Good vibrations

I start each morning with 10 minutes of Qi Gong.  Which translated simply means vibrating and shaking my body around.

This simple activity give me an amazing energy burst that lasts most of the day.  Sometimes, if I have seen a lot of patients I have to do it again in the afternoon.  It always helps.

Here is a NASA article from 2001 talking about research showing standing on a vibrating plate for a few minutes everyday drastically improves bone density.

Health care is not rocket science.  Staying healthy is a daily responsibility, please take care of yourself.

Dr D

http://science.nasa.gov/science-news/science-at-nasa/2001/ast02nov_1/

Osteoporosis Drugs May Be Linked to Cancer Risk

Original article

Side Effects of Osteoporosis Drugs can Be Far Worse than Brittle Bones…

Osteoporosis drugs have become increasingly well-known for their dangerous side effects, many of which could easily be worse than your original concern.

Acid reflux and related esophageal inflammation were a couple of the side effects that quickly became apparent when these drugs hit the market. This is why you’re instructed to take them with food and avoid lying down shortly after taking them.

But as I predicted over a decade ago, that’s just the beginning of the health nightmare these drugs can bring about.

Since their release, bisphosphonate drugs have also become associated with:

  • Hypocalcemia (blood calcium levels are too low)
  • Serious eye inflammation and possible blindness
  • Severe musculoskeletal pain
  • Stomach ulcers – particularly when taken together with anti-inflammatory drugs.

    In one study, 8 percent of participants taking Fosamax and 12 percent of those receiving the anti-inflammatory Naprosyn developed stomach ulcers. But when the two drugs were taken in combination, the rate of stomach ulcers rose to a whopping 38 percent.

    This is important, as many elderly, particularly women, are likely to suffer from both arthritis and osteoporosis, increasing the likelihood of bisphosphonates and anti-inflammatory drugs being taken at the same time.

  • Liver damage –Although the mechanism is still unknown, researchers believe drugs like Fosamax may inhibit the synthesis of cholesterol in your liver, which may alter liver function.

    Regardless of the mechanism, if you’re taking Fosamax or related bisphosphonate drugs you need to beware of the possibility of liver dysfunction, and your doctor should monitor you properly for it.

  • Kidney failure (renal failure)
  • Atrial fibrillation — Women who have used Fosamax are nearly twice as likely to develop atrial fibrillation (quivering of your heart’s upper chambers), which is the most common kind of chronically irregular heartbeat

    One study published in the Archives of Internal Medicine found that Fosamax was associated with an 86 percent higher risk of atrial fibrillation compared to those who had never used the drug.

    Atrial fibrillation can cause palpitations, fainting, fatigue, or congestive heart failure. It can also lead to embolic strokes.

  • Thigh bone (femur) fractures – Although you’ve only started hearing about this recently, the FDA asked Merck (the maker of Fosamax) to “add information about the report of femur fractures” to the medication’s package insert back in 2008, according to an ABC News report.

    Sixteen months later they finally added it to the list of fine print side effects, but neither Merck nor the FDA properly informed doctors and patients of this newfound risk.

    According to a recent report by a US panel of experts reviewing the evidence of increased risk of unusual femur fractures, 94 percent of patients who had experienced a femur break had been on bisphosphonate drugs. Most of them had taken the drugs longer than five years.

    More than half of those who broke their thigh bones had reported groin or thigh pain for a period of weeks or months before fractures occurred.

    In addition, “more than a quarter of patients who experienced atypical femur fractures in one leg experienced a fracture in the other leg as well,” Canadian CTV reports.

  • Osteonecrosis of your jaw bone (jaw bone death) — This is a serious condition that can also cause disfiguration as the bone in your jaw dies and begins to decay.

    Symptoms include jaw pain, infection, and loosening of your teeth. However, some people experience no symptoms until they suddenly notice exposed bone. If you’ve had teeth extracted, or wear full dentures, you may also be at greater risk.

    Interestingly, an animal study published in the June issue of Journal of Bone and Mineral Research concluded that osteonecrosis of the jaw may involve the interaction between bisphosphonate drugs and vitamin D deficiency! As you will see below, optimizing your vitamin D levels is imperative for healthy bones, and this finding further strengthens that recommendation.

Osteoporosis & Heart Disease Linked

By Bob Livingston • Apr 17th, 2009 •

original article here

Osteoporosis & Heart Disease Linked Studies show an inverse correlation between bone mineral density and calcification of the arteries—a major contributor to heart disease. This means that if our bone mineral density is low, the calcification of our arteries is high. This makes osteoporosis and heart disease twins.

