But I am taking at least 3 heaping teaspoons of bone meal, daily, 10,000 IU of vitamin D (look up Sarfraz Zaidi’s The Power of Vitamin D, his clinical patients have taught him that the need for D averages about 10,000 IU per day, his practice is in Ventura , sunny S CA (I am at 40 latitude, I lose IVB rays about Sept through May), he found only ONE patient to have optimal D, she was a lifeguard, in a swimsuit 5 hours a day 5 days a week, so much for 15 minutes a day on the arms and legs.
There is also sulfur needed to combine the D, see Stephanie Seneff’s great interview with Dr Mercola on that fascinating subject.
There is also the Study published on the Weston Price website on true vitamin A and Vitamin D working as a team to remove risk of toxicity; https:///health-topics/abcs-of-nutrition/vitamin-a-on-trial-does-vitamin-a-cause-osteoporosis/
So I’m on sulfur (MSM 1 gram a day), D(10,000 IU), K2 (60 mg , yes you read that right, no puny micrograms for me), magnesium (at least 1 gram or more a day), vitamin A (25,000 IU a day, I have high needs, I have to go optimal until I get results), natural B complex, C (12 grams a day), natural E 1000 IU, etc. ZInc/copper for bones too.
Figure B shows a picture of a male with Gigantism (over-secretion of growth hormone) who had a final height of nearly 9 feet. Longitudinal bone growth occurs at the growth plate by a process called endochondral ossification in which cartilage is first formed and then remodeled into bone tissue. The growth plate consists of three principal layers: the resting zone, proliferative zone, and hypertrophic zone. Growth hormone acts preferentially at the proliferative zone where it stimulates longitudinal bone growth.
Figure A represents Spondyloepiphyseal dysplasia (SED) where there is disproportionate dwarfism, spinal involvement, and a barrel chest from a COL2A1 mutation. Figure C represents diastrophic dysplasia with a "hitch-hikers" thumb, "cauliflower ear", cleft palate, and short-limbed dwarfism due to a sulfate transport mutation. Figure D represents cleidocranial dysplasia due to defect in core-binding factor alpha 1 (CBFA-1) causing dwarfism and absent clavicles. Figure E represents Multiple epiphyseal dysplasia (MED) causing disproportionate dwarfisim with multiple epiphyses involved, shortened metacarpals, valgus knees, but no spinal involvement, all of which are due to a COMP mutation.
Testosterone is significantly correlated with aggression and competitive behaviour and is directly facilitated by the latter. There are two theories on the role of testosterone in aggression and competition.  The first one is the challenge hypothesis which states that testosterone would increase during puberty thus facilitating reproductive and competitive behaviour which would include aggression.  Thus it is the challenge of competition among males of the species that facilitates aggression and violence.  Studies conducted have found direct correlation between testosterone and dominance especially among the most violent criminals in prison who had the highest testosterone levels.  The same research also found fathers (those outside competitive environments) had the lowest testosterone levels compared to other males.