IMT at common carotid arteries. At the stepwise multiple regression, the variables most significantly related to IMT in GH-deficient patients were total cholesterol levels (t = 5.2, P < 0.001), followed by disease duration (t = 2.4, P = 0.02), while in controls the variables most significantly related to IMT were IGF-1 levels (t = -9.9, P < 0.001), followed by low density lipoprotein (LDL)-cholesterol levels (t = -2.3, P = 0.02). Compared to patients with normal IGF-1 levels, those with low IGF-1 levels had lower high density lipoprotein (HDL)-cholesterol levels (1.0 +/- 0.2 vs. 1.3 +/- 0.2 mmol/l, P = 0.0002), and higher glucose (54.3 +/- 6.1 vs. 48.9 +/- 5.9 mmol/l, P = 0.008), insulin (25.2 +/- 6.8 vs. 18.8 +/- 6.0 mUl/l, P = 0.004), total cholesterol (7.1 +/- 1.1 vs. 4.9 +/- 0.6 mmol/l, P < 0.0001), total/HDL-cholesterol ratio (7.2 +/- 1.8 vs. 3.9 +/- 0.7, P < 0.0001), fibrinogen levels (319.8 +/- 56.9 vs. 241.8 +/- 53.0 mg/dl, P < 0.0001) and mean IMT at common carotid arteries (1.05 +/- 0.25 vs. 0.69 +/- 0.07 mm, P < 0.0001). Atherosclerotic plaques were found only in GH-deficient patients with low IGF-1 levels. CONCLUSIONS: GH-deficient patients have alterations in lipid profile with an increase in the total/HDL-cholesterol ratio, which is an index of increased cardiovascular risk, but only patients with IGF-1 deficiency have increased IMT.
______________________________________

Arterioscler Thromb Vasc Biol. 1998 Feb;18(2):277-82.

Erratum in:
* Arterioscler Thromb Vasc Biol 1998 Jul;18(7):1197.

Serum total IGF-I, free IGF-I, and IGFB-1 levels in an elderly population: relation to cardiovascular risk factors and disease.

Janssen JA, Stolk RP, Pols HA, Grobbee DE, Lamberts SW.
Department of Internal Medicine III, Erasmus University, Rotterdam, The Netherlands.
Recently, a method to measure free insulin-like growth factor-I (IGF-I) levels has been developed. Free IGF-I levels may have greater physiological and clinical relevance than total (bound and free) IGF-I. The associations between the circulating IGF-I/IGF binding protein (IGFBP) system and cardiovascular disorders was studied. In a cross-sectional study of 218 healthy persons (103 men, 115 women) aged 55 to 80 years, fasting serum (total and free) IGF-I and IGFBP-1 levels, lipid profile, insulin, and glucose were measured. In addition, blood pressure, body mass index (BMI), and waist-hip ratio (WHR) were measured. Ultrasonography of both carotid arteries was performed to investigate the presence of atherosclerotic lesions. A history of angina pectoris, the presence of a possible or definite myocardial infarction on the ECG, and plaques in the carotid arteries were used as indicators of presence of cardiovascular signs and symptoms. Free IGF-I was inversely related to serum triglycerides (P=.04, adjusted for age and sex). Mean free IGF-I levels in subjects without signs or symptoms of cardiovascular diseases were significantly higher than in those with at least one cardiovascular symptom or sign (P=.002, adjusted for age and sex). Free IGF-I levels were also higher in subjects who had no atherosclerotic plaques in the carotid arteries (P=.02, adjusted for age and sex) and who had never smoked (P=.02, adjusted for age and sex). IGFBP-1 showed an inverse relation with insulin, BMI, and WHR and a positive relation with HDL cholesterol. The associations between IGFBP-1 levels and HDL cholesterol, WHR, and BMI remained significant after adjustment for fasting insulin levels. High fasting serum free IGF-I levels are associated with a decreased presence of atherosclerotic plaques and coronary artery disease and lower serum triglycerides, whereas high fasting IGFBP-1 levels are associated with a more favorable cardiovascular risk profile. The findings suggest that the IGF-I/IGFBP system is related to cardiovascular risk factors and atherosclerosis.
_________________________________________

