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MIM Health - December 2007

 
In this issue:

Doctor's Corner
Upcoming Appearances
Health Topic: Osteoporosis
Natural Tip™: Turmeric
Recipe: A Healthier Pumpkin Bread


Winter in Bozeman

Doctor's Corner

December is a busy month for most of us. While many people love this time of year, it can cause anxiety in others. Holiday shopping, dinners, parties and other commitments can leave people physically and mentally exhausted. While Christmas, Hanukkah and Kwanzaa, the major holidays during this month were intended to focus people on reaffirming their connection to God, this message has largely been lost in our consumer-oriented country. Just remember this--true love and commitment can never be bought; can never be wrapped in a shiny box. Or, as the Beatles' sang, "The best things in life are free."

My step mom is a clinical social worker who has been practicing for more than 25 years in Baltimore, MD. She and I were talking the other day about the holidays and its effects on people. We agreed that the basic consequences are: (1) people over-commit to holiday events; (2) they put added pressure on themselves to cook more, buy more, give more and be more during this month; and (3) when their expectations are not met, they feel sad, disappointed and unfulfilled.

Studies show that during the holidays there is an increase in anxiety, depression, suicide attempts, visits to the emergency room and spousal abuse. Financial pressures increase with each present purchased. And many people find themselves without the family members they miss, or stuck with family they'd rather avoid.

So, what to do about all this? If you love the holidays and just can't get enough of them, then go for it. Enjoy! But if this season increases your anxiety and heightens your depression, here are a few things you can do so you don't sacrifice your mental, emotional and physical health. Focus on quality and not quantity in everything--gift-giving, food, commitments. Only schedule yourself for events that don't cause you anxiety, and keep your schedule light enough to accommodate last-minute invitations that invariably come up during the season. Equally important, give yourself the gift of relaxation so you can truly enjoy the delights of the season.

Wishing you good health and much joy,

Dr. Neustadt

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Upcoming Appearances

On Sunday morning, December 16, from 7:00-10:00 AM MST, Dr. Neustadt, along with Dr. Pieczenik, MD, PhD, will be appearing on the radio show, Gesundheit! with Jacobus on KMMS 1450 AM in Bozeman. Drs. Neustadt and Pieczenik will be discussing Men's Health. So grab a warm cup of coffee or tea and curl up in front of the fire and your radio for a lively discussion of men's health that may just save your life or the life of someone you love.

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Health Topic: Osteoporosis
(Note: This article is an excerpt from a more technical, professional article Dr. Neustadt is writing for the October-November 2008 issue of the journal, Integrative Medicine: A Clinician's Journal. Dr. Neustadt was contacted by the editors and asked to write this article, which will be titled, "New Findings on Osteoporosis." )

Osteoporosis is a major health concern in the United States and leads to an inability to do normal, daily tasks and even early death. More than 10 million people in the U.S. have been diagnosed with osteoporosis, and the National Osteoporosis Foundation indicates that 44 million people are at risk for the disease by virtue of having low bone mineral densities. Each year 1.5 million fractures occur in people with osteoporosis. The cost of treating fractures of the spine alone is more than $745 million. Hip fractures are more expensive still.

People with osteoporosis are at an increased risk for fractures, particularly of weight-bearing bones such as the hip and spine. Debilitating acute and chronic pain in the elderly is often attributed to fractures from osteoporosis and can lead to further disability. Fractures of the hip and spine have a 15% greater chance of dying within five years than people without these fractures. After a hip fracture, only 50% of people regain the same level of independence they had before the injury, and 12 to 40% of patients who suffer hip fractures die within 6 months.

Although osteoporosis can occur in men and women of any age, and many medical conditions increase one's risk for developing osteoporosis, it's most frequently seen in postmenopausal women between 50 to 70 years old. It's been estimated that half of all women and one quarter of all men over 50 will break a bone due to osteoporosis.

During childhood and throughout puberty, the rate of bone creation is faster than the rate of bone loss; therefore, bones become larger and stronger. Bones continue to grow from birth until age 30 to 35. Once peak bone mass has been achieved, men and women begin to lose bone at 0.5 to 2% per year. There is considerable individual variation in this rate of bone loss, and an accelerated rate of loss in women occurs during menopause and for about 10 years thereafter.

