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Doctor Mariano,
I have been using HGH for two years and my IGF-1 continues to slowly plummet. Three ius a day, every night.
Generally is around 170 but has hit 130 recently. I am 48. I started on it when I found my IGF-1 to be 122. Has hit the 200s when I was overeating. Recent fasting insulin was about 3.7. This was near the bottom of the range, which I believe to be good.
I think the HGH is working for fat loss and hopefully helping me out of osteopenia, but is there anything I can do to increase the IGF-1. I mean, it is low enough for treatment!
Am I just fine the way it is? I am 175 pounds and 6 foot 2, in good shape I think. On TRT with level of high 600s on 70 mg twice a week. Bio only in the low 300s. This too had been higher.
Thank you.
Bob
@00slotiv 2957 wrote:
I have been using HGH for two years and my IGF-1 continues to slowly plummet. Three ius a day, every night.
Generally is around 170 but has hit 130 recently. I am 48. I started on it when I found my IGF-1 to be 122. Has hit the 200s when I was overeating. Recent fasting insulin was about 3.7. This was near the bottom of the range, which I believe to be good.
I think the HGH is working for fat loss and hopefully helping me out of osteopenia, but is there anything I can do to increase the IGF-1. I mean, it is low enough for treatment!
Am I just fine the way it is? I am 175 pounds and 6 foot 2, in good shape I think. On TRT with level of high 600s on 70 mg twice a week. Bio only in the low 300s. This too had been higher.
Although I have my own ideas, I am curious.
What have you and your doctor done to evaluate and improve the response to growth hormone?
@DrMariano 2958 wrote:
Although I have my own ideas, I am curious.
What have you and your doctor done to evaluate and improve the response to growth hormone?
Nothing. She wonders if the HGH is doing any good but it certainly is. It is Genotropin made by the company I work for. It is very high quality.
She has not propounded a way to improve the response.
I had a similar response after initiating Sermorelin a couple of years ago. Started at 122 IGF-1, got as high as 265, then down in stages to 126.
I don’t doubt that there is ample growth hormone circulating, but don’t know if the IGF-1 I have now is high enough in spite of that, or if I am getting adequate repair from it.
Is this something you have encountered in your practice?
I covet your ideas Doctor Mariano.
Thanks for responding so rapidly too! 🙂
Bob
@00slotiv 2961 wrote:
Nothing. She wonders if the HGH is doing any good but it certainly is. It is Genotropin made by the company I work for. It is very high quality.
She has not propounded a way to improve the response.
I had a similar response after initiating Sermorelin a couple of years ago. Started at 122 IGF-1, got as high as 265, then down in stages to 126.
I don’t doubt that there is ample growth hormone circulating, but don’t know if the IGF-1 I have now is high enough in spite of that, or if I am getting adequate repair from it.
Growth hormone levels can be verified using a 24-hour urine test.
When growth hormone fails to increase IGF-1 signaling, a person has Growth Hormone Resistance. Growth Hormone Resistance has multiple possible causes. It is important to examine for each of those causes to help improve response to growth hormone.
The partial circuitry involved in IGF-1 production is as follows:
1. Growth Hormone Receptors are produced in Liver Cells.
2. Growth hormone from the pituitary or exogenous source stimulates Growth Hormone Receptors.
3. Stimulation of the Growth Hormone Receptor triggers within-cell signaling processes called signal transduction. Signal transduction includes activation of a protein called STAT5b.
4. STAT5b triggers the production of IGF-1.
5. Stimulation of the Growth Hormone Receptor also leads to the production of IGF Binding Protein 3 (IGFBP3) and Acid Labile Subunit (ALS).
6. In circulation, IGF-1 Binds to IGFBP3. The two then bind to ALS. This combination lengthens the half-life of IGF-1 to 12-hours.If IGF-1 does not bind to proteins (free IGF-1), its half-life is 4.5 minutes. There are about 6 IGF Binding Proteins. 75-80 % of IGF-1 is bound to IGFBP3. About 1-2 % of IGF-1 is free. Growth Hormone triggers the production of IGF-1, IGFBP3, and ALS.