J Clin Endocrinol Metab. 1998 Feb;83(2):499-502. Related Articles, Links

The insulin-like growth factor axis and plasma lipid levels in the elderly.
Ceda GP, Dall'Aglio E, Magnacavallo A, Vargas N, Fontana V, Maggio M, Valenti G, Lee PD, Hintz RL, Hoffman AR.
Cattedra di Geriatria, Universita di Parma, Italy.
The activity of the hypothalamic-GH-insulin-like growth factor (IGF) network declines with age. It has recently been shown that increased cardiovascular mortality occurs in adults with GH deficiency. As hypercholesterolemia is common in GH-deficient adults, and because there is experimental evidence that GH may play a role in regulating plasma cholesterol, we decided to investigate the activity of the GH-IGF axis in an elderly population by measuring serum IGF-I, IGF-II, and IGF-binding protein-3 (IGFBP-3) levels and to study their relationship with blood lipid levels. One hundred and thirty-two elderly subjects, 52 men and 80 women, were studied (age range, 60-91 yr). Men had significantly lower levels of IGFBP-3, high density lipoprotein cholesterol (HDL-C) and apoprotein A1 (ApoA1) compared to the women, whereas IGF-I and IGF-II were only slightly lower. Using linear regression analysis, we observed an inverse relationship of age with IGF-I (r = -0.35; P < 0.001), IGF-II (r = 0.40; P < 0.001), IGFBP-3 (r = 0.52; P < 0.001), body mass index, and lipid levels. Univariate regression analysis showed a strong and positive correlation of both IGF-I and IGFBP-3 with HDL-C and ApoA1. Partial correlation analysis, after adjustment for age and body mass index, showed that IGFBP-3 and IGF-II were still significantly and positively related to HDL-C and ApoA1. Furthermore, a strong association was documented among IGF-I, IGF-II, and IGFBP-3. These data demonstrate that even in an elderly population, further aging is accompanied by a progressive decline in circulating IGF-I, IGF-II, and IGFBP-3, suggesting a continuing diminution of the GH-IGF axis throughout aging. Moreover, the strong correlation between HDL-C and an index of GH secretion, such as IGFBP-3, suggests that GH might play an important role in lipid metabolism in healthy elderly subjects.
_________________________________________
J Clin Endocrinol Metab. 1999 Feb;84(2):453-7.

Comment in:
* J Clin Endocrinol Metab. 1999 Dec;84(12):4749-50.
* J Clin Endocrinol Metab. 2000 Dec;85(12):4923.


Growth hormone (GH) treatment reverses early atherosclerotic changes in GH-deficient adults.
Pfeifer M, Verhovec R, Zizek B, Prezelj J, Poredos P, Clayton RN.
Department of Endocrinology, Diabetes and Metabolic Diseases, University Medical Center, Ljubljana, Slovenia.
Hypopituitary patients have increased mortality from vascular disease, and in these patients, early markers of atherosclerosis [increased carotid artery intima-media thickness (IMT) and reduced distensibility] are more prevalent. As GH replacement can reverse some risk factors of atherosclerosis, the present study examined the effect of GH treatment on morphological and functional changes in the carotid and brachial arteries of GH-deficient (GHD) adults. Eleven GHD hypopituitary men (24-49 yr old) were treated with recombinant human GH (0.018 U/kg BW x day) for 18 months. IMT of the common carotid artery (CCA) and the carotid bifurcation (CB), and flow-mediated endothelium-dependent dilation (EDD) of the brachial artery were measured by B mode ultrasound before and at 3, 6, 12, and 18 months of treatment, and values were compared with those in 12 age-matched control men. Serum concentrations of lipids, lipoprotein(a), insulin-like growth factor I (IGF-I), and IGF-binding protein-3 (IGFBP-3) were also measured. In GHD men before treatment the IMTs of the CCA [mean(SD), 0.67(0.05) mm] and CB [0.75(0.04) mm] were significantly greater (P < 0.001) than those in control men [0.52(0.07) and 0.65(0.07) mm, respectively]. GH treatment normalized the IMT of the CCA by 6 months [0.53(0.04) mm] and that of the CB by 3 months [0.68(0.05) mm]. The IMT of the carotid artery (CCA and CB) was negatively correlated with serum IGF-I (r = -0.53; P < 0.0001). There was a significant improvement in flow-mediated EDD of the brachial artery at 3 months, which was sustained at 6 and 18 months of GH treatment (P < 0.05). GH treatment increased high density lipoprotein cholesterol at 3 and 6 months, but did not reduce total or low density lipoprotein cholesterol and was without effect on lipoprotein(a). There was no correlation between plasma lipids and changes in IMT or EDD of the arteries examined. In conclusion, GH treatment of hypopituitary GHD men reverses early morphological and functional atherosclerotic changes in major arteries and, if maintained, may reduce vascular morbidity and mortality. GH seems to act via IGF-I, which is known to have important effects on endothelial cell function.
___________________________________________________

Am J Hypertens. 2003 Sep;16(9 Pt 1):754-60.

