If you’re implementing nutritional or pharmaceutical strategies to increase Growth Hormone, and you’re not getting enough Vitamin D, you may be wasting your efforts.
Vitamin D is actually technically a steroid, and one that is produced in the skin during exposure to ultraviolet rays. Many people have mistakenly assumed spending time in the sun will take care of deficiencies, but it’s important to know that even regular sun exposure might not be enough if you live in certain latitudes that aren’t close enough to the equator. Another thing to consider is that sunscreens inhibit the formation of 25-hydroxyvitamin D, the active form of Vitamin D. Will it completely prevent it? Not necessarily, but supplementing with Vitamin D is cheap, and the concern we used to have for overdoses of it have been found to be unwarranted. In some studies, upwards of 50,000 IUS of Vitamin D were given to MS patients with no side effects reported. The daily recommended amount is 1000 IUs. But if you are deficient, and Vitamin D deficiency is quickly becoming one of the most common vitamin deficiencies there is, then supplementing with 5000 IUs for a few weeks and then backing down to 1000 IUs daily could be seen as a successful way to balance out Vitamin D levels, which leads to a host of benefits.
Vitamin D is essential for the absorption of calcium and magnesium into bones. Without adequate Vitamin D, someone could consume copious amounts of calcium and never fully absorb it where it matters most. In fact, in some studies, it has been shown that boosting Vitamin D levels, while leaving Calcium levels constant, is a much more viable strategy to prevent osteoporosis. In addition to bone health, Vitamin D plays a role in muscular function. Vitamin D actually activates a receptor in muscle tissue which enhances RNA activated Muscle Protein synthesis. In addition to bone health and muscular development, Vitamin D has also been shown to positively affect mood. Studies suggest that Vitamin D deficiency can slow down the production of Serotonin, the neurotransmitter typically targeted in anti-depressant medications.
A recent study I dug up shows that Vitamin D may also enhance circulating levels of IGF-1. IGF-1 is created when growth hormone levels stimulate the liver to produce this unique anabolic peptide. Many people today are employing methods of raising Growth Hormone levels, by using supplements, diet or sometimes the use of rHGH, a pharmaceutical version of Growth Hormone. But many of the positive benefits of GH come indirectly as a result of increased IGF-1 levels, so it’s essential that Vitamin D levels be maintained in order to adequately take advantage of this effect.
Vitamin D increases circulating IGF1 in adults: potential implication for the treatment of GH deficiency.
Ameri P1, Giusti A, Boschetti M, Bovio M, Teti C, Leoncini G, Ferone D, Murialdo G, Minuto F.
Previous studies suggested that vitamin D modulates circulating IGF1. We investigated this effect in adults and its clinical relevance in the management of GH deficiency (GHD).
DESIGN AND METHODS:
IGF1 levels were prospectively measured before and after 12 weeks of treatment with oral vitamin D3 (5000 or 7000 IU/week) vs no intervention in 39 subjects 61.9±7.9 years old. The frequency of IGF1 values ≥50th age- and sex-specific percentile in relation to vitamin D status, as determined by the concentration of 25-hydroxyvitamin D (25(OH)D), was retrospectively assessed in 69 GHD patients (57.4±16.6 years) on stable hormone replacement and with 25(OH)D and IGF1 concurrently measured.
Treatment with 5000 and 7000 IU vitamin D3/week significantly raised 25(OH)D by 12.7±8.4 and 13.1±6.5 ng/ml respectively (both P<0.001 vs baseline). In the 7000 IU group, IGF1 levels also significantly increased by 31.3±36.7 ng/ml (P=0.01). Neither 25(OH)D nor IGF1 significantly varied in controls. IGF1 was ≥50th percentile more frequently in GHD patients with 25(OH)D levels ≥15 than <15 ng/ml (65.9 vs 40.0%, P<0.05). Logistic regression with adjustment for recombinant human GH (rhGH) dose, vitamin D supplements, gender, use of thyroid hormones, corticosteroids or estrogen/testosterone, and season revealed a significant positive association between ≥15 ng/ml 25(OH)D and IGF1 ≥50th percentile (OR 4.4, 95% CI 1.0-18.8, P<0.05). A significant negative correlation between 25(OH)D concentrations and rhGH dose was found after correcting for age and IGF1 (β -0.042, P<0.01), but not after further adjusting for sex, thyroid, adrenal or gonadal replacement, and season (β -0.037, P=0.06).
Vitamin D increases circulating IGF1 in adults. As a result, a better vitamin D status may ease the achievement of normal IGF1 values in GHD.
Another very recent study backs up this finding by showing that Vitamin D significantly influences glucose tolerance and insulin sensitivity in women. Again, researchers noted the variant responsible for this increase in glucose tolerance? You guessed it, Vitamin D.
J Nutr. 2014 Apr 9. [Epub ahead of print]
Evidence for Threshold Effects of 25-Hydroxyvitamin D on Glucose Tolerance and Insulin Resistance in Black and White Obese Postmenopausal Women.
Sorkin JD1, Vasaitis TS, Streeten E, Ryan AS, Goldberg AP.
We identified normal vs. abnormal 25-hydroxyvitamin D [25(OH)D] concentrations by examining the relation of 25(OH)D to non-bone-related measures (plasma glucose, insulin resistance, lipids, blood pressure, fitness, obesity, and regional adiposity) and asking whether there is a 25(OH)D concentration above and below which the relation between 25(OH)D and outcome changes. We examined the relation between 25(OH)D and outcome by race to see whether race-specific normal ranges are needed, and we examined the role of insulin-like growth factor-1 (IGF-1) in modulating the relation between 25(OH)D and outcome. In a cross-sectional study of 239 overweight and obese, sedentary postmenopausal women without diabetes (83 black, 156 white), outcome measures included plasma lipids, glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), IGF-1, parathyroid hormone (PTH), aerobic fitness, body composition, subcutaneous abdominal and visceral fat, and blood pressure. We identified threshold effects in the association between 25(OH)D and these variables using piecewise linear regressions. We found that 25(OH)D was inversely related to fasting glucose, fasting and 2-h insulin, HOMA-IR, visceral abdominal fat, percentage fat, PTH, and triglycerides. Evidence for a threshold effect of 25(OH)D was found for 2-h glucose, 2-h insulin, fasting insulin, and HOMA-IR. There was no evidence suggesting the need for race-specific normal 25(OH)D concentrations. IGF-1 modulated the relation between 25(OH)D and outcome but only below, and not above, a threshold 25(OH)D concentration. Our findings suggest a threshold effect of 25(OH)D on glucose-insulin metabolism such that 25(OH)D ≥ ∼26 μg/L (65.0 pmol/L) supports normal glucose homeostasis and that the same cut point defining normal 25(OH)D concentration can be used in black and white women. This study was registered at clinicaltrials.gov as NCT01798030.
If you’re not supplementing with Vitamin D, I highly recommend it. As with any fat-soluble vitamin, take it with a fatty meal, which if you follow my blog with any regularity you should know that would be just about any meal 😉