haidut

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I was shocked to find this "editorial" in, of all places, the BMJ since it is known as one of the bastions of modern "medicine" (together with NEJM). I hope this is a good sign that not all allopathic doctors are villains. Either way, it makes for a very interesting read and it reads as if Peat himself wrote it.

http://www.bmj.com/rapid-response/2011/ ... ficiencies

"... Jean-Yves Reginster writes that besides all these pharmacological agents, calcium and vitamin D should be a first line strategy for the management of osteoporosis—unless an individual's dietary assessment shows a satisfactory intake.

Contrary to popular belief the available published evidence suggests that osteoporosis is not primarily due to deficiencies of either calcium or oestrogen but is related to deficiencies of key nutrients. Low serum serum bone alkaline phosphatase (ALP) activity (a measure of poor bone formation), relates to reduced zinc, magnesium and manganese concentrations. ALP activity improves when these nutrients are supplemented, both in vitro and in vivo.

Among women with confirmed or suspected osteoporosis, those taking hormone replacement therapy (HRT) had abnormally high serum copper levels and decreased ALP activity compared with non-users with osteoporosis. HRT takers also had significantly lower white cell zinc, lower red cell magnesium and lower serum bone ALP concentrations, and significantly higher mean serum phosphate levels, than other women with osteoporosis. Hormone takers also tended to have lower serum manganese, tartrate-resistant acid phosphatase (a measure of bone resorption), and vitamin C levels, and higher urinary excretion of zinc and hydroxyproline. Taking exogenous steroid sex hormones is associated with a reduction in essential bone nutrients and reduced bone formation.

International incidence data show that fractures among women aged 35-65 years have increased dramatically in hormone prescribing countries, and this may be mediated by reduction in essential nutrients for bone formation.

Dr Kitty Little, the author of Bone Behaviour, wrote that observations on osteoporosis from the sixth century onwards have shown that stress is the main causative factor. This has been confirmed by animal experiments, using rabbits, with stress simulated by the administration of cortisone. For normal health, the hormonal anticatabolic/catabolic ratio should remain on the anticatabolic side.

Stress, emotional or otherwise, can tip the balance over to the catabolic side. In the presence of progestational compounds (in the pill or hormone replacement therapy), much lower levels of stress are needed. The main types of osteoporosis are disuse, with a lower blood flow through bone, steroid-induced and thrombus-induced osteoporosis. When the anticatabolic/catabolic ratio tips to the catabolic side, cell membranes become more rigid. Osteogenic precursor cells coalesce to form osteoclasts, which remove bone. Memory cells are affected, and also those responsible for the absorption of food from the gut. Increased catabolic levels also lead to the production of abnormal megakaryocytes. These produce sticky platelets that immediately coalesce to form thrombi. Many can block blood vessels in cortical bone, killing the osteocytes. Later the dead bone is removed by phagocytic cells. Other thrombi are deposited elsewhere in the body, including the coronary arteries. In these ways, hormone replacement therapy may cause osteoporosis, thrombi, heart attacks and senility, rather than preventing them.

It is likely that the changes in vascularity and clotting caused by HRT have given clinicians a misleadingly false impression of favourable increases in bone density. The WHI study underestimated adverse effects like fractures by not comparing current HRT users with never users of hormones."
 

Amazoniac

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I was shocked to find this "editorial" in, of all places, the BMJ since it is known as one of the bastions of modern "medicine" (together with NEJM). I hope this is a good sign that not all allopathic doctors are villains. Either way, it makes for a very interesting read and it reads as if Peat himself wrote it.

http://www.bmj.com/rapid-response/2011/ ... ficiencies

"... Jean-Yves Reginster writes that besides all these pharmacological agents, calcium and vitamin D should be a first line strategy for the management of osteoporosis—unless an individual's dietary assessment shows a satisfactory intake.

