Quote from Dr. Garrett Smith on November 8, 2018, 7:15 pm

There is a worldwide osteoporosis epidemic.  This goes hand-in-hand with the worldwide Poison/"Vitamin A" epidemic, and it is well-established that the more Poison/"Vitamin A" is in the body, the greater the bone loss.

From the National Institute of Health, pointing out what is not just a coincidence:

Vitamin A and Bone Health

Older adults are at significant risk for osteoporosis and related fractures, and their serum (blood) levels of retinol increase with age.

The next paper shows that intakes of retinol that are barely at or slightly above the RDA (adult male RDA is 5,000 IU, adult female RDA is 4,000 IU) reduced bone density and increased fracture risk:

Excessive dietary intake of vitamin A is associated with reduced bone mineral density and increased risk for hip fracture.

BACKGROUND: The highest incidence of osteoporotic fractures is found in northern Europe, where dietary intake of vitamin A (retinol) is unusually high. In animals, the most common adverse effect of toxic doses of retinol is spontaneous fracture.

"Spontaneous fractures" in animals are a lot like when older people suddenly fall down BECAUSE their femur suddenly snapped.  In osteoporosis, it is all too often the case that a person doesn't  "fall and break their hip"...it is that their hip/femur bone BROKE and that is why they FELL.  From the NIH: "It is known as a silent disease because it progresses without symptoms, osteoporosis involves the gradual loss of bone tissue or bone density and results in bones so fragile they break under the slightest strain."

Anybody would fall if a bone they were standing on suddenly snapped underneath them, right?

OBJECTIVE: To investigate whether excessive dietary intake of vitamin A is associated with decreased bone mineral density and increased risk for hip fracture.

For the "food-based Vitamin A is always safe and innocent and wonderful and harmless" folks...the researchers assessed their DIETARY AKA FOOD INTAKE of Vitamin A.

DESIGN: A cross-sectional study and a nested case-control study.

SETTING: Two counties in central Sweden.

PARTICIPANTS: For the cross-sectional study, 175 women 28 to 74 years of age were randomly selected. For the nested case-control study, 247 women who had a first hip fracture within 2 to 64 months after enrollment and 873 age-matched controls were selected from a mammography study cohort of 66,651 women 40 to 76 years of age.

MEASUREMENTS: Retinol intake was estimated from dietary records and a food-frequency questionnaire. Bone mineral density was measured with dual-energy x-ray absorptiometry. Hip fracture was identified by using hospital discharge records and was confirmed by record review.

RESULTS: In multivariate analysis, retinol intake was negatively associated with bone mineral density. For every 1-mg increase in daily intake of retinol, risk for hip fracture increased by 68% (95% CI, 18% to 140%; P for trend, 0.006). For intake greater than 1.5 mg/d compared with intake less than 0.5 mg/d, bone mineral density was reduced by 10% at the femoral neck (P = 0.05), 14% at the lumbar spine (P = 0.001), and 6% for the total body (P = 0.009) and risk for hip fracture was doubled (odds ratio, 2.1 [CI, 1.1 to 4.0]). [this is ONLY 5000 IU of Poison/"Vitamin A", that's not much at all!]

CONCLUSION: High dietary intake of retinol seems to be associated with osteoporosis.

More DIETARY intake of RETINOL = more osteoporosis.

Let me do a calculation for you, in terms of intakes of some foods you might have been duped into giving yourself osteoporosis with:

• 1 ounce (28 grams) of beef liver = ~5000 IU
• 1 tsp of cod liver oil = ~5000 IU
• 25 grams of sweet potato = ~5000 IU

Those are TINY amounts, folks!  It only takes ONE of the above things to get the 5000 IU that showed increased osteoporosis!  What about the people who are being encouraged to eat as much of ALL of these things as possible?!?!  Do you think the osteoporosis epidemic is an ACCIDENT?  I don't!

In case you thought this association between Poison/"Vitamin A" and osteoporosis/fractures was only in women, it's not.  Here's one in men:

Serum Retinol Levels and the Risk of Fracture

RESULTS:  The risk of fracture was highest among men with the highest levels of serum retinol. Multivariate analysis of the risk of fracture in the highest quintile for serum retinol (>75.62 μg per deciliter [2.64 μmol per liter]) as compared with the middle quintile (62.16 to 67.60 μg per deciliter [2.17 to 2.36 μmol per liter]) showed that the rate ratio was 1.64 (95 percent confidence interval, 1.12 to 2.41) for any fracture and 2.47 (95 percent confidence interval, 1.15 to 5.28) for hip fracture. The risk of fracture was further increased within the highest quintile for serum retinol. Men with retinol levels in the 99th percentile (>103.12 μg per deciliter [3.60 μmol per liter]) had an overall risk of fracture that exceeded the risk among men with lower levels by a factor of seven (P<0.001).

CONCLUSIONS:  Our findings, which are consistent with the results of studies in animals, as well as in vitro and epidemiologic dietary studies, suggest that current levels of vitamin A supplementation and food fortification in many Western countries may need to be reassessed.

Another study with men and women, same thing:

Retinol intake and bone mineral density in the elderly: the Rancho Bernardo Study.