Increased levels of insulin-like growth factor binding protein-3 in hypertensive patients with carotid atherosclerosis.
Watanabe T, Itokawa M, Nakagawa Y, Iguchi T, Katagiri T.
Division of Internal Medicine, Showa University Karasuyama Hospital, 6-11-11 Kita-karasuyama, Setagaya-ku, Tokyo 157-8577, Japan. karas@js9.so-net.ne.jp
BACKGROUND: It has been proven that the intima-media thickness (IMT) of the carotid artery increases in patients with essential hypertension. Serum levels of insulin-like growth factor-1 (IGF-1) increase in hypertensive patients with ventricular hypertrophy. However, the relationship between carotid atherosclerosis and serum levels of IGF-1 and its binding protein-3 (IGFBP-3) in patients with essential hypertension has not been established. METHODS: The carotid IMT, blood pressure (BP), serum lipid profiles, and serum IGF-1 and IGFBP-3 contents were determined in 54 hypertensive patients (19 with and 35 without carotid plaque) and 52 normotensive controls without plaque. RESULTS: Systolic, diastolic, and mean BPs and serum IGFBP-3 level were significantly higher in the hypertensive patients (with and without plaque) than in the normotensive controls. The IGFBP-3 level correlated with systolic BP (r = 0.204, P =.0354). Age, gender, body mass index, and serum levels of HDL cholesterol, triglycerides, lipoprotein(a), lipid peroxides, insulin, and fasting plasma glucose did not differ significantly among the three groups. Hypertensive patients with plaque, compared with those without plaque or the normotensive controls, had the highest values of carotid IMT, LDL cholesterol, IGF-1, and IGFBP-3. Multiple logistic regression analysis revealed that the IGFBP-3 level was associated with a ninefold (95% confidence interval 2.6-31) higher risk of carotid plaque formation compared with LDL cholesterol or IGF-1 levels. CONCLUSIONS: These results suggest that an increased level of IGFBP-3 may play a crucial role in the development of carotid atherosclerosis in hypertensive patients.
_____________________________________________
J Clin Endocrinol Metab. 1997 Jul;82(7):2204-9. Related Articles, Links

Serum levels of insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 in healthy centenarians: relationship with plasma leptin and lipid concentrations, insulin action, and cognitive function.
Paolisso G, Ammendola S, Del Buono A, Gambardella A, Riondino M, Tagliamonte MR, Rizzo MR, Carella C, Varricchio M.
Department of Geriatric Medicine and Metabolic Diseases, II University of Naples, Italy.
It has been demonstrated that healthy centenarians have more favorable anthropometric characteristics and insulin-mediated glucose uptake than aged subjects. The plasma insulin-like-growth factor I (IGF-I) concentration may account for such differences. Three groups of subjects were studied: 1) adults (< 50 yr; n = 30), 2) aged subjects (75-99 yr; n = 30), 3) centenarians (> 100 yr; n = 19). In all subjects, fasting plasma IGF-I, IGF-binding protein-3 (IGFBP-3), leptin, and lipid concentrations were determined; body composition was assessed by bioimpedance analysis; and insulin-mediated glucose up-take was evaluated by euglycemic hyperinsulinemic glucose clamp. IGF-I declined with advancing age, but no differences between aged subjects and centenarians were found. IGFBP-3 showed a trend similar to IGF-I, but lower values were present in centenarians than in aged subjects. Nevertheless, centenarians had a plasma IGF-I/IGFBP-3 molar ratio greater than that in aged subjects. Centenarians had also a whole body glucose disposal (WBGD) greater than that in aged subjects, but similar to that in adults. Mini Mental State Examination (27 +/- 2.1 vs. 18.3 +/- 3.1; P < 0.02) and Instrumental Activities Daily Living (26 +/- 2.6 vs. 8.4 +/- 4.1; P < 0.001) scores were significantly different in aged subjects and centenarians, respectively. In centenarians, the plasma IGF-I/IGFBP-3 molar ratio correlated with the body mass index (r = -0.55; P < 0.009); the amount of body fat (r = -0.62; P < 0.003); fat-free mass (r = 0.56; P < 0.008); fasting plasma leptin (r = -0.63; P < 0.004), triglycerides (r = -0.58; P < 0.01), free fatty acid (r = -0.64; P < 0.005), and low density lipoprotein cholesterol (r = -0.59; P < 0.009) concentrations; Mini Mental State Examination (r = 0.53; P < 0.0.03); and WBGD (r = 0.64; P < 0.005). All correlations were independent of daily fat and carbohydrate intake and WBGD (P < 0.05 for all). No significant correlations between the plasma IGF-I/IGFBP-3 molar ratio and plasma total (r = 0.31; P = NS) and high density lipoprotein cholesterol (r = 0.34; P = NS) concentrations were present. The correlation between the plasma IGF-I/IGFBP-3 molar ratio and WBGD persisted after adjustment for body fat, fasting plasma insulin concentration, daily carbohydrate and fat intake, and daily physical activity (r = 0.55; P < 0.009), but not after further adjustment for plasma free fatty acid concentration (r = 0.30; P = 0.17). In conclusion, healthy centenarians have plasma IGF-I/IGFBP-3 molar ratio greater than aged subjects. A more elevated plasma IGF-I/IGFBP-3 molar ratio might improve insulin action and plasma lipid concentration in centenarians.
_____________________________________
J Clin Endocrinol Metab. 2005 Sep;90(9):5146-55. Epub 2005 Jun 28.

