There is no evidence to show that the supplements boost bones or prevent fractures, study finds. There is no evidence to show that the supplements boost bones or prevent fractures, study finds.
Foods rich in calcium include dairy products, green leafy vegetables such as broccoli, cabbage, soya beans, nuts, bread and anything made with fortified flour. The NHS says adults need 700mg of calcium a day, and does not recommend supplements of it, though older people are advised to boost their Vitamin D. But some doctors and international organisations recommend higher calcium intakes in order to improve bone density and prevent fractures.
Foods rich in calcium include dairy products, green leafy vegetables such as broccoli, cabbage, soya beans, nuts, bread In the new studies New Zealand scientists looked at diet and supplements on bone health in women and men aged over 50. The first research found that increasing calcium intake from dietary sources or by taking supplements produces small (1-2 per cent) increases in bone mineral density, which "are unlikely to lead to a clinically meaningful reduction in risk of fracture." The second found that dietary calcium intake is not associated with risk of fracture, and found no evidence from clinical trials that increasing the amount consumed prevented such breaks. In an editorial Professor Karl Michaelsson from Uppsala University in Sweden said: "The official recommendations in the UK and Nordic countries of 700-800 mg/day of dietary calcium for adults seem at present to be enough. "This intake can be achieved with a normal varied diet. In the UK, up to 11 per cent of British adults are estimated take calcium supplements. However there have been repeated safety concerns about the pills, which have been shown to double the risk of a heart attack. Researchers said it was “puzzling” that organisations such as the International Osteoporosis Foundation continued to promote intakes so high that most people over the age of 50 would need to take a supplement. “Most will not benefit from increasing their intakes and will be exposed instead to a higher risk of adverse events such as constipation, cardiovascular events, kidney stones, or admission for acute gastrointestinal symptoms,” Prof Michaelsson said.
DHT, via its metabolite 3α-androstanediol (produced by 3α-hydroxysteroid dehydrogenase (3α-HSD)), is a neurosteroid that acts via positive allosteric modulation of the GABAA receptor. Testosterone, via conversion into DHT, also produces 3α-androstanediol as a metabolite and hence has similar activity. Some AAS that are or can be 5α-reduced, including testosterone, DHT, stanozolol, and methyltestosterone, among many others, can or may modulate the GABAA receptor, and this may contribute as an alternative or additional mechanism to their central nervous system effects in terms of mood, anxiety, aggression, and sex drive
He also suggested "the profitability of the global supplements industry probably plays its part” in some of the advice to take supplements. A spokesman for the Health Supplement Information Service said: “It is important to note that there were disparities in the calcium supplementation trial methodologies which make comparisons between trials and hence conclusions difficult. "Fourteen of the 26 trials studied calcium alone, eight studied calcium and vitamin D, and four were multi-arm or factorial studies of both agents. “In addition, the majority did not take vitamin D status into account; calcium cannot be absorbed or utilized without vitamin D and there is a wealth of evidence to suggest that a combination of these nutrients is effective for reducing the risk of both fracture and falls.”
Non-17α-alkylated testosterone derivatives such as testosterone itself, DHT, and nandrolone all have poor oral bioavailability due to extensive first-pass hepatic metabolism and hence are not orally active. A notable exception to this are AAS that are androgen precursors or prohormones, including dehydroepiandrosterone (DHEA), androstenediol, androstenedione, boldione (androstadienedione), bolandiol (norandrostenediol), bolandione (norandrostenedione), dienedione, mentabolan (MENT dione, trestione), and methoxydienone (methoxygonadiene) (although these are relatively weak AAS). AAS that are not orally active are used almost exclusively in the form of esters administered by intramuscular injection, which act as depots and function as long-acting prodrugs. Examples include testosterone, as testosterone cypionate, testosterone enanthate, and testosterone propionate, and nandrolone, as nandrolone phenylpropionate and nandrolone decanoate, among many others (see here for a full list of testosterone and nandrolone esters). An exception is the very long-chain ester testosterone undecanoate, which is orally active, albeit with only very low oral bioavailability (approximately 3%). In contrast to most other AAS, 17α-alkylated testosterone derivatives show resistance to metabolism due to steric hindrance and are orally active, though they may be esterified and administered via intramuscular injection as well. In addition to oral activity, 17α-alkylation also confers a high potential for hepatotoxicity, and all 17α-alkylated AAS have been associated, albeit uncommonly and only after prolonged use (different estimates between 1 and 17%), with hepatotoxicity. In contrast, testosterone esters have only extremely rarely or never been associated with hepatotoxicity, and other non-17α-alkylated AAS only rarely, although long-term use may reportedly still increase the risk of hepatic changes (but at a much lower rate than 17α-alkylated AAS and reportedly not at replacement dosages).[additional citation needed] In accordance, D-ring glucuronides of testosterone and DHT have been found to be cholestatic. Aside from prohormones and testosterone undecanoate, almost all orally active AAS are 17α-alkylated. A few AAS that are not 17α-alkylated are orally active. Some examples include the testosterone 17-ethers cloxotestosterone, quinbolone, and silandrone, which are prodrugs (to testosterone, boldenone (Δ1-testosterone), and testosterone, respectively), the DHT 17-ethers mepitiostane, mesabolone, and prostanozol (which are also prodrugs), the 1-methylated DHT derivatives mesterolone and metenolone (although these are relatively weak AAS), and the 19-nortestosterone derivatives dimethandrolone and 11β-MNT, which have improved resistance to first-pass hepatic metabolism due to their 11β-methyl groups (in contrast to them, the related AAS trestolone (7α-methyl-19-nortestosterone) is not orally active). As these AAS are not 17α-alkylated, they show minimal potential for hepatotoxicity.