If there is any problem at any step of the circuitry described, the production of IGF-1 from Growth Hormone will be reduced and Growth Hormone Resistance occurs.
Some Conditions That Can Cause Growth Hormone Resistance:
* Alcohol. One drink is toxic enough to impair cellular metabolism in the liver such that growth hormone receptor production is reduced, inflammatory signaling is raised to the point production of IGF-1 and its binding proteins are reduced. One drink wastes an entire day’s worth of growth hormone.* Fasting. Fasting inhibits growth hormone receptor production. Fasting also reduces production of IGF Binding Proteins.
* Nutritional Deficiencies. Nutrient deficiencies (such as in Vitamin A, iron, protein, etc.) directly or indirectly impair IGF-1 and IGFPB3 production.
* Hypoglycemia or low insulin levels can reduce IGF Binding Proteins other than IGFBP3. This can reduce the half-life of IGF-1, lowering blood levels.
* Hypothyroidism. Suboptimal thyroid hormone signaling impairs production of growth hormone receptors.
* Excessive Inflammatory Cytokine Signaling from the Immune System. Inflammatory cytokines (such as Tumor Necrosis Factor Alpha (TNF-alpha), InterLeukin 1a, 1b, and 6) can inhibit growth hormone receptor production, impair signal transduction, impair IGF-1 gene expression, leading to impaired IGF-1 production and impaired IGFBP3 and ALS production.
* Excess Estrogen. Excessive estrogen (e.g. estradiol and the numerous other estrogens.) binding to its receptor can directly reduce IGF-1 gene expression and hence IGF-1 production. Estrogen can increase inflammatory cytokine signaling and reduce thyroid hormone signaling. These can lead to reduced growth hormone receptor production and reduced IGF-1 production. Oral estrogen is particularly bad. It is a waste to use growth hormone when taking oral estrogens. Tamoxifen (Nolvadex) acts like estrogen in the liver, leading to a reduction in IGF-1. Arimidex may block estradiol production, but it doesn’t block the production of other estrogens. And, if the Arimidex dose is too high, even estradiol can be produced via alternative pathways.
* Liver Disease. Liver disease may involve impaired cellular metabolism and excessive inflammatory signaling which impairs IGF-1, IGFBP3, and ALS production.
* Renal Disease. Renal disease can cause multiple problems including nutritional, electrolyte, hormonal problems, and the production of inhibitors (including inflammatory signals) which lead to reduced growth hormone receptor production, impaired signal transduction and gene expression, which lead to decreased IGF-1. The ALS protein can also be lost from the kidney into the urine in protein-losing kidney diseases, leading to reduced half-life of IGF-1, leading to reduced IGF-1 level.
* Infections. Infections can cause excessive inflammatory cytokine production which decrease IGF-1. Some infections may not have obvious symptoms – such as periodontal disease, some gut infections, etc.
* Stress and trauma. Stress (either internal or external) increases norepinephrine signaling (the primary stress signal) and/or histamine signaling (another stress signal). These can increase inflammatory cytokine production which decrease IGF-1.
* Diabetes Type 2. Diabetes Type 2 and pre-diabetes have multiple pathophysiologies which can impair IGF-1 including increased stress/norepinephrine signaling, suboptimal thyroid signaling, increased immune system inflammatory signaling, cellular metabolic problems which impairs growth hormone receptor, IGF-1 and binding protein production.
* Autoimmune diseases, such as the inflammatory bowel diseases, can cause excessive production of inflammatory cytokines, which decrease IGF-1.
* Growth Hormone inhibiting antibodies. There is a rare condition where a person has a mutation in growth hormone which causes the immune system to recognize exogenous growth hormone as foreign. The body produces antibodies which inactivate growth hormone. This can cause response to exogenous Growth Hormone to progressively go down.
* Genetic Growth Hormone Resistance. Genetic defects can cause growth hormone receptor deficiency, impaired signal transduction, impaired gene expression and production of IGF-1, IGFBP3, and ALS, leading to low IGF-1 levels.
* Xenobiotics. Environmental toxins (including some plastics) can act like estrogen or lead to increased inflammatory cytokine signaling, leading to reduced IGF-1.