Early detection and treatment of risk factors for osteoporosis is essential for preventing its progression. Family physicians will frequently recommend screening for osteoporosis and are uniquely positioned to ensure early detection and appropriate treatment. Understanding histology of bone, the physiology of bone turnover and the current research on the prevention and treatment of osteoporotic fractures can contribute toward the development of a successful integrative approach to treating this condition.

What is bone?

Bone is a complex mixture of minerals and protein. The mineral component of bone is 95% hydroxyapatite, which contains the minerals calcium and phosphorous. The remaining 5% is made up of magnesium, sodium, potassium, fluoride and chloride. The protein component of bone is 95% collagen, comprised of repeating sequences of the three amino acids glycine, proline and hydroxyproline.

Osteoblasts create bone and osteoclasts cause bone loss. Both are required for normal, healthy bones. Since it is a living tissue, the size, shape and density of bone changes over time. Old bone is broken down and new bone is continually created. Through the activity of these cells bone is continually being dissolved and produced, a process referred to as bone remodeling. In addition to the nutrients found in bone, "helper" nutrients are needed to build bones, including, boron, zinc and phosphorous; vitamins C, D and K; and hormones.

The popular press and the general public tend to focus solely on the importance of bone minerals, such as calcium, while ignoring the vital role collagen plays in maintaining healthy bone. Collagen is just as important as is mineral density for protecting against fractures. Collagen is responsible for the flexibility of bone. This can be demonstrated by kitchen science. Take a chicken bone and soak it in vinegar for 48 to 72 hours. It will become extremely elastic and difficult to break. That's because the minerals have dissolved away, leaving behind the flexible collagen.

Healthy bone is a mixture of proteins and minerals and requires other minerals, vitamins and hormones to stay healthy. Take away minerals and the health of the bone is decreased. Take away the collagen and all that's left is the minerals, which leaves the bone like a column of chalk that easily crumbles.

What causes osteoporosis?

Osteoporosis is caused when the process of breaking down bone speeds up or the process of creating new bone slows down. While there are many factors that influence the development of osteoporosis, several of the most common appear to be inactivity, poor diets, stress, inflammation, medications and low vitamin and mineral status.

Inactivity

Lack of exercise is highly associated with the development of osteoporosis and other degenerative conditions such as cardiovascular disease, diabetes and depression. Muscles are attached to bones. Exercise moves muscles, which puts mechanical stress on bones and stimulates an increase in bone formation. This occurs in resistance exercises such as weight lifting. Additionally, during aerobic exercises such as jogging, the impact of the feet on the ground promotes the production of new bone, again by creating mechanical stress. Lack of routine aerobic, weight-bearing and resistance exercises increases your risk of osteoporosis, broken bones and an early death.

Poor diet

The intricate relationship between diet and bone health are still being worked out, but much is already known. What is beyond dispute is that diet affects bone health. A diet that is high in meat and low in fruits and vegetables increases the risk for osteoporosis. Unfortunately, this describes the standard American diet.

Animal protein is acid forming because it contains high amounts of sulfur-containing amino acids (e.g., methionine). Calcium carbonate and citrate and magnesium hydroxyapatite are released from bone and used by the body to decrease the acidity of blood when it gets too high. Experimentally this is detected in the urine by an increase in calcium and the proteins involved in breaking down bone, and decreases in the osteocalcin, the protein responsible for building bone. Dozens of clinical studies have demonstrated this effect.

Conversely, diets rich in dark green, leafy vegetables (e.g., chard and kale) reduce the risk for osteoporosis. In addition to opposing the acidifying effect of meat, fruits and vegetables are rich sources for bone-building vitamins and minerals. The importance of vitamins and minerals in maintaining bone health was demonstrated in a study of postmenopausal women ages 50 to 60. Those women who took a supplement containing calcium, magnesium, zinc and vitamins D and K lost significantly less bone mineral density compared to those who didn't take the supplement.

Coffee is worth mentioning because it has often been cited as increasing the risk for osteoporosis. Coffee can increase calcium excretion in the urine; however, this does not occur if people consume the RDA or more of calcium per day. A study conducted in Norway found that there was only an increase risk for fracture when people drank nine or more cups of coffee per day. However, when consumed in moderation in combination with a healthy diet and adequate calcium intake, the studies suggest that coffee increases one's risk for osteoporosis or fractures.