Does a gender-related effect of growth hormone (GH) replacement exist on cardiovascular risk factors, cardiac morphology, and performance and atherosclerosis? Results of a two-year open, prospective study in young adult men and women with severe GH deficiency.
Colao A, Di Somma C, Cuocolo A, Spinelli L, Acampa W, Spiezia S, Rota F, Savanelli MC, Lombardi G.
Department of Molecular and Clinical Endocrinology and Oncology, "Federico II" University of Naples, via S. Pansini 5, 80131 Naples, Italy. colao@unina.it
CONTEXT: GH secretion and response to GH replacement are gender-related. OBJECTIVE: The objective of this study was to investigate the effects of GH deficiency (GHD) and replacement on the cardiovascular system according to gender. DESIGN: The design was open and prospective. SETTING: The study was conducted at a university hospital. SUBJECTS: Subjects included 36 severe adult-onset GHD patients (18 men, 20 women, aged < 45 yr); 36 gender-, age-, and body mass index-matched healthy subjects served as controls. INTERVENTIONS: Subjects received GH replacement at a median dose of 6.5 microg/kg.d in men and 7.7 microg/kg.d in women for 2 yr. MAIN OUTCOME MEASURES: Homeostasis model assessment index, total to HDL cholesterol ratio, fibrinogen and C-reactive protein levels, left ventricular mass index, blood pressure, heart rate, diastolic filling, and systolic function at rest and at peak exercise and intima-media thickness (IMT) at common carotid arteries were measured. RESULTS: Basal prevalence and/or degree of insulin resistance, lipid alterations, compromised cardiac function, and IMT were similar in women and men. Diastolic dysfunction was more prevalent in men (61 vs. 25%, P = 0.036). After GH replacement, IGF-I levels normalized in all patients. Lipid profile, fibrinogen, and C-reactive protein levels normalized in all cases. The total to HDL ratio (P = 0.04) was higher in women than men. The homeostasis model assessment index persisted higher in GHD patients than controls and decreased only in GHD men (P = 0.017). Left ventricular mass index normalized during treatment in both women and men, abnormal diastolic function persisted in three women (P = 0.031), and abnormal systolic performance persisted in six women and one man (P = 0.13). IMT decreased similarly in women and men, persisting higher than in controls. Exercise performance normalized in all. CONCLUSIONS: Two-year GH replacement has similar beneficial effects on cardiac and exercise performance and atherosclerosis in women and men with severe GHD.



_______________________________________________________________________________________

Clin Endocrinol (Oxf). 2004 Jul;61(1):81-7.

Different effects of short- and long-term recombinant hGH administration on ghrelin and adiponectin levels in GH-deficient adults.
Giavoli C, Cappiello V, Corbetta S, Ronchi CL, Morpurgo PS, Ferrante E, Beck-Peccoz P, Spada A.
Institute of Endocrine Sciences, University of Milan, Ospedale Maggiore IRCCS, Milan, Italy.
OBJECTIVE: To evaluate circulating levels of ghrelin and adiponectin (ApN) in GH-deficient (GHD) adults before and after short- and long-term recombinant human GH (rhGH) administration. PATIENTS AND METHODS: Twenty-three patients were studied. Seventeen subjects (Group A, 12 men, five women) were evaluated at baseline and after 1 year rhGH therapy (dose mean +/- SD: 0.3 +/- 0.1 mg/day) with the assessment of serum IGF-I, ghrelin, ApN, leptin, insulin and glucose levels, percentage of body fat (BF%), HOMA-IR and QUICKI. Seventeen age-, sex- and body mass index (BMI)-matched healthy subjects were recruited for comparisons. Six patients (Group B, three men, three women) underwent IGF-I generation test (rhGH 0.025 mg/kg/day for 7 days), blood sampled at baseline and on day 8 for determination of IGF-I, ghrelin and ApN levels. RESULTS: Group A: at baseline GHD patients showed low IGF-I levels and BF% significantly higher than controls (31.4 +/- 2.5 vs. 26.4 +/- 1.3, P < 0.05). Glucose, insulin, leptin, tryglicerides, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels, as well as HOMA-IR and QUICKI values were similar in the two series, while total cholesterol levels were higher in GHD. In GHD, ghrelin levels were significantly lower than in controls (193.9 +/- 27.1 vs. 298.1 +/- 32.5 pmol/l, respectively, P = 0.02), while ApN levels were similar (10.2 +/- 1.1 and 9 +/- 1 mg/l, respectively, P = ns). After 1 year of rhGH therapy, BF%, BMI, serum total and LDL cholesterol significantly decreased, serum leptin levels showed a trend to decrease, while HOMA-IR and QUICKI did not change. Ghrelin and ApN levels significantly increased from 193.9 +/- 27.1 to 232.4 +/- 26.3 pmol/l (P < 0.01) and from 8.6 +/- 0.8 to 10.3 +/- 1.1 mg/l (P < 0.05), respectively. In group B, the expected increase in IGF-I levels was associated with a significant decrease in ghrelin levels, while ApN did not change. CONCLUSION: GHD patients showed serum ghrelin lower than controls, probably due to the higher BF%. No difference in ApN was observed. Ghrelin and ApN increments induced by long-term treatment may be related to the significant BMI and BF% reduction that is the predominant metabolic effect of rhGH therapy. Conversely, the decrease in ghrelin levels observed after short-term rhGH administration may be consistent with an inhibitory feedback of GH and/or IGF-I on ghrelin release.
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Eur J Endocrinol. 2004 May;150(5):671-9.

