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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
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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. |
|
* * *
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
1087 Stoneridge Drive, Suite 1, Bozeman, MT 59718, tel. 406-582-0034 |