Interestingly, one study analyzed both diet and coffee consumption and the risk of fractures. It was conducted in Norway and more than 40,000 men and women, ages 47-68 years old participated. Only in women consuming a diet high in non-dairy animal protein and low in calcium was the risk for fractures increased. Women drinking 9 or more cups of coffee per day combined with low calcium intake also had an increased risk. While this association does not prove cause and effect, it does show that risk factors for hip fracture are increased by low calcium.

Maintaining a balanced diet with adequate calcium intake and a mixture of other vitamins and minerals appears to provide the safest dietary protection against osteoporosis. Osteoporosis risk is increased by a high ratio animal protein to a predominant fruits and vegetables diet; low intakes of calcium, boron, potassium, magnesium and vitamin K; and low concentrations of vitamin D. Additionally, people with low bone mineral density have lower zinc concentrations in their bones.

Methionine, an amino acid found in high concentrations in animal protein, is converted in the body to homocysteine. This is a sulfur-containing amino acid that can be elevated in people who eat a diet rich in animal protein. Homocysteine interrupts the proper formation of collagen, the main protein in bone and joints, which leads to its degradation. But in addition to its bone-destroying effect, homocysteine directly damages blood vessels and also reduces levels of glutathione, an important antioxidant. Not only is homocysteine an independent risk factor for osteoporotic hip fractures, it is also a risk factor for cardiovascular disease.

Stress

There are many different types of stress--emotional, physical and psychological. But they all stimulate the body to secrete cortisol. This hormone is known as the "stress hormone." It is produced naturally by the body, but is also used pharmacologically to treat inflammatory disease such as arthritis, collagen vascular diseases, lung inflammation and asthma, certain types of liver inflammation, some skin diseases and granulomatous diseases. As a drug it is classified as a glucocorticoid and is marketed as cortisone, prednisone, hydrocortisone, dexamethasone and methylprednsone.

Even very small doses of oral glucocorticoids (<2.5 mg per day) are associated with a 20 to 200% increase in the risk of vertebral fractures. And each 10 mg per day increase is associated with a 62% increase in risk for bone fracture. This risk may be necessary and acceptable in order to control a disease process. However, if there are ways to reduce the dosage of corticosteroids, it would be advisable, since the risk for fracture decreases after stopping the medication. If you must take corticosteroid drugs, its deleterious effects on bone density may be reduced by supplementation with vitamin K. Do not reduce your medication or change its dosage without guidance from a qualified health care professional. Doing so can be dangerous.

The body's own production of cortisol can also contribute to osteoporosis. People with Cushings disease, a rare condition in which the body produces excessively high, uncontrolled amounts of cortisol, are at an increased risk for osteoporosis and bone fractures. Two studies have shown that even normal, healthy people can also be producing enough cortisol to negatively affect bone. In one study of thirty-four "healthy" men ages 61 to 72 years, bone density was inversely correlated with cortisol levels. This means that the men with the highest cortisol levels had lower bone mineral density and those with the lowest cortisol levels had higher bone mineral density.

Poor diet also increases cortisol. The standard American diet, with its high meat protein and low fruits and vegetable intake increases cortisol, and long-term may contribute to the known osteoporosis-promoting effects of this diet. Alkalinizing the diet by eating more fruits and vegetables reduces cortisol.

Excessive inflammation

Inflammation is important for the proper immune system functioning. However, when there is too much or it goes on for too long, inflammation becomes more damaging than beneficial. Among other illnesses, it can contribute to cardiovascular disease, depression, anorexia and osteoporosis. And, in turn, since cardiovascular disease and depression can increase inflammation in the body, they can contribute to osteoporosis.

Cardiovascular disease deserves special attention here, since it is the number one killer in the U.S. Inflammation is now regarded as the initiating factor for the development of atherosclerosis. Many different lifestyle, dietary and metabolic factors can contribute to this inflammation. One blood marker that is elevated in many people with cardiovascular disease is homocysteine. Homocysteine is a protein that directly damages blood vessel walls, including the blood vessels that deliver blood and nutrients to bones, and, among other deleterious effects, can initiate and maintain inflammation. Elevated homocysteine is a risk factor for cardiovascular disease and it is an independent risk factor for osteoporotic bone fractures.