Dose-, IGF-I- and sex-dependent changes in lipid profile and body composition during GH replacement therapy in adult onset GH deficiency.
Abrahamsen B, Nielsen TL, Hangaard J, Gregersen G, Vahl N, Korsholm L, Hansen TB, Andersen M, Hagen C.
Department of Endocrinology M, Odense University Hospital, Odense, Denmark.
OBJECTIVE: Patients with GH deficiency of adult onset (GHDA) exhibit dyslipidaemia and increased cardiovascular morbidity. GH replacement potently reduces body fat and serum lipids in GHDA. In recent years, lower GH doses have been introduced. The purpose of this analysis was to explore the response relationship between GH doses, lipids and body composition. DESIGN: Two consecutive, randomized 12-month GH replacement studies covering placebo and three different doses of GH (0.5, 1.0 and 1.7 IU/m(2) per day). Low and intermediate doses were IGF-I titrated. PATIENTS: Fifty-eight patients with severe GHDA, not previously treated with GH and stably substituted for other endocrine deficiencies, were included in the study. METHODS: Serum lipoproteins, serum IGF-I and body composition analysis by dual energy X-ray absorptiometry (DXA) were used. RESULTS: Fifty-seven percent of patients exhibited low density lipoprotein (LDL) cholesterol levels above 4.16 mmol/l, corresponding to the American Heart Association threshold of 160 mg/dl. GH treatment resulted in significant decreases in total and LDL cholesterol, with no significant change in high density lipoprotein cholesterol or triglycerides. The low dose induced no significant changes in lipid levels, whereas the medium dose reduced LDL cholesterol and the high dose decreased both LDL and total cholesterol. The effects depended significantly on the GH dose and the level of IGF-I obtained, but not on gender. GH replacement induced dose-dependent reductions in fat mass and sex-dependent increases in lean mass. CONCLUSIONS: GH given for 1 year at a dosage between 0.5 and 1.7 IU/m(2) per day reduced fat mass in a dose-dependent manner, increased lean body mass and lowered total and LDL cholesterol in patients with severe GHDA. Low dose GH treatment with normal IGF-I levels induced smaller changes compared with high dose therapy, and may need a longer treatment time.
______________________________________________

J Clin Endocrinol Metab. 2004 Apr;89(4):1801-7

Effects of growth hormone (GH) replacement therapy on low-density lipoprotein apolipoprotein B100 kinetics in adult patients with GH deficiency: a stable isotope study.
Christ ER, Cummings MH, Jackson N, Stolinski M, Lumb PJ, Wierzbicki AS, Sonksen PH, Russell-Jones DL, Umpleby AM.
Department of Endocrinology and Diabetology, University Hospital of Bern, Bern CH-3100, Switzerland.
GH replacement therapy has been shown to improve the dyslipidemic condition in a substantial proportion of patients with adult GH deficiency. The mechanisms are not yet fully elucidated. Low-density lipoprotein (LDL) apolipoprotein B100 (apoB) formation and catabolism are important determinants of plasma cholesterol concentrations. This study examined the effect of GH replacement therapy on LDL apoB metabolism using a stable isotope turnover technique. LDL apoB kinetics was determined in 13 adult patients with GH deficiency before and after 3 months GH/placebo treatment in a randomized, double-blind, placebo-controlled study. LDL apoB (13)C-leucine enrichment was determined by isotope-ratio mass spectrometry. Plasma volume was assessed by standardized radionuclide dilution technique. GH replacement therapy significantly decreased LDL cholesterol, LDL apoB concentrations, and LDL apoB pool size compared with placebo. Compared with baseline, GH replacement therapy resulted in a significant increase in plasma volume and fractional catabolic rate, whereas LDL formation rate remained unchanged. LDL lipid content did not significantly change after GH and placebo. This study suggests that short-term GH replacement therapy decreases the LDL apoB pool by increasing removal of LDL particles without changing LDL composition or LDL apoB production rate. In addition, it is possible that the beneficial effects of GH on the cardiovascular system contribute to these findings.
______________________________________________