Retinol is involved in bone remodeling, and excessive intake has been linked to bone demineralization, yet its role in osteoporosis has received little evaluation. We studied the associations of retinol intake with bone mineral density (BMD) and bone maintenance in an ambulatory community-dwelling cohort of 570 women and 388 men, aged 55-92 years at baseline. Regression analyses, adjusted for standard osteoporosis covariates, showed an inverse U-shaped association of retinol, assessed by food-frequency questionnaires in 1988-1992, with baseline BMD, BMD measured 4 years later, and BMD change. Supplemental retinol use, reported by 50% of women and 39% of men, was an effect modifier in women; the associations of log retinol with BMD and BMD change were negative for supplement users and positive for nonusers at the hip, femoral neck, and spine. At the femoral neck, for every unit increase in log retinol intake, supplement users had 0.02 g/cm2 (p = 0.02) lower BMD and 0.23% (p = 0.05) greater annual bone loss, and nonusers had 0.02 g/cm2 (p = 0.04) greater BMD and 0.22% (p = 0.19) greater bone retention. However, among supplement users, retinol from dietary and supplement sources had similar associations with BMD, suggesting total intake is more important than source. In both sexes, increasing retinol became negatively associated with skeletal health at intakes not far beyond the recommended daily allowance (RDA), intakes reached predominately by supplement users. This study suggests there is a delicate balance between ensuring that the elderly consume sufficient vitamin A and simultaneously cautioning against excessive retinol supplementation.

This is a KEY sentence:  "However, among supplement users, retinol from dietary and supplement sources had similar associations with BMD, suggesting total intake is more important than source."

PLEASE stop with the "food-based Vitamin A" is somehow magickally different and immune to causing humanity-wide disease than supplements.  The RESEARCH and FACTS do NOT agree with you.  You are, quite simply, incorrect.

Two more papers definitively linking higher Poison/"Vitamin A"--one by blood level, the other by intake-- to lowered bone density:

High Serum Retinol as a Relevant Contributor to Low Bone Mineral Density in Postmenopausal Osteoporotic Women.

There is controversial information about the impact of vitamin A on bone. Some epidemiological studies show that excessive intake of vitamin A, or an excess of serum vitamin A, has related with adverse impact on bone mass; however, other studies did not find these links, and some authors have proposed that this vitamin might promote a better bone health. The present work aims to contribute to clarify the real role of vitamin A in bone tissue. For this purpose, a cross-sectional study of 154 osteoporotic non-treated postmenopausal women (> 65 years old) was carried out.
[...]
 It is concluded that elevated serum-retinol levels are associated with an increased risk of low bone mass and thus with osteoporotic fractures. Therefore, osteoporosis-risk assessment should include quantification of serum metabolite of vitamin A.

Vitamin A intake and osteoporosis: a clinical review.

RESULTS:  Of 20 clinical studies, 3 were randomized controlled trials (RCTs), 14 were observational studies, and 3 were case reports. Most (8) observational studies were cross-sectional. Oral retinyl palmitate (RP) in high doses induces fractures and radiographic osteoporosis in animals. Retinol intake from diet or supplements is negatively associated with lumbar, femoral neck, and trochanter bone mineral density (BMD). There is a graded increase in relative risk of hip fracture with increasing retinol intake, attributable primarily to retinol (either from diet or supplements) but not beta-carotene intake. Higher serum retinol levels are associated with higher risk of any fracture and with higher risk of hip fracture, whereas there is no evidence of harm associated with beta-carotene intake. The few RCTs involve serum markers of bone metabolism, not bone density or fracture outcomes. Observational studies are generally consistent in finding harm from either dietary or supplemental retinol intake on BMD and hip fracture risk. Total Vit A intake is more important than source in determining harm. Adverse effects may occur at a level of retinol intake that is only about twice the current recommendation for adult females.

CONCLUSIONS:  It is not yet possible to set a specific level of retinol intake above which bone health is compromised. Pending further investigation, Vit A supplements should not be used with the express goal of improving bone health.

Apparently this process has not only been shown in adults, but also in infants, mice, and zebrafish:

Excessive dietary intake of vitamin A reduces skull bone thickness in mice

Calvarial thinning and skull bone defects have been reported in infants with hypervitaminosis A. These findings have also been described in humans, mice and zebrafish with loss-of-function mutations in the enzyme CYP26B1 that degrades retinoic acid (RA), the active metabolite of vitamin A, indicating that these effects are indeed caused by too high levels of vitamin A and that evolutionary conserved mechanisms are involved. To explore these mechanisms, we have fed young mice excessive doses of vitamin A for one week and then analyzed the skull bones using micro computed tomography, histomorphometry, histology and immunohistochemistry. In addition, we have examined the effect of RA on gene expression in osteoblasts in vitro. Compared to a standard diet, a high dietary intake of vitamin A resulted in a rapid and significant reduction in calvarial bone density and suture diastasis. The bone formation rate was almost halved. There was also increased staining of tartrate resistant acid phosphatase in osteocytes and an increased perilacunar matrix area, indicating osteocytic osteolysis. Consistent with this, RA induced genes associated with bone degradation in osteoblasts in vitro. Moreover, and in contrast to other known bone resorption stimulators, vitamin A induced osteoclastic bone resorption on the endocranial surfaces.

This should be fairly clear.  It should be noted that I am anti-Poison/"Vitamin A", and I am also anti-Vitamin D supplementation in all its forms.  The latter part will be a whole other forum section...for now, if you want to see my older writings on the problems with "eating" Vitamin D, go to my FaceBook Notes (linked below in my signature).