Some other conditions associated with chronic inflammation include rheumatoid arthritis, inflammatory bowel disease, allergies and gout. These conditions increase inflammatory immune signals and increase bone resorption (release of bone minerals into the blood stream).

Low estrogen also contributes to inflammation. Estrogen is a potent anti-inflammatory, and when it declines with a hysterectomy or menopause, the risk for osteoporosis increases. When estrogen decreases, molecular markers of inflammation increase and osteoclasts are stimulated to break down bone.

Pathological inflammation occurs when the biochemical pathways involved in the creation and cessation of inflammation are blocked. Among their many functions, antioxidants help decrease inflammation by protect cells from free radical damage. Free radicals are molecules that attach to, damage and destroy parts of cells. During this reaction new free radicals are created, which can go on to damage more cellular components and create additional free radicals. This process continues unabated until an antioxidant comes in contact with the free radical and deactivates it.

Free radicals are created by the immune system to fight viruses, bacteria and other pathogens. In this respect they are necessary for our survival. However, free radicals also come from the environment and foods, such as fried foods. Antioxidants that protect the body from free radical damage come from food (eg, vitamin C from peppers or citrus fruits; quercetin from yellow onions, beta carotene from carrots; flavonoids from blueberries, cherries, pomegranate and other fruit) and some are produced by the body (e.g., glutathione and superoxide dismutase), but need vitamins and minerals to synthesize them. Damage by free radicals contributes to the development of cancer, heart disease, arthritis, cataracts, allergies and more rapid aging.

In healthy bone free radicals are used by osteoclasts to "chisel away at older bone," which creates small holes in bone that are filled by new bone by osteoblasts. This is bone remodeling. However, when estrogen levels decline after menopause, osteoblasts decrease their activity, which shifts the balance towards bone breakdown and unopposed free radical generation.

Low vitamin D

Vitamin D also plays a major role in bone health. Vitamin D is required for proper absorption of calcium. This reduction in dietary calcium absorption is most frequently caused by a decrease in vitamin D production by the body. Vitamin D is a steroid molecule stored in the skin at pre-vitamin D. Once activated by UVB rays from sunlight, pre-vitamin D is released. It travels to the liver where it is transformed into vitamin D2 (calcidiol or 25-hydroxyvitamin D), and then to the kidney where it becomes the active form or vitamin D, vitamin D3 (calcitriol, or 1,25-hydroxyvitamin D).

To activate pre-vitamin D in the skin, people must be exposed to 18 to 20 mJ/cm2 of UVB light. This is not generally reached during the winter in the northern United States above 40 degrees North latitude. All of Montana is above this latitude, as is about a third of the United States. Anyone in Montana is at elevated risk for vitamin D deficiency strictly based on geography. From November through February the sun simply doesn't get high enough in the sky to activate pre-vitamin D. But even if it did, which it does in throughout the country in summer, many people apply sunscreen that blocks UVB radiation from activating vitamin D. And people also tend to go outside with most of the skin covered up, further decreasing the activation of vitamin D.

Low vitamin D is now understood to be a risk factor for many conditions and is extremely common. Vitamin D has many roles in the body. It is required to absorb calcium and also helps prevent cancers, type 1 diabetes and heart disease. Low levels of vitamin D can be caused by inadequate exposure to sunlight, liver and renal disease or advanced age. For example, elderly people may have decreased synthesis of pre-vitamin D in the skin, decreased absorption of dietary or supplemental vitamin D in the intestines, decreased ability of vitamin D to increase calcium absorption in the gut or an inability to transform pre-vitamin D into active vitamin D.

Without vitamin D, the intestines can absorb no more than 10 to 15% of dietary calcium, while if someone is simply deficient in vitamin D their absorption of dietary calcium is still not more than 30%. Since the body tries at all costs to closely regulate the amount of calcium in the blood, when vitamin D is low the body compensates by extracting calcium from bones, thereby decreasing bone mineral density and contributing to osteoporosis.

