Mechanisms Linking Low Bone Mineral Density to Coronary Artery Disease

Pam Flores @phflores Health Guide
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    February is American Heart Month so it's a good time to look through the causes, prevention and cure for those of us with coronary artery disease and osteoporosis.  If we can further understand these two diseases, and their connection to one another, maybe we can prevent one or both of these conditions.

     

    For years we've heard about the connection between bone loss - osteopenia and osteoporosis - and coronary artery disease.  Maybe you know someone with both of these disorders and wondered what caused them and if both disease states have something in common to produce these two disorders in one individual.  To further understand this, we've broken down the risk factors for each and start with an explanation of what these disorders mean for our health.

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    First let's look at the definition of coronary artery disease.  According to the National Institute of Health, Coronary artery disease (CAD), also called coronary heart disease, is a condition in which plaque builds up inside the coronary arteries. These arteries supply your heart muscle with oxygen-rich blood.

     

    Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. When plaque builds up in the arteries, the condition is called atherosclerosis.

     

    Plaque narrows the arteries and reduces blood flow to your heart muscle. It also makes it more likely that blood clots will form in your arteries. Blood clots can partially or completely block blood flow.

     

    When your coronary arteries are narrowed or blocked, oxygen-rich blood can't reach your heart muscle. This can cause angina or a heart attack (U.S. Department of Health and Human Services and National Institute of Health 2010).

     

    Image of coronary artery disease

     

    There are risk factors that are prevalent in coronary artery disease.  The risk factors are broken into modifiable and non-modifiable risk factors.  By discussing these we'll understand the connection between these two medical disorders and what they have in common.

     

    Non-Modifiable Risk Factors:

    • Family history
    • Male and Female sex
    • Advancing age

    Modifiable Risk Factors:

     

    • Elevated blood pressure
    • Unhealthy diets
    • Tobacco use
    • Excessive alcohol use
    • Physical inactivity
    • Obesity

     

    • Abnormal lipid lipoprotein profiles (e.g. high total cholesterol, LDL cholesterol and triglycerides levels, and low levels of HDL cholesterol)

     

    • Diabetes

     

      

    Merging Blood Level Factors:

      

    • Lipoprotein (packages that transport cholesterol)
    • Vitamin D deficiency
    • Fibrinogen (protein that stops bleeding)
    • Calcium levels

     

    • C-reactive protein (a protein whose levels rise in response to inflammation)
    • Vitamin K deficiency
    • Homocysteine (protein usually produced by consuming meat)
    • Cytokines  [1]

     

  • Since we can't change non-modifiable risks like, family history, age, and sex, we need to concentrate on the modifiable risk factors to prevent and treat coronary artery disease.  By concentrating on modifiable risk factors we can improve our blood pressure, quit smoking, increase physical activity, improve our diets and cholesterol levels, limit alcohol use and watch our weight, and monitor Homocysteine levels to achieve an overall healthier heart.  It is also very important to watch and control all the other blood level scores listed on the merging blood level factors that are implicated in CAD.

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    Vascular health appears to have a strong effect on skeletal health, and vice versa.  To explain this we'll also look at the risk factors for osteoporosis and its connection to CAD.

     

    Osteoporosis, according to worldnetweb.princeton.edu, is an abnormal loss of bony tissue resulting in fragile porous bones attributable to a lack of calcium; most common in postmenopausal women (Princeton University 2010).

     

     

     

    Non-modifiable risk factors for osteoporosis:

     

    • Female/Male sex
    • Family history of osteoporosis
    • Advancing age
    • European or Asian ancestry
    • Family history of fracture
    • Dementia

     

    Modifiable risk factors:

     

    • Low BMI
    • Smoking
    • Calcium and D deficiency
    • Excessive alcohol consumption
    • Physical inactivity
    • Early menopause
    • Certain medications (corticosteroids, etc)
    • Pre-menopausal amenorrhea
    • Estrogen deficiency
    • Vitamin K deficiency  [1]

     

    One major link between osteoporosis and CAD are its risk factors they have in common.  If you look at these, there are nine or more shared risk factors.  These risk factors may promote or inhibit atherosclerosis and demineralization of bone, which is the loss of minerals in the bone.  Common mechanisms involving inflammatory cytokines, sex hormones, oxidized lipids, vitamin K, calcium and D are implicated in the progression of CAD and osteoporosis.

     

    Elevated blood level factors like Homocysteine, which are produced from consuming meat, could result in nutritional factors that lead to CAD and osteoporosis. [2]

     

    Genetic markers also contribute to both of these disease states; an example would be the lack of osteoprotegerin (OPG).  Mice lacking the OPG gene, developed early onset of both CAD and osteoporosis.  [3]

     

    Oxidized lipids inhibit osteoblasts and plasma levels of LDL and HDL; each negatively and positively relate to both CAD and osteoporosis. [4]

     

    Modifiable risk factors for osteoporosis like, calcium, D and K, physical inactivity, certain medications, smoking, excessive alcohol use, pre-menopausal amenorrhea are all under our control through changes in lifestyle.

     

    There have been a lot of medical studies done recently on the correlation between calcium, vitamin D, osteoporosis and coronary artery disease.  The link between D deficient individuals and early onset of osteoporosis is well documented.  Reduced levels of vitamin D are also a predictor for CAD as seen in the Framingham Offspring Study.  These studies will no doubt help us on our path to greater health, but looking at just these two risk factors seems a bit short sighted to me.  There are many more risk factors that these two disorders have in common, so only looking at two of them doesn't make much sense.  I believe there is no doubt about the ramifications that will occur from low D and calcium irregularities that will hinder many, but what about those who don't have these vitamin and mineral problems. If you are like me and have friends or family members who are not D deficient or don't have any calcium problems, and still suffer from CAD or premature cardiac death, how do we explain this without looking at all the possibilities that could cause this?  There's always the possibility that those with osteoporosis may acquire artery problems somewhere down the road, but if our calcium and D levels are good and have been that way for years should we only look at this connection, or look at the whole picture?  We need more than one or two explanations for this comorbidity between these disorders.

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    We hope you can do what is necessary to prevent these disorders, but know that if this does happen we have more than several explanations for this and possible treatment options to help you towards a healthy life free of calcified arteries and bone loss.

     

    Sources: 

     

    1. Warburton et al. Cardiovascular Disease and Osteoporosis: Balancing   Risk  Management. Vasc Health Risk Manag. 2007; 3(5): 673-689

     

    2. Boushey et al.  A Quantitative Assessment of Plasma Homocysteine as a Risk Factor for Vascular Disease. Probable Benefits of Increasing Folic Acid Intakes. JAMA 1995 Oct 4;274(13):1049-57

      3.  Bucay et al. Osteoprotegerin-deficient Mice Develop Early Onset Osteoporosis and Arterial Calcification. Genes Dev. 1998 May 1;12 (9):1260-8.

       

      4.  Hanson.  Inflammation, Atherosclerosis, and Coronary Artery Disease. N Engl J Med. 2005 Apr 21;352(16):1685-95.

       

    Published On: February 26, 2010