What is the common thread between osteoporosis and heart disease? It’s vitamin D and vitamin K deficiency. Vitamin K is commonly known for its ability to activate blood clotting factors, but it is equally important and responsible for the activation of two other important proteins: osteocalcin, which is involved in the mineralization of bone matrix, and matrix Gla protein (MGP), which protects soft tissues from calcification. Vitamin D is also necessary for proper bone mineralization. Vitamin K is needed in smaller amounts than vitamin D to abate toxic effects of soft tissue calcification. Bone health requires both vitamins D and K. Clinical trials show that vitamin K supplementation increases the activation of osteocalcin, decreasing bone loss and increasing bone mineral density.

Gone is osteoporosis and calcification of the arteries. Calcification of the arteries is a clinical predictor of heart disease. And studies show that those with the highest intake of vitamin K have less severe artery calcification. Can vitamin D and vitamin K reverse artery calcification? There is no evidence that they can but they could stop further calcification.

My choice to clean out calcification is oral EDTA chelation. Warfarin (a blood thinner) does its work by inhibiting vitamin K recycling, causing soft tissue calcification. Those on this drug might consider talking to your doctor about switching to fish oil and cod liver oil, the best natural blood thinners. Otherwise you might change the effect of your prescribed blood thinner. So don’t take them both. It’s vitamin K or Warfarin. The best vitamin K that I know of is by Standard Process. It is an oil based chlorophyll complex (perle) product containing A, K, E and F. Chlorophyll is the essence of the life-supporting nutritional pattern of the planet earth. Cooking our green foods destroys the chlorophyll content. Most chlorophyll supplements sold are water soluble and mostly void of any nutrition.

Fosomax has been shown to cause strokes

Women who have used Fosamax are nearly twice as likely to develop atrial fibrillation (quivering of your heart’s upper chambers), which is the most common kind of chronically irregular heartbeat.

Fosamax is the most widely used drug treatment for the bone-thinning disease osteoporosis. The FDA approved the first generic version (called alendronate) in February.

The drug was associated with an 86 percent higher risk of atrial fibrillation compared with never having used the drug. Atrial fibrillation can cause palpitations, fainting, fatigue, or congestive heart failure. They can also lead to embolic strokes.

Medicine’s New Direction:

By: Dr. Jeffrey S. Bland, PhD

 Osteoarthritis, rheumatoid arthritis, osteoporosis, periodontal disease, coronary heart disease, metabolic syndrome, and type-2 diabetes — these common and very different diseases typically require separate and different medical protocols.

 In August 2007, a collaborative group of medical scientists from Columbia University, University of Cambridge, Penn State Medical Center, Northwestern University School of Medicine, and the Laboratory for Endocrinology Research in Lyon, France, authored a research paper that caught the attention of the medical world.

Their conclusion: The skeleton is an endocrine organ and has an effect on insulin signaling and adiponectin expression in adipocytes (fat cells). (1)

 This extraordinary discovery links obesity, insulin resistance/metabolic syndrome, diabetes, and heart disease to bone physiology and the bone-derived hormone osteocalcin that regulates energy metabolism and the insulin/glucose axis.  Osteocalcin “speaks” to adipocytes and insulin secreting beta-cells of the pancreas, and influences both insulin action and insulin-sensitizing and the anti-inflammatory protein adiponectin.  In essence, the report defined skeletal health and function as principle factors in the risk to diseases of metabolism and demonstrated a direct relationship between skeletal health and the prevention of diabetes and heart disease.

 BEYOND ‘WEAR AND TEAR’

Skeletal health is dependent upon lifestyle, genetic, structural, and nutritional factors.  The lack of weight-bearing activities reduces the activity of the bone rebuilding osteoblast, in turn reducing the release of osteocalcin.  The reduction in osteocalcin adversely influences insulin signaling and increases the risk to many chronic diseases. These same factors play important roles in maintaining the functional health of the bone remodeling cells: osteoblasts and osteoclasts.

The complex interconnections among these various cell types help explain the recent recognition of the connection between osteoarthritis and rheumatoid arthritis.  We now know osteoarthritis is not simply the result of “wear and tear” on the joint.  Rather, it results from an inflammatory process that engages bone, synovium, connective tissue, and joint lubricant substances.