Decreased production of active vitamin D can also be caused by cadmium toxicity. At high doses cadmium is toxic to the kidneys, which decreases the body's ability to make active vitamin D. This decreases the ability to absorb dietary calcium and the body reacts by taking calcium from bones to use in the blood stream and other tissues such as muscles and nerves. Small, chronic cadmium exposure may also lead to osteoporosis, although not by damaging kidneys. It decreases bone mineral density by directly disrupting the balance between bone formation and destruction.

Cadmium is a metal used in many manufacturing processes, such as jewelry brazing, soldering, manufacture of nickel-cadmium batteries, metal plating, zinc and lead refining, smelting of cadmium and lead and the production of plastics. People who smoke have twice the average cadmium in their bodies than nonsmokers. In the United States, sewage sludge is used as fertilizer, which can legally contain many different contaminants. Cadmium accumulates in the soil from fertilizer and taken up by growing plants, which become the food we eat. It also accumulates in shellfish, and a 1996 study showed that women who ate shellfish once a week consumed twice the amount of cadmium than those not eating shellfish.

Dietary mineral deficiencies such as low copper, calcium, zinc, and iron, or low protein intake, increase cadmium absorption. For example, iron deficiency leads to a 5 to 20% increase in the body's ability to absorb cadmium. And once it gets in the body, about 50% accumulates and is stored in the kidneys, with the rest being deposited in other tissues such as bones, pancreas and adrenal glands. Without treatment cadmium remains in the body for decades and contribute to osteoporosis.

Poor digestion and absorption

A good diet is the foundation for good health. It is obviously important for preventing and treating osteoporosis; however, if you are not digesting and absorbing the nutrients in food adequately, they do you no good. Anything that decreases the optimal functioning of the digestive system increases the risk for osteoporosis and other chronic, degenerative conditions. Among the most prevalent conditions in the aging population are Celiac disease, Crohn's disease and hypochlorhydria, all of which disrupt healthy digestion.

Gut dysbiosis (when the amount of healthy gut is reduced and the harmful bacteria increased) may contribute to osteoporosis. Gut bacteria manufacture vitamin K2 in our small intestine. Taking broad spectrum antibiotics can reduce the vitamin K production nearly 74% compared to people not taking these antibiotics. Additionally, in the elderly there is a reduction in vitamin K2, and diets low in vitamin K also decrease the body's vitamin K concentration. Vitamin K is necessary for proper blood clotting and bone formation. The amount of vitamin K needed for proper bone formation is much greater than for proper blood clotting, so decreased bone formation will appear much earlier than increases in bleeding disorders.

Multiple clinical trials have shown that high doses of vitamin K2 significantly increases bone mineral density and reduces the risk of fracture. Vitamin K2 (45 mg/d) alone and in combination with vitamin D3 and calcium has been shown to increase bone mineral density by up to about 11% and decrease fracture risk by 30% compared those participants who did not take these nutrients. This matches or exceeds the benefits in clinical trials that prescribed medications such as Fosamax, without the dangerous side effects. Additionally, vitamin K2 has also been tested and shown to decrease the risk of osteoporosis in people taking such medications as prednisone and leuprolide. Vitamin K2 has also been shown in clinical trials to increase the effects of bisphosphonate medications (e.g., etidronate [Didronel], alendronate [Fosamax] and risendronate [Actonel]).

Drugs

Some prescription drugs increase the risk for osteoporosis. Taking anticonvulsant medications such as phenytoin, phenobarbital, topiramate and lamotrigine increases the risk. This is due to an acidifying effect that these drugs have, which stimulates the destruction of bone to modulate the blood pH. Systemic corticosteroid use, such as oral prednisone, for more than 6 months also increases the risk for osteoporosis. One major reason for this is likely due to fact that corticosteroids modulate the immune system towards the production of tumor necrosis factor alpha (TNF), a marker of inflammation that stimulates bone resorption. Additionally, these drugs can deplete the body of important nutrients such as biotin, calcium, folic acid and vitamins B1, B12, D and K. If you are on any drugs, it is prudent to ask your doctor if the medications you are taking are associated with an increased risk of osteoporosis.