J Clin Endocrinol Metab. 1999 Apr;84(4):1277-82. Related Articles, Links

The growth hormone (GH) response to the arginine plus GH-releasing hormone test is correlated to the severity of lipid profile abnormalities in adult patients with GH deficiency.
Colao A, Cerbone G, Pivonello R, Aimaretti G, Loche S, Di Somma C, Faggiano A, Corneli G, Ghigo E, Lombardi G.
Department of Molecular and Clinical Endocrinology and Oncology, Federico II University of Naples, Italy. colao@unina.it
The aim of the present study was to correlate the degree of the GH response to the combined arginine and GHRH (ARG+GHRH) test with clinical status in 157 adult hypopituitary patients and 35 healthy controls. On the basis of the GH response to ARG+GHRH, the 192 subjects were subdivided into 5 groups: group 1, very severe GH deficiency (GHD; 65 patients with GH peak <3 microg/L); group 2, severe GHD (37 patients with GH peak between 3.1-9 microg/L); group 3, partial GHD (25 patients with GH peak between 9.1-16.5 microg/L); group 4, non-GHD (30 patients with GH peak >16.5 microg/L); and group 5 (35 controls with GH peak >16.5 microg/L). Plasma insulin-like growth factor I (IGF-I) concentrations were lower (P < 0.001) in patients of group 1 (74.4 +/- 6.7 microg/L) and group 2 (81.4 +/- 6.8 microg/L) than in those of group 3, 4, and 5 (163.6 +/- 40.6, 185.9 +/- 21, and 188.8 +/- 11.1 microg/L, respectively). Plasma IGF-binding protein-3 concentrations were lower (P < 0.01) in group 1 (2.1 +/- 0.2 mg/L) and group 2 (2.0 +/- 0.2 mg/L) than in group 3 (3.4 +/- 0.7 mg/L) and group 5 (3.8 +/- 0.2 mg/L). In patients of group 1, total cholesterol (228.3 +/- 5.7 mg/dL) and triglycerides levels (187.4 +/- 15.3 mg/dL) were higher than those in group 3 (196.6 +/- 9.6 and 115.8 +/- 10.1 mg/dL, respectively), group 4 (176.8 +/- 11.3 and 101.4 +/- 12.5 mg/dL, respectively), and group 5 (160 +/- 6.9 and 99.3 +/- 5.4 mg/dL, respectively). High density lipoprotein cholesterol levels were lower in patients of group 1 (45.2 +/- 2.4 mg/dL) than in those of group 4 (54.7 +/- 3.5 mg/dL; P < 0.05) and group 5 (53.6 +/- 2 mg/dL; P < 0.001), whereas low density lipoprotein cholesterol levels were higher in patients of group 1 (127.3 +/- 7.9 mg/dL), group 2 (129.2 +/- 9.5 mg/dL), and 3 (133 +/- 9 mg/dL) than in those of group 5 (102.4 +/- 7.4 mg/dL; P < 0.05). Patients of group 2 had total cholesterol, high density lipoprotein cholesterol, and triglycerides levels at an intermediate level with respect to those in groups 1, 3, and 4. Among the five groups, no difference was found in fasting glucose concentrations, heart rate, or systolic and diastolic blood pressures. A significant increase in fat body mass and a decrease in lean body mass and total body water were found in all patients compared to controls. Disease duration was significantly shorter in patients of group 4 than in those of the remaining three groups (P < 0.001). A significant correlation was found between the GH peak after ARG+GHRH and disease duration (r = -0.401; P < 0.001), plasma IGF-I (r = 0.434; P < 0.001), total cholesterol (r = -0.324; P < 0.001), and triglycerides levels (r = -0.219; P < 0.05). A significant multiple linear regression coefficient was found between the GH peak after ARG+GHRH and plasma IGF-I levels (t = 2.947; P < 0.005), total cholesterol levels (t = -2.746; P < 0.01), and disease duration (t = -2.397; P < 0.05). In conclusion, the results of the present study indicate that the degree of the GH response to ARG+GHRH is correlated with the severity of lipid profile abnormalities and substantiate the reliability of the ARG+GHRH test for the diagnosis of GHD in adults. Because at present GH treatment is recommended only in adult patients with severe GHD, patients with a GH response below 9 microg/L to the ARG+GHRH test should be treated with GH, as should patients with a peak GH response to an insulin tolerance test below 3 microg/L.
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[HeadDoc]