 Inflammatory processes are found in the joint space with increased osteoclastogenesis and angiogenesis, the hallmarks of progressive osteoarthritis. (2)  Musculoskeletal integrity is critically important in reducing the risk to inflammation.  The problem in osteoarthritis is not just wear and tear; it is how the musculoskeletal system responds to stress factors influencing the release of inflammatory mediators, such as interleukin-1, interleukin-6, or tumor necrosis factor alpha.  That these characteristics are also factors in the etiology of rheumatoid arthritis suggests a common therapeutic approach to the prevention and management of both conditions.

 MODIFYING KINASE ACTIVITY

The inflammatory signaling process connecting the etiology of these seemingly disparate diseases is, to a great extent, regulated by the activity of a family of enzymes termed “kinases.”  Produced in every cell, kinases regulate the translation of events that occur outside the cell to the genes of the cell, triggering various cellular events, such as the inflammatory response.   The activation of the inflammatory family of kinases may result in a variety of clinical effects, such as type-2 diabetes, arthritis, heart disease, metabolic syndrome, and even certain forms of cancer. (3)

 Certain phytonutrients and other natural compounds have been found to modulate kinase function and serve as “brakes” that help prevent the inflammatory process from running out of control. (4)  Well-publicized examples of such compounds include hops-derived reduced iso-alpha acids and O-methylated catechins from tea leaves. (5, 6)

These compounds may be used in supplementary form to “reset” inflammatory kinase signaling, thereby influencing any cell types that have enhanced inflammatory functions.  Their role in regulating the signaling that induces the primary cause of the disease suggests these compounds have promise as a new class of therapeutics that treats the intersection of the cause of a family of chronic diseases with a shared mechanism of origin. (7)

 CROSS TALK AND SYSTEMIC DISEASE

Altered mechanical signaling through the connective tissue and fascia has been found to increase the production of inflammatory mediators that may contribute to the potentiation of the underlying cause of diseases as far ranging as arthritis, type-2 diabetes, and bone loss of osteoporosis. (8)  This discovery suggests a mechanistic role for physical medicine, structural medicine, and acupuncture in the treatment of these conditions. (9)  Interesting, too, is the fact that in September 2007 the National Institutes of Health provided funding for the first international conference on fascia. (10)  This conference brought together bodywork practitioners with basic scientists to better understand the role of fascia in chronic disease and what can be done to improve its function.

 Out of the conference emerged the recognition that the extracellular matrix, with its component connective tissue, serves not only a structural role, but also a signaling role, translating outside information to various cells.  The translation of these messages through the fascia affects kinase signaling and different inflammatory responses.

This once again demonstrates the “cross talk” that occurs among different tissues that sets up the potential for many different diseases.  In another example, it is increasingly accepted that obesity, in and of itself, does not cause diabetes and heart disease. Rather, obesity is an effect of a process associated with the infiltration of various tissues, such as the fat tissue, with pro-inflammatory immune cells. (11)  This inflammatory process triggers the pathology of obesity and relates to the cause of type-2 diabetes and heart disease.  For obese patients, a treatment plan that seeks to nutritionally modulate kinases associated with the inflammatory process while improving body composition may be a more effective approach than weight loss alone.

 CLINICAL APPLICATIONS

These extraordinary recent advances in the understanding of the etiology of chronic diseases that previously seemed so different from one another have now created the understanding that they all share common mechanisms of etiology.  Rather than treating the disease effect, the new medicine is to treat the cause.   Additionally, environmental factors, such as chronic infection, xenobiotic or heavy-metal toxicity, or intestinal dysbiosis and food allergy can increase the inflammatory response.  These are modifiable if the practitioner asks the patient the correct questions, including questions about family history, personal health history, diet, environment, lifestyle, and exercise patterns.

 Consequently, a patient with a history of chronic inflammatory disorders would be a candidate for a personalized intervention program that incorporates regular musculoskeletal therapy and a healthy diet, plus nutritional intervention that might include a low-allergy-potential diet; supplementary intake of anti-inflammatory phytonutrients that modulate kinase function; fish oils containing omega-3 EPA/DHA; and botanicals, such as Curcumin, Boswellia serata, and ginger.

Supplementation with probiotics, such as specific strains of Lactobaccilli and Bifidobacterium, might also be administered to improve gastrointestinal immune function and reduce inflammation.

 These are exciting times related to the advancement in the understanding of the mechanisms of origin of chronic disease.  These advancements are timely because, if a new model for the prevention and management of chronic disease is not soon found, the rising tide of age-related chronic disease will economically drown the aging baby boomers in healthcare expenditures.  The news from the latest research indicates a new paradigm in healthcare is evolving, and with it, a validation of the importance of a functional medicine approach to chronic disease that integrates lifestyle, environment, physical and structural medicine, diet, and nutrient therapies, with the focus on managing the intersection of the root cause of the diseases.