Other important causes

There are other causes of osteoporosis that may need to be ruled out. Bone metabolism is closely regulated by hormones and the proper functioning of the liver and kidneys. Calcitonin, a hormone produced by specialized cells in the thyroid gland, stimulates bone growth. Parathyroid hormone (PTH), which is produced by the parathyroid gland that rests on the thyroid gland, stimulates bone resorption. Proper functioning of the liver and kidneys is necessary for the activation of vitamin D. Tumors or dysregulation of the adrenal glands can produce excessive amounts of cortisol. Low body weight, as is seen in anorexia nervosa and occasionally in people who exercise a lot, can decrease a woman's production of estrogen. Stroke also increases the risk of osteoporosis, as well as malnutrition.

Any condition that disrupts the optimal performance of these organs and hormones can potentially contribute to osteoporosis. While these "secondary" causes of osteoporosis are rarer than postmenopausal osteoporosis, a proper diagnosis is required if a rational treatment is to be recommended.

Are you at risk?

Many factors influence bone health. These are generally grouped into two categories: modifiable and non-modifiable. Those that cannot be modified include someone's gender, age, body (frame) size, genetics, family history of osteoporosis, ethnicity and early menopause (<45 years old). Modifiable factors include hormonal status, nutrient deficiencies, physical activity, smoking, alcohol consumption, weight and diet. Additionally, accumulation of toxic metals, such as cadmium, also puts you at risk.

The number one risk factor for osteoporosis in women is having a mother with osteoporosis. This is most likely because behaviors, such as exercise (or lack of it) and diet tend to be learned and passed along from one generation to the next, and because the post-menopausal increase in bone loss obviously only effects women. Genetic predisposition may also play a role, but the Center for Disease Control and Prevention's (CDC) position on genetics and disease is that the longer someone is alive, the more lifestyle and diet, and the less genetics, play in the development of diseases.

How is osteoporosis diagnosed and monitored?

The gold standard for diagnosis of osteoporosis is dual energy x-ray absorption scan, which is referred to as a DEXA scan, a bone mineral density study or, simply a DEXA. Low-energy x-rays are passed through bones, such as the spine and hip. This test exposes someone to a very-low dosage of radiation and takes only about 10 minutes to complete. It indicates a person's bone mineral density and can determine someone's risk for fracture.

Bone density scans are not 100% accurate. Some people with very "dense" bones develop fractures, whereas many people with bone loss never break a bone. Bone mineral content is only one factor making up the health of bone. The quality of the bone crystal (which cannot be readily measured) and the integrity of the bone collagen (which can be indirectly measured) also appears to be important.

One criticism of DEXA scans is that their precision is low. Bone turnover is a slow process. Bone density my change by less than 3% per year, while bone density may change by less than 3% per year. Therefore, DEXA scans only yield clinically valuable results if they are done at 18-24 month intervals. Repeating the test too soon may simply provide expensive and unreliable information.

So while DEXA scans show the direction in which bone mineral density has headed over the past couple of years, it cannot show whether it is continuing or reversing itself. It has also been argued that, while bone mineral density may correlate to the risk for fracture, just as driving a car is associated with an increased risk for automobile accidents, loss of bone minerals may not be the underlying cause of the increased risk for fracture.

One of my mentors, Thomas Dorman, MD, was fond of telling patients the analogy of a brick house. He would ask them, "What's makes up the strength of the house? The bricks, or the metal rods (the re-bar) inside the walls." He would answer that while the bricks are important, it's the re-bar that creates the true structural integrity of the walls. Take away some of the bricks and the wall will remain strong. Yet remove the rebar, and the wall crumbles like chalk.

The collagen protein inside bones is the rebar and the minerals that attach to the collagen are the bricks and mortar. When I was in medical school and learning about the microscopic structure of bones, my professor brought a chicken bone to lab one day. She wanted to illustrate the point that collagen is flexible and that loss of collagen is the real reason why people develop osteoporotic fractures. She had taken this ordinary chicken bone and soaked it in vinegar for several days. The acid environment in the vinegar dissolved the minerals from the bone and left the collagen mostly intact. She was then able to hold up the demineralized bone and bend it without it breaking. Collagen is flexible, minerals are not.

In addition to testing bone mineral density, markers for bone collagen destruction, such as and deoxypyridinoline, and of bone formation, such as osteocalcin and bone-specific alkaline phosphatase are also important tests to consider. Unlike a bone mineral scan that can only detect clinically relevant differences over 18-24 months, deoxypyridinoline, osteocalcin and bone-specific alkaline phosphatase tell if bone is being destroyed or built on the day the test is taken.