Will thanks for posting the studies. Here's reference to a doc who does alot of lecturing on the same. You'll find lectures and citations.

http://ehealthspan.com/references/lectures.asp

The figure of 10% has come up in a few places as the reciprocal elevation of HGH to testosterone and vicaversa. Regardless the IGF-1 and IGFBP3 both are needed for effective and safe replacement. For most, HGH would be an expensive route to TRT. From the lectures I attended thru A4M it makes more sense to consider the use of testoserone and HGH as separate issues and treat them accordingly. If you have access to Dr. Rothenberg, he is more than versed in this. He has taught many of current generation of antiaging docs.

 

[WillBrink]

Will thanks for posting the studies. Here's reference to a doc who does alot of lecturing on the same. You'll find lectures and citations.

http://ehealthspan.com/references/lectures.asp

The figure of 10% has come up in a few places as the reciprocal elevation of HGH to testosterone and vicaversa. Regardless the IGF-1 and IGFBP3 both are needed for effective and safe replacement. For most, HGH would be an expensive route to TRT. From the lectures I attended thru A4M it makes more sense to consider the use of testoserone and HGH as separate issues and treat them accordingly. If you have access to Dr. Rothenberg, he is more than versed in this. He has taught many of current generation of antiaging docs.

Yes, my intent was not that one can treat the other, only that there was a relationship and effect between the two. Bang for the biological buck, I would take the T personally. Considering how little GH is needed and how low the cost og GH, it's at least getting within reason as a treatment, but T is dirt cheap compared to GH.

 

[hackskii]

What a great thread.
A nice refreshing read.

marianco, I didnt know about dehydration and test levels, thanks for that.

 

[marianco]

Here is an updated list of the labs I may run:

LAB TESTING IN PSYCHIATRY

Conventional Lab Tests

GENERAL:
Comprehensive Metabolic Panel (glucose, urea nitrogen, creatinine, calcium, sodium, potassium, CO2, chloride, total protein, albumin, globulin, total bilirubin, alkaline phosphatase, AST, ALT)
CBC (complete blood count)
Lipid Profile (including total cholesterol, triglycerides, HDL cholesterol, VLDL cholesterol, LDL cholesterol)
Urinalysis
Homocysteine
Uric Acid (if gout is a possibility)
Serum Myoglobin (if muscle aches are present)

TOXICITY:
Heavy Metal Screen (blood)
Urine Drug Screen
Specific Plasma or Serum Drug Level

REPRODUCTIVE:
Free and Total Testosterone, Sex Hormone Binding Globulin, Estradiol, Luteinizing Hormone, Follicle Stimulating Hormone, Prolactin, Prostate Specific Antigen, Dihydrotestosterone, Androstanediol glucucoronide

THYROID:
Free T4 (Free Thyroxine), Free T3 (Free Liothyronine), Thyroid Stimulating Hormone, Total T4, Total T3, Thyroglobulin, Reverse T3, antithyroglobulin antibody, antithyroid peroxidase antibody, thyroid stimulating immunoglobulin.

ADRENAL:
Cortisol AM, Cortisol PM, Cortisol-Binding Globulin, Adrenocorticotropic Hormone (ACTH), Dehydroepiandrosterone Sulfate (DHEA-s), Progesterone , Pregnenolone-sulfate

CARBOHYDRATE METABOLISM:
fasting glucose (included in comprehensive metabolic panel when fasting), Hemoglobin A1c, fasting insulin
3-Hour Glucose Tolerance Test (samples of blood for measuring glucose and insulin are taken at 0, 60, 120, and 180 minutes after ingesting a 1.75 g/kg glucose solution)

GROWTH HORMONE (if this was a consideration in treatment):
IGF-1 (Insulin-like growth factor I / Somatomedin-C), IGF-BP-3, 24-hour Urine Growth Hormone
Growth Hormone Stimulation Test using GHRH (growth hormone releasing hormone) plus Arginine (samples of blood for measuring growth hormone are taken at 0, 30, 60, 90, and 120 minutes)

INFLAMMATION:
C-reactive Protein
Erythrocyte Sedimentation Rate
Rheumatoid Factor