 Jeffrey Bland, PhD, FACN, is the chief science officer of Metagenics Inc. and president of MetaProteomics in Gig Harbor, Wash.  In 1991, he founded the Institute for Functional Medicine.  He can be reached at (800) 692.9400 or through the Web site, www.metagenics.com.

 References

1 Lee NK, Sowa H, Hinoi E, et al. Endocrine regulation of energy metabolism by the skeleton. Cell. 2007;130(3):456-469.

2 Bonnet CS, Walsh DA. Osteoarthritis, angiogenesis and inflammation. Rheumatology. 2005;44:7-16.

3 Bain J, McLauchlan H, Elliott M, Cohen P. The specificities of protein kinase inhibitors: an update. Biochem J. 2003;371(Pt 1):199-204.

4 Suzuki T, Miyata N. Epigenetic control using natural products and synthetic molecules. Curr Med Chem. 2006:13(8):935-958.

5 Minich DM, Bland JS, Katke J, et al. Clinical safety and efficacy of NG440: a novel combination of rho iso-alpha acids from hops, rosemary, and oleanolic acid for inflammatory conditions. Can J Physiol Pharmacol. 2007;85(9):872-883.

6 Maeda-Yamamoto M, Inagaki N, Kitaura J, et al. O-methylated catechins from tea leaves inhibit multiple protein kinases in mast cells. J Immunol. 2004;172(7):4486-4492.

7 Lila MA. From beans to berries and beyond: teamwork between plant chemicals for protection of optimal human health. Ann N Y Acad Sci. 2007;1114:372-380.

8 Langevin HM, Churchill DL, Cipolla MJ. Mechanical signaling through connective tissue: a mechanism for the therapeutic effect of acupuncture. FASEB J. 2001;15(12):2275-2282.

9 Langevin HM, Yandow JA. Relationship of acupuncture points and meridians to connective tissue planes. Anat Rec. 2002;269(6):

257-265.

10 Grimm D. Cell biology meets rolfing. Science. 2007;318:

1234-1235.

11 Segenès C, Miranville A, Lolmède K, Curat CA, Bouloumiè A. The role of endothelial cells in inflamed adipose tissue. J Intern Med. 2007;262:415-421.

Obesity reduces bone size and strength

It looks like contrary to popular belief, obese people are not “just big boned”  In fact, the following study shows a smaller bone size and strength for obese college age women versus those with less that 32% body fat. 

American Journal of Clinical Nutrition, Vol. 86, No. 5, 1530-1538, November 2007
  

Is adiposity advantageous for bone strength? A peripheral quantitative computed tomography study in late adolescent females1,2,3

Norman K Pollock, Emma M Laing, Clifton A Baile, Mark W Hamrick, Daniel B Hall and Richard D Lewis 1 From the Departments of Foods and Nutrition (NKP, EML, CAB, and RDL) and Statistics (DBH), The University of Georgia, Athens, GA, and the Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, GA (MWH)

Background: Whereas excess adiposity is presumed to be advantageous for the skeleton, studies investigating relations between bone strength and fat during youth have been equivocal.

Objectives: Relations of percentage body fat (BF) and bone strength indexes were assessed in late adolescent females, taking into consideration surrogates of muscle force [ie, muscle cross-sectional area (MCSA) and bone length]. Bone measurements in the normal- and high-fat groups were also compared.

Design: Late adolescent females (n = 115; aged 18.2 ± 0.4 y) participated in this cross-sectional study. Fat-free soft tissue mass, fat mass, and percentage BF were measured with the use of dual-energy X-ray absorptiometry. Tibial and radial peripheral quantitative computed tomography measurements were taken at the 4% (trabecular bone), 20% (cortical bone), and 66% (for measurement of MCSA) sites from the distal metaphyses.

Results: Percentage BF was inversely related to radial cortical bone area, total bone cross-sectional area (CSA), cortical bone mineral content (BMC), periosteal circumference, and strength-strain index (SSI) (20% site; all P < 0.05). After control for MCSA and limb length, negative relations remained between percentage BF and radial measurements and were also observed at the tibia (20% site). Unadjusted bone measures were not different between groups. After control for MCSA, the high- compared with the normal-fat group had lower bone measures at the 20% site (cortical bone area and cortical BMC at the tibia, total bone CSA at the radius, and SSI at both the tibia and radius; P < 0.05 for all).

Conclusion: Excess weight in the form of fat mass does not provide additional benefits, and may potentially be negative, for adolescent bone.