Testing for osteoporosis provides an estimate of fracture risk. No single test or combination of tests is 100% reliable. Considering the epidemic nature of osteoporosis, everyone should consider a prevention program, including a diet of whole foods, supplementation with calcium and other micronutrients, regular weight-bearing exercise, and abstaining from cigarettes and excessive amounts of caffeine and alcohol. The tests mentioned above may help identify individuals who are at increased risk. In those cases, treatment with hormones and possibly other medications may be advisable.

A comprehensive testing approach to osteoporosis may include a DEXA scan, a urine test to for "bone specific collagen" (deoxypyridinoline), osteocalcin, PTH, whole blood or urine toxic metals, vitamin D status, intracellular mineral concentrations (e.g., zinc, magnesium), serum calcium, plasma amino acids, homocysteine, markers of inflammation, antioxidants, and markers of free radical damage. Only then can you get the most comprehensive picture of bone health and even predict possible future bone degeneration. And because this approach to testing actually looks at the underlying biochemical determinants of disease, it can be incredibly effective at generating data to improve many facets of health, including increasing energy, mood, stamina, and immune function and decreasing cardiovascular disease and dementia risk.

References

There were too many references to list in the newsletter. Click here to view the references.

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Natural Tip: Turmeric for Cardiovascular Disease and Inflammation

Cardiovascular disease (CVD) is the number one killer in the United States. One third of American adults (more than 71 million people) have one or more types of CVD, including 13.2 million cases of atherosclerosis. In 2003, 37.3% of all deaths were caused by CVD and was "an underlying or contributing cause" for approximately 58% of deaths in 2002. Most people get their cholesterol checked at one time or another and believe excellent cholesterol numbers will protect them against CVD. Unfortunately, cholesterol is only one risk factor for CVD, and having excellent cholesterol numbers alone isn't adequate protection.

There are many risk factors for atherosclerosis, including high cholesterol triglycerides, and chronic inflammation. Inflammation can cause free radical damage to cholesterol, which in turn damages blood vessels and causes plaques (atherosclerosis). Fortunately, nature has provided many plants with powerful cholesterol-lowering and anti-inflammatory actions. One of these is turmeric (Cucuma longa).

Turmeric root has been used for centuries in India, China and Indonesia for food and medicine, and is one of the spices found in the Indian spice, curry. Turmeric root has a rich yellow color and is ground for food and medicine.

Traditionally, turmeric has been used to treat a wide range of ailments. Topically it has been applied to wounds and burns and taken internally for liver and digestive complaints. Turmeric has many beneficial actions, including anti-inflammatory, antioxidant, anticancer, liver protective, stimulant of bile excretion and cholesterol lowering.

Turmeric is a potent anti-inflammatory. There are two main ways in which it does this. One is by suppressing an enzyme, called cyclooxygenase (COX) that creates pro-inflammatory signals in the body. The other is by inhibiting a gene, called nuclear factor kappa beta (NFκB) that also produces pro-inflammatory molecules.

The antioxidants in turmeric also prevent damage to cholesterol, thereby protecting against atherosclerosis. In fact, the ability of the antioxidants in turmeric to decrease free radicals is similar to vitamins C and E. Additionally, the antioxidant activities of turmeric are not degraded by heat, so using the spice to cook may also provide benefits.

Curcumin, the principle active compound, has been studied for its cholesterol-lowering effects. Rats were fed a high cholesterol diet with or without turmeric, for 8 weeks. Cholesterol was 12% lower in the rats fed turmeric. Additionally, triglycerides, another fat that circulates in the blood stream and is a risk for cardiovascular disease, was 53% lower in the rats fed curcumin.

In a recent study of atherosclerosis, mice were fed a standard American diet, which is rich in refined carbohydrates and saturated fat and low in fiber. Some of the mice, however, received this diet plus turmeric mixed in with their food. After 4 months on these diets, the mice that consumed the turmeric with their food had 20% less blockage of the arteries than the mice fed the diet without the turmeric. In another study, rabbits, which were specially bred to study atherosclerosis, were fed turmeric plus a diet designed to cause atheroslcerosis. Several risk factors for atherosclerosis were improved, including a decrease in cholesterol, triglycerides and free radical damage.

