Latest Osteoporosis News ‘Decoded’
I’m always on the look out for the latest osteoporosis news. Today, I’ll do more than just share the most recent news with you. I’ll also decode them. Why would I decode news you might wonder?
The answer is a lot simpler than you might think. By “decoding”, I mean that I have dug deeper into the news content, and will explain their real meaning to you.
So let’s get started.
1. Prolia’s Maker Amgen Exceeds Profit Estimates
Amgen, the largest biotech company in the world and maker of the osteoporosis drug Prolia, has topped Wall Street’s expectations for their second quarter earnings.1 With $1.27 billion for the second quarter, and total revenue up by double digits, at $4.48 billion, the company’s CEO has pledged to focus on expanding its international market and to increase bone drugs sales.2
The osteoporosis drug market is hugely profitable, with just about every post-menopausal woman diagnosed and therefore, prescribed an osteoporosis drug. Both Prolia and its stronger-dosed twin Xgeva (the latter used in cancer patients) contributed to the company’s bottom line by more than $500 million in 2011.
While Amgen’s best-selling immune-suppressing drug Enbrel, prescribed for rheumatoid arthritis, has brought in no less than $3.5 billion in 2010, the bone health arena is viewed as having more potential for increasing sales. Plus who’s to say that in the not-so distant future, new and more horrific side effects linked to Prolia won’t be discovered? This might explain the rush to increase Amgen’s bone drug sales.
If you don’t have the Osteoporosis Reversal Program, I urge you to read my review of Prolia. If you have the Osteoporosis Reversal Program, you already know in great detail its mechanism of action, side effects, and numerous scientifically backed reasons why you should never use it.
2. Moderate Alcohol Consumption Has a Positive Effect on Bones
Daily intake of alcohol, equivalent to one or two glasses of wine a day, helps to maintain bone strength, according to the latest study published in the journal Menopause.3
Scientists from the International Scientific Forum on Alcohol Research have observed that just 19 grams of alcohol a day decreased old bone loss, helping maintain bone strength.
Further confirming the beneficial action of alcohol, bone turnover markers increased with no alcohol supplementation. This observation has led to the conclusion that moderate alcohol consumption has a similar effect on bone turnover as bisphophonate drugs.3
The study is flawed from its very inception. I’ll explain. Titled “Moderate alcohol intake lowers biochemical markers of bone turnover in postmenopausal women”, the 40 study participants had their bone formation marker osteocalcin (s-OC) and their resorption marker C-terminal telopeptide (CTx) measured daily and 14 days after stopping the alcohol.4
Osteocalcin is secreted by osteoblasts – cells that are responsible for replacing old bone with new bone. It is involved in bone-building, bone mineralization, and in maintaining calcium levels. High osteocalcin levels can therefore be linked to increases in bone density.
C-terminal telopeptide (CTx) is an indicator of bone turnover, as it measures the presence of collagenous tissue found in bone, specifically the portion cleaved by osteoclasts as they remove old bone.
Since mainstream science views osteoporosis as a disease that causes excessive bone turnover and insufficient bone deposition – without understanding why this happens – they conclude that an increase in both osteocalcin and C-terminal telopeptide reflect accelerated bone loss. For that reason, the latest observation that alcohol reduced levels of both, has lead to the conclusion that alcohol can help “build bones”.
As I wrote in the Osteoporosis Reversal Program, the correct equilibrium of bone resorption and deposition is crucial. But what if reduced osteocalcin and C-terminal telopeptide levels could actually be detrimental?
For the answer, let’s take a look at another study conducted by oral and maxillofacial surgeons. Their retrospective study also measured osteocalcin and C-terminal telopeptide to establish if these markers could help predict bisphosphonate-related osteonecrosis of the jaw (BRONJ).5
They found that study subjects who had been diagnosed with BRONJ had lower levels of both markers than those in the control group (also on bisphosphonate therapy but without BRONJ). Can we still believe that low levels of these markers are necessarily good for bones? Not according to this study, whose authors conclude that:
“As a result of the s-CTX and s-OC testings at the diagnosis of BRONJ, the values of the two markers were decreased.The decrease of the s-OC values implies a problem during the bone-formation process… This result may imply that, during bisphosphonate therapy, simultaneous consideration of s-CTX showing inhibition of bone resorption and s-OC indicating the degree of bone formation might be a set of risk markers assessing risk prediction for BRONJ before invasive dental surgery.”
And one more inconsistency: osteoporosis treatment with Forteo (teriparatide) increases osteocalcin serum levels, which is seen as a benefit, since its presence indicates bone formation.6 Go figure!
These are yet more examples of the confusing “double speak”, typical of Mainstream Medicine. It is quite obvious that relying on their skewed scientific findings can lead to disaster. Fortunately, with the Osteoporosis Reversal Program by your side, you don’t have to…
Till next time!
4 Marrone JA, et al. “Moderate alcohol intake lowers biochemical markers of bone turnover in postmenopausal women.” Menopause 2012.
5 Kwon YD, et al. “Retrospective study of two biochemical markers for the risk assessment of oral bisphosphonate-related osteonecrosis of the jaws: can they be utilized as risk markers? Clin. Oral Implants Res. 2011 Jan;22(1):100-5. doi: 10.1111/j.1600-0501.2010.01965.x. Epub 2010 Oct 13.
6 Cosman F et al. Retreatment with teriparatide one year after the first teriparatide course in patients on continued long-term alendronate. J Bone Miner Res. 2009 Jun;24(6):1110-5.