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How to Protect Yourself from Radiation

Posted By Administration, Thursday, March 17, 2011
Updated: Friday, April 18, 2014

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by Hyla Cass, MD

We are all saddened as we watch the unfolding events in Japan. There is a growing sense of fear, as well.

The nuclear catastrophe raging through Japan's nuclear power complex is generating an intense fear of radioactive fallout potentially reaching North America. My patients and friends have been asking about how best to protect themselves and their families, as there is considerable confusion in the media about the issue.

Even as government officials and health experts downplay the health risk to U.S. citizens, pharmacies up and down the West Coast of the United States have been stripped bare of their stock of potassium iodide tablets -- a frontline treatment for radiation exposure. Anxious buyers turning to the internet are faced with a similar lack of available supplies. So, what do we do? It's a growing, ever-changing scenario, and here are my current thoughts, certainly open to modification.

Are we really at risk of exposure from radioactive fallout generated by a nuclear meltdown in Japan? I believe this is a question best left to qualified nuclear scientists and meteorologists. But after serving as a consultant to the Independent Safety Committee for the Diablo Canyon Nuclear Power Plant from 1990 to 2002, I know firsthand how important it is to be prepared for all possibilities when dealing with nuclear radiation.

One of the greatest dangers following a nuclear accident comes from exposure to gases containing radioactive isotopes of iodine. These highly carcinogenic isotopes are readily taken up by the thyroid gland, resulting in the development of thyroid cancer. Exposure to radioactive iodine calls for immediate treatment with another form of iodine, potassium iodide, to saturate the thyroid and block the absorption of radioactive iodine. This is especially critical for children, pregnant women, and nursing mothers, who are most at risk following a nuclear disaster. A lack of adequate supplies of potassium iodide tablets after theChernobyl nuclear disaster in 1986 resulted in thyroid cancer for thousands of untreated children.

Potassium Iodide (KI)
Potassium iodide tablets are commonly stockpiled near nuclear power plants to allow for rapid distribution in case of a radioactive accident. In the absence of tablets, potassium iodide may also be administered as a "saturated solution of potassium iodide" (SSKI) which in the U.S.P. generic formulation contains 1000 mg of KI per ml of solution. Two drops of U.S.P. SSKI solution is equivalent to one 130 mg KI tablet (100 mg iodide).


Recommended Doses 
According to the World Health Organization (WHO), the following doses of potassium iodide should be taken as a single dose within three hours of exposure, or up to 10 hours after exposure, although this is less effective.

• Adults : 130 mg (see below as well for CDC addendum) 

• Adolescents: 12-18: WHO -- adult dose; CDC -- children's dose; if adult size (150 pounds or over) they should take the full adult dose, regardless of their age.
• Children age 3-12 years: 65 mg

• Infants : 1 mo. to 3 years, 32. 25 mg (ie half tablet)
• Newborns to 1 mo., 1/4 capsule.

Note: Dosages may be crushed and taken mixed with milk or water. For kids, chocolate milk or raspberry syrup disguise the unpleasant taste.

Precautions
While potassium iodide can be taken by a majority of people without any problems, it should only be used in case of a nuclear emergency. Doses in excess of the single (one time only) daily dose listed above should be taken only upon recommendation by a physician or public health authority. Patients should ask their doctor if taking quinidine, captopril, or enalopril, amiodarone, or if they are sensitive to iodine, or suffer from dermatitis herpetiformis, thyrotoxicosis or kidney problems before taking potassium iodate (or any thyroid blocker).

Prophylaxis
It is best to take iodide prophylactically, prior to exposure. Every family should have a good supply in their homes. At this time we may recommend taking 10-40mg per day. A dose of 30-50mg is the range of dietary intake in Japan and relatively safe to take long term but under practitioner monitoring. Build up gradually: 10mg-20mg-30mg-40mg.