Contrary to popular belief the available published evidence suggests that osteoporosis is not primarily due to deficiencies of either calcium or oestrogen but is related to deficiencies of key nutrients. Low serum serum bone alkaline phosphatase (ALP) activity (a measure of poor bone formation), relates to reduced zinc, magnesium and manganese concentrations. ALP activity improves when these nutrients are supplemented, both in vitro and in vivo.

Among women with confirmed or suspected osteoporosis, those taking hormone replacement therapy (HRT) had abnormally high serum copper levels and decreased ALP activity compared with non-users with osteoporosis. HRT takers also had significantly lower white cell zinc, lower red cell magnesium and lower serum bone ALP concentrations, and significantly higher mean serum phosphate levels, than other women with osteoporosis. Hormone takers also tended to have lower serum manganese, tartrate-resistant acid phosphatase (a measure of bone resorption), and vitamin C levels, and higher urinary excretion of zinc and hydroxyproline. Taking exogenous steroid sex hormones is associated with a reduction in essential bone nutrients and reduced bone formation.

International incidence data show that fractures among women aged 35-65 years have increased dramatically in hormone prescribing countries, and this may be mediated by reduction in essential nutrients for bone formation.

Dr Kitty Little, the author of Bone Behaviour, wrote that observations on osteoporosis from the sixth century onwards have shown that stress is the main causative factor. This has been confirmed by animal experiments, using rabbits, with stress simulated by the administration of cortisone. For normal health, the hormonal anticatabolic/catabolic ratio should remain on the anticatabolic side.

Stress, emotional or otherwise, can tip the balance over to the catabolic side. In the presence of progestational compounds (in the pill or hormone replacement therapy), much lower levels of stress are needed. The main types of osteoporosis are disuse, with a lower blood flow through bone, steroid-induced and thrombus-induced osteoporosis. When the anticatabolic/catabolic ratio tips to the catabolic side, cell membranes become more rigid. Osteogenic precursor cells coalesce to form osteoclasts, which remove bone. Memory cells are affected, and also those responsible for the absorption of food from the gut. Increased catabolic levels also lead to the production of abnormal megakaryocytes. These produce sticky platelets that immediately coalesce to form thrombi. Many can block blood vessels in cortical bone, killing the osteocytes. Later the dead bone is removed by phagocytic cells. Other thrombi are deposited elsewhere in the body, including the coronary arteries. In these ways, hormone replacement therapy may cause osteoporosis, thrombi, heart attacks and senility, rather than preventing them.

It is likely that the changes in vascularity and clotting caused by HRT have given clinicians a misleadingly false impression of favourable increases in bone density. The WHI study underestimated adverse effects like fractures by not comparing current HRT users with never users of hormones."
Toxic 5 year silence, but I'm breaking it:
- Impacts of Psychological Stress on Osteoporosis: Clinical Implications and Treatment Interactions
- Chronic Psychological Stress as a Risk Factor of Osteoporosis
 

Blossom

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Amazoniac

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Thanks for breaking the silence. It should be regulated like a drug. :):
If the person is under stress, it's better to fail with movement because it can trick the brain that there is escape, that the person ainn't doomed. A walking failure is safe. However, there are times when walking is not possible, such as waiting on a line or minutes before a public presentation, in these cases the stress is temporary and inescapable, so, chewing a gum makes sense because it will provide relief without perforating the stomach. If it's prolonged, the alternatives to walking would be viewing everyone that gets close as kalingas and attack them because they're a threat to your stability; or retract, get depressed and begin self-harm to distract your brain with a physical injury; both are toxic, shouldn't be promoted as drugs.
 

LucyL

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Dr Kitty Little, the author of Bone Behaviour, wrote that observations on osteoporosis from the sixth century onwards have shown that stress is the main causative factor.

Wow, that's a heck of a rabbit hole - thanks @Amazoniac for opening this back up.