Herb-Drug Interactions

There are no known interactions. However, turmeric theoretically might interfere with antiplatelet medications. If you are taking any medications, consult a licensed healthcare professional who is knowledgeable in botanical medicine and pharmacology.

Dosage

Turmeric is available in different forms, including whole root and powdered root and standardized to the amount of curcumin, one of the medicinal compounds in the root.

Cut root: 1.5-3 grams per day
For inflammation, curcumin: 400-600 mg three times daily

References
Heart Disease and Stroke Statistics--2006 Update. American Heart Association [pdf]. Available at: http://www.americanheart.org/downloadable/heart/1140534985281Statsupdate06book.pdf. Accessed April 11, 2006.
Snow JM. Herbal Monograph: Curcuma longa L. (Zingiberaceae). Protocol Journal of Botanical Medicine. Autumn 1995:43-46.
Shishidia S, Sethi G, Aggarwal BB. Curcumin: Getting Back to the Roots. Annals of the New York Academy of Sciences. 2005;1056(1):206-217.
Kulkarni AP, Ghebremariam YT, Kotwal GJ. Curcumin Inhibits the Classical and the Alternate Pathways of Complement Activation. Annals of the New York Academy of Sciences. 2005;1056(1):100-112.
Rakel DP, Rindfleisch A. Inflammation: nutritional, botanical, and mind-body influences. South Med J. Mar 2005;98(3):303-310.
Singh S, Aggarwal BB. Activation of Transcription Factor NF-kappaB Is Suppressed by Curcumin (Diferuloylmethane). J. Biol. Chem. 1995;270(42):24995-25000.
Cronin JR. Curcumin: Old Spice Is a New Medicine. Alternative & Complementary Therapies. 2003;9(1):34-38.
Selvam R, Subramanian L, Gayathri R, Angayarkanni N. The anti-oxidant activity of turmeric (Curcuma longa). J Ethnopharmacol. 1995;47(2):59-67.
Olszanecki R, Jawien J, Gajda M, et al. Effect of curcumin on atherosclerosis in apoE/LDLR-double knockout mice. J Physiol Pharmacol. Dec 2005;56(4):627-635.
Ramirez-Tortosa MC, Mesa MD, Aguilera MC, et al. Oral administration of a turmeric extract inhibits LDL oxidation and has hypocholesterolemic effects in rabbits with experimental atherosclerosis. Atherosclerosis. Dec 1999;147(2):371-378.

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Recipe: A Healthier Pumpkin Bread
(
Have a recipe you want to share? Email it to us and it may appear in a future issue of MIM Health.)

'Tis the season for entertaining and gift giving. So here's a nutrition-packed pumpkin bread recipe that is a huge hit with our family and friends. Unlike the majority of sweetbread recipes, it uses higher-fiber whole wheat flour, unsweetened apple sauce and a lot less sugar. And pumpkin is packed with fiber and beta-carotene, which acts as an antioxidant and immune system booster. This makes two loaves, so you'll have one to give away, and one to enjoy!

 Ingredients

1 cup canola oil
0.5 cup unsweetened applesauce (cinnamon-flavored works well, too)
0.5 cup sugar
3 large eggs
1 16-ounce can of solid pack pumpkin
2.5 cups whole wheat flour (Bob's Red Mill brand is terrific)
0.5 cup unbleached all-purpose flour

1 t ground cloves

1 t ground cinnamon
1 t ground nutmeg

1 t baking soda

0.5 t salt

0.5 t baking powder

1 cup raisins

1 cup coarsely chopped walnuts

Preheat the oven to 350 degrees. Prep two 9x5x3-inch loaf pans with non-stick spray (Pam Organic is my wife's favorite). Beat sugar, oil and applesauce in a large bowl to blend. Mix in eggs and pumpkin. In another large bowl, combine flour, spices, baking soda, salt and baking powder. Stir half flour combo into pumpkin mixture, then add the other half. Mix in walnuts and raisins.

Divide batter equally between two loaf pans. Bake until toothpick or knife inserted into the center comes out clean, about 1.25 hours. Set loaf pans on cooling racks and let sit for 10-15 minutes. Using a sharp knife, cut around the edge of the loaves. Turn over onto racks and cool completely.

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Montana Integrative Medicine
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