Then, in case there is an official announcement of significantly increased radiation, adults should go to the dose mentioned above: 130mg/day and children to lower doses per body weight, generally 65 mg, age 3-12 years. You can use a loading dose of two drops daily of Lugol's Iodine, a commonly available pharmaceutical form of potassium iodide, or SSKI, and increase to 130 mg if needed. See the U.S. Centers for Disease Control recommendations. Adults over 40 should not take KI unless public health officials say that contamination with a very large dose of radioactive iodine is expected, since have the lowest risk of developing thyroid cancer or thyroid injury after such contamination. They also have a greater chance of having allergic reactions to KI. Everyone should check with their doctor, in any case.

Other supplements that may be protective are: vitamin D and vitamin K as they support appropriate apoptosis, which is programmed death of cells that accumulate various DNA errors (due to radiation and other causes), and vitamin D also supports DNA repair.

Avoid exposure to rain that may be laden with radiation if we are exposed. You'll be informed by authorities if that is the case.

Other Radiation Dangers
Besides I-131, there are other toxic radio-isotopes, including cerium 137 and plutonium. Dr. Gabriel Cousens has provided some excellent advice in his book "Conscious Eating." To protect yourself from cesium poisoning, consume plenty of high potassium foods, as potassium competitively inhibits cesium uptake. Foods high in potassium include avocados, sea vegetables, and leafy green vegetables, and are more effective than taking a potassium supplement.

To protect yourself from plutonium poisoning, eat lots of dulse and consume iron from plant sources, namely sea algaes such as spirulina and chlorella, which provide more iron than red meat. Miso soup has also been shown to have a protective effect. See also Michio Kushi's well-referenced book, "The Cancer Prevention Diet." The mineral, zeolite, is being investigated for taking most radioactive materials out of the body.

Additionally, foods and supplements high in antioxidants, will also help the body cope with these higher toxic levels as radioactive materials cause antioxidant depletion and ill health.

Summary
The Nuclear Regulatory Commission has admitted it is 'quite possible' that fallout from the Japanese reactors could reach America, though levels expected to be so low as to be almost undetectable. Given the unprecedented circumstances of the current crisis, though, it would be prudent to keep some potassium iodide on hand as a precautionary measure.

Stay tuned to news sources for ongoing information, as this story is clearly developing by the minute.

For both those directly affected and those of us who feel the stress of this tragedy, check out some simple trauma-releasing methods, such as EMDREFT: or download free EFT audio "Tapping for Japan."

If I am able to find sources of tablets, I'll put a note here in comments, and list them on my website, as well. Otherwise, I'd recommend using SSKI which I'll likely be getting for my patients in the absence of tablets or capsules.

Our prayers are with the people of Japan, those who have lost their lives and those who have survived, and are dealing with trauma, grief and unspeakable loss.

 

Tags:  radiation 

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Compounding Pharmacy Quality Assurance Checklist

Posted By Administration, Tuesday, March 15, 2011
Updated: Friday, April 18, 2014

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Fill006lighted 
Safety and Consistency is Our Priority

There is no compromise when it comes to health.

At McGuff compounding pharmacy, we have independent Quality Assurance and Quality Control programs to ensure that our products and patient care meet high quality standards and requirements. Our commitment is to provide a level of service that delivers safe compounded products consistently that patients and physicians can depend upon.

We use industry leading practices to meet your needs. We model our operations to meet manufacturing FDA Current Good Manufacturing Practice standards whenever possible.

When choosing a compounding pharmacy you want to feel confident that you will receive the highest quality compounded products and unparalleled patient care.