My oncologist insists osteoporosis is due to estrogen depletion by AIs, and wants to do regular bone scans. So this is fascinating. After all, what cancer patient isn't stressed?
Impacts of Psychological Stress on Osteoporosis: Clinical Implications and Treatment Interactions
IGFs may also play a role in psychological stress (47) and osteoporosis (48). Circulating IGF-1 is increased in individuals with depression or anxiety disorders (49, 50) and has been shown to be a biomarker for vulnerability of an individual to stress following traumatic brain injury (51). Yu et al. found that, in a single prolonged stress model, IGF-1 levels were up-regulated by approximately 25% in the stressed group, although this data was not statistically significant (52).

In bone health, IGF-1 and−2 regulate osteoblast-osteoclast interactions, thus making them important regulators of bone remodeling (54). IGF-1 has also been shown to activate mammalian target of rapamycin (mTOR) remodeling to stimulate MSC differentiation into osteoblasts (55). Knockout of IGF-1 impairs osteoblast differentiation and leads to decreased trabecular bone formation (56). Its role in fracture healing is still not fully understood, as some studies suggest beneficial effects of IGF-1 treatment, while other studies demonstrate non-significant effects (5759).
It is this mTOR activation that makes many people leery of IGF-1 when dealing with cancer, but in the end, it may all go back to our old friend Serotonin.

Antidepressant-like behavioral effects of IGF-I produced by enhanced serotonin transmission
Because the pattern of antidepressant-like effects of IGF-I resembled those of selective serotonin reuptake inhibitors, the role of serotonin in the behavioral effects of IGF-I was studied. Depletion of serotonin, by the tryptophan hydroxylase inhibitor para-chlorophenylalanine, blocked the antidepressant-like effects of IGF-I. Administration of IGF-I increased basal serotonin levels in the ventral hippocampus and altered the effects of acute citalopram.
...
Thus, IGF-I administration initiates a long-lasting cascade of neurochemical effects involving increased serotonin levels that results in antidepressant-like behavioral effects.
From this article The two faces of serotonin in bone biology

The free circulating form of gut-derived serotonin directly signals to the osteoblast by binding to the Htr1b receptor. This binding inhibits the phosphorylation of CREB by PKA, leading to decreased expression of Cyclin (Cyc) genes and decreased osteoblast proliferation. As a result, bone formation is slowed down.

so I try to tie this to another post by haidut
Lower Growth Hormone (hGH) And IGF-1 Levels In Men Extends Lifespan in which haidut wrote:
The hormone IGF-1 is driven primarily by etsrogen, so high IGF-1 levels are typically found in hyperestrogenic conditions. This is actually the only reason why estrogen appears beneficial to bone health in studies - i.e. through its boosting of IGF-1. However, with age and declining health, the prolactin release that estrogen also triggers overcomes the effects (and release) of IGF-1 and estrogen ends up destroying the bones when chronically elevated.

So perhaps when the AI's lower estrogen, and subsequently IGF-1, seratonin is no longer countered by IGF-1's positive bone effects and wreaks havoc? Hence Ray's recommendation to drink milk, does give IGF-1, but also the IGF binding proteins which may mitigate it's carcinogenic nature.
 

Blossom

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If the person is under stress, it's better to fail with movement because it can trick the brain that there is escape, that the person ainn't doomed. A walking failure is safe. However, there are times when walking is not possible, such as waiting on a line or minutes before a public presentation, in these cases the stress is temporary and inescapable, so, chewing a gum makes sense because it will provide relief without perforating the stomach. If it's prolonged, the alternatives to walking would be viewing everyone that gets close as kalingas and attack them because they're a threat to your stability; or retract, get depressed and begin self-harm to distract your brain with a physical injury; both are toxic, shouldn't be promoted as drugs.
Thanks. I’ve felt much stronger after incorporating regular walks in nature back into my life. I joined a gym yesterday which is something I never thought I’d do again but I think building more muscle can only help at this point.
 

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