* Cancer. Some cancers increase inflammatory cytokine signaling.
* Etc., Etc., Etc.
This is quite a response Doctor Mariano. Thank you for putting it together. I may have forgotten to mention that my last IGFBP-3 was a little under the range. The second one before that was the same exact way. Usually it is on the low side of normal.
I’ve done the Rhein’s urine test and the GH there is above the range. I believe it. Just not doing much for the IGF-1.
In perusing your list, I am on Thyroid and those #s are good and getting better. Anastrozole has E2 mid range on the Mayo Clinic ultrasensitive. I eat healthy most of the time and shouldn’t be deficient unless it is vitamin A. Drink once a year maybe, don’t fast.
Fasting insulin is low. Don’t recall being hypoglycemic. Inflammation markers have always been good.
I am not over stressed. I work a lot of hours but exercise and get eight hours of bed time a night usually. Am happy with life and work generally.
As far as liver and renal issues, how would they be manifested? Maybe there is something to this.
If nothing is able to be changed, am I alright with high GH but IGF-1 between 130 and 150?
Thank you again for your five star response. Very thorough!
Bob
@00slotiv 2967 wrote:
I may have forgotten to mention that my last IGFBP-3 was a little under the range. The second one before that was the same exact way. Usually it is on the low side of normal.
I’ve done the Rhein’s urine test and the GH there is above the range. I believe it. Just not doing much for the IGF-1.
In perusing your list, I am on Thyroid and those #s are good and getting better.
Anastrozole has E2 mid range on the Mayo Clinic ultrasensitive.
I eat healthy most of the time and shouldn’t be deficient unless it is vitamin A.
Drink once a year maybe, don’t fast.
Fasting insulin is low. Don’t recall being hypoglycemic.
Inflammation markers have always been good.
I am not over stressed. I work a lot of hours but exercise and get eight hours of bed time a night usually.
Am happy with life and work generally.
As far as liver and renal issues, how would they be manifested? Maybe there is something to this.If nothing is able to be changed, am I alright with high GH but IGF-1 between 130 and 150?
Inflammation markers do not always indicate if one has an infection or even inflammation. They may not be specific enough for certain illnesses. They may be specific for some illnesses but not many others. Thus, it is up to the physician to decide which of the tons tests available to use to diagnosis for specific illnesses based on the patient’s history and exam. For example, C-Reactive Protein, for example, may be fairly specific for cardiac risk, but is poor for everything else. Erythrocyte Sedimentation Rate may be useful for diagnosing temporal arteritis and polyarthralgia rheumatica, but it can be very insensitive and may be “normal” for other inflammatory illnesses and infections.
Some infections are not obvious.
I seldom see anyone who is not deficient in many nutrients. Since the 1920s, nutritional status has decreased tremendously. Modern diets just do not give sufficient nutrition for health.
The list I presented is fairly technical. Self-diagnosis without the expertise is problematic. Even I would consult my physician if I reach the end of my expertise. This is why I usually recommend that people consult their physicians, particularly those who are prescribing the failing treatment in the first place, for reevaluation.
Thanks Doctor Mariano.
Bob
@DrMariano 2968 wrote:
Inflammation markers do not always indicate if one has an infection or even inflammation. They may not be specific enough for certain illnesses. They may be specific for some illnesses but not many others. Thus, it is up to the physician to decide which of the tons tests available to use to diagnosis for specific illnesses based on the patient’s history and exam. For example, C-Reactive Protein, for example, may be fairly specific for cardiac risk, but is poor for everything else. Erythrocyte Sedimentation Rate may be useful for diagnosing temporal arteritis and polyarthralgia rheumatica, but it can be very insensitive and may be “normal” for other inflammatory illnesses and infections.
Some infections are not obvious.
I seldom see anyone who is not deficient in many nutrients. Since the 1920s, nutritional status has decreased tremendously. Modern diets just do not give sufficient nutrition for health.
The list I presented is fairly technical. Self-diagnosis without the expertise is problematic. Even I would consult my physician if I reach the end of my expertise. This is why I usually recommend that people consult their physicians, particularly those who are prescribing the failing treatment in the first place, for reevaluation.
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