NUTRITIONAL:
Magnesium
Vitamin D, 1, 25-Dihydroxy
Vitamin B12
Folate
24-hour urine iodine - or Random urine iodine if 24-hour urine iodine is not available
(best is iodine excretion test with 50 mg loading dose of iodine given orally then 24-hour urine iodine done).
Vitamin A
Ferritin
Zinc
Copper

IMMUNE SYSTEM:
Interleukin-1 beta
Interleukin-2
Tumor Necrosis Factor-Alpha
Interleukin-6
Interleukin-10 (antiinflammatory cytokine)

The tests are done in the morning after fasting overnight (no food or drink after dinner except for water). The patient should drink 0.5 liters of water before the test to avoid dehydration. The patient should avoid strenuous activity the day before, avoid restaurant food and stimulants such as coffee, eat their regular meals, and avoid stressful situations for at least 2 days before the test.

Cortisol-PM is done in the afternoon between 4-6 PM on the same day as the morning test.

The 3-hour glucose tolerance test and growth hormone stimulation tests should be done on different days.


SPECIALTY LAB TESTS (Paid for by Patient Out-Of-Pocket):

NEUROTRANSMITTER PROFILE:
Spot-urine test which includes: Serotonin, Dopamine, GABA, Glutamate, Norepinephrine, Epinephrine.

SALIVARY CORTISOL AND DHEA PROFILE:
Four saliva samples during the day for Cortisol and DHEA

Comprehensive 24-hour urine hormone panel
Which may include: DHEA, Androsterone, Etiocholanolone, Pregnanetriol, Cortisone, Cortisol, Tetrahydrocortisone, Tetrahydrocortisol, Allo-tetrahydrocortisol, Aldosterone, Tetrahydrocorticosterone, Allo-tetrahydrocorticosterone, Estrone, Estradiol, Estriol, Pregnanediol, Testosterone, Androsterone, 2-hydroxyestrogens, 16a-hydroxyestrone, 4-hydroxyestrone, 2-methoxyestrone, 2-methoxyestradiol, 5a-androstanediol, 5b-androstanediol, 11b-hydroxyandrosterone, 11b-hydroxyetiocholanolone, Free T3, Free T4, Sodium, Potassium, Calcium, Phosphorus, Magnesium

MRI of Brain
Chest X-Ray
EKG

 

[Grimnuruk]

Hi Marianco,
Could you expound on this a bit more: the testing for Serum Myoglobin (if muscle aches are present).
I have major problems with myofascial pain all over my body and only get (temporary) relief from: 1) extremely deep regular massage therapy (very expensive and difficult finding /keeping a therapist who is willing and able (strong enough) to do it. 2) constantly working trigger points against hard rubber ball and 3) TRT, initially it seemed to almost all go away after starting and now it is creeping back. regular exercise and stretching is a must or it hurts worse. It is obvious to me that my pain perception was highly skewed due to low T and fatigued adrenals but my muscles actually knotting up and needing an extreme amount of maintenance work to keep functional is what bothers me.

 

[marianco]

Serum Myoglobin

Hi Marianco,
Could you expound on this a bit more: the testing for Serum Myoglobin (if muscle aches are present).
I have major problems with myofascial pain all over my body and only get (temporary) relief from: 1) extremely deep regular massage therapy (very expensive and difficult finding /keeping a therapist who is willing and able (strong enough) to do it. 2) constantly working trigger points against hard rubber ball and 3) TRT, initially it seemed to almost all go away after starting and now it is creeping back. regular exercise and stretching is a must or it hurts worse. It is obvious to me that my pain perception was highly skewed due to low T and fatigued adrenals but my muscles actually knotting up and needing an extreme amount of maintenance work to keep functional is what bothers me.

Serum myoglobin is released from muscle cells when they experience injury or destruction.

It is commonly elevated in agitated mental states, seizures, high fevers, and other conditions which cause muscle injury or destruction. Untreated, the elevated serum myoglobin is toxic to the kidneys and may result in kidney failure.

It is frequently elevated when using anticholesterol medications such as Lipitor, Zocor, Crestor, etc. when they cause weird muscle pains - and some other medications.

The condition of muscle destruction is called Rhabdomyolysis - a serious, potentially life threatening condition. When it is obvious - such as when people have delirium and an agitated state, then someone may think of getting the serum myoglobin done.

Unfortunately, in more subtle situations, very few physicians (if any at all) in my experience, check this very basic test when they prescribe patients anticholesterol medications. They all test for liver function as indicated by the prescribing information. But they don't think deeply enough to do the serum myoglobin.

In some of my paitents, this resulted in unnecessary E.R. visits and hospitalizations due to unusual pains such as unexplained facial pains until I myself checked their serum myoglobin.