The following are some questions that you should ask when selecting a compounding pharmacy. Each affirmative answer should be followed by one additional question… "If so, how can you prove this to me?". The answer to this question, without independent audit reports of their pharmacy from national and international standards organizations, will more than likely be “because we said so”. If a pharmacy is not accredited by PCAB™ or ISO there must be a reason.:

Quality Assurance Checklist

 

TopicQuestionMcGuff Compounding Pharmacy
The Organization Does your pharmacy have specific assignment of quality functional responsibilities as defined in a Quality Assurance plan? Checkmark 
Does your pharmacy have an independent Quality Systems Department whose responsibility is to ensure that the facility, equipment and personnel meet the demanding standards set forth the United States Pharmacopeia? Checkmark 
Does your independent Quality Assurance department have the authority to over-ride the pharmacist-in-charge and stop the release of any compounded medication if the medication quality attributes are suspect? Checkmark 
Independent Standards Reviews Is your pharmacy PCAB Accredited™ which assures that the pharmacy is dedicated to protecting patients by practicing safe, high-quality compounding ? Checkmark 
Is your pharmacy ISO 9001:2008 certified by an independent organization to assure compliance to international standards of customer care and product development? Checkmark 
In addition to your pharmacy license do you have a State Board of Pharmacy sterile compounding license? Checkmark 
The Commitment Is your pharmacy committed to and in compliance with USP <1075>, Good Compounding Practices? Checkmark 
Is your pharmacy committed to and in compliance with USP <795>, Pharmaceutical Compounding – Non-sterile Preparations? Checkmark 
Is your pharmacy committed to and in compliance with USP <797> guidelines for sterile compounding? Checkmark 
Documentation Are all significant procedures performed in the pharmacy covered by Standard Operating Procedures (SOPs)? Is there documentation that the pharmacy staff has been trained and understands the SOPs? Checkmark 
Is the Pharmacy’s Quality Assurance plan reviewed annually and when changes are made to the plan? Checkmark 
Does the pharmacy maintain both a master formula and lot-specific compounding history records for all compounds? Checkmark 
Does the pharmacy's master formula document the name, strength, and dosage form of the compounded product, all ingredients and their quantities, assigned a beyond-use date, record the equipments to be used, mixing instructions, packaging instructions, and Quality Assurance checklist? (This documentation ensures that the compound is prepared consistently to reproduce the same each and every time.) Checkmark 
Does your pharmacy prepare a formulation checklist and perform a design review process to determine acceptable strength, quality, and purity of a new formulation request? Checkmark 
The Facility Does your pharmacy’s facility meet or exceed U.S.P. Guidelines for compounding pharmacies? Checkmark 
Does your pharmacy perform sterile filling in a class 100 (ISO Class 5) laminar flow hood located within class 10,000 (ISO Class 7) clean room? Checkmark 
Does your pharmacy have separate areas dedicated to perform sterile and non-sterile compounding, product inspections, labeling, raw material storage, and dispensing? Checkmark 
Is the air quality in your compounding pharmacy engineered for HEPA filtration to reduce particulates? Checkmark 
Environmental Monitoring Does your pharmacy perform daily monitoring and documentation of raw material storage, sterile and non-sterile compounding areas, and final product storage for temperature and humidity? Checkmark 
Does your pharmacy conduct daily tests of air and surface samples of your clean-room and other controlled environments? Checkmark 
Does your pharmacy perform daily, weekly, and quarterly cleaning to assure a clean and safe facility? Checkmark 
Personnel Are your pharmacy’s pharmacists, technicians, and customer service staff dedicated exclusively to compounding? Checkmark 
Is your pharmacy’s staff properly trained to perform aseptic manipulation skills, gowning technique, clean-room use, and successfully perform media fills every six months? Checkmark 
Does your pharmacy’s staff take steps to minimize error and maximize the prescriber’s intent for the patient during the compounding process? Checkmark 
Compounding Materials Does your pharmacy purchase pharmaceutical-grade chemicals (USP, NF equivalent) from FDA-registered suppliers? Checkmark 
Does your pharmacy obtain and keep Certificates of Analysis for all raw materials used in compounding? Checkmark 
Quality Control Does your pharmacy perform sterility testing according to USP <71> - Sterility Tests and USP <85> - Bacterial Endotoxin Test on every lot prepared? Checkmark 
Does your pharmacy verify the potency of finished compounds through weight, volume and yield checks? Checkmark 
Does your pharmacy perform post-filtration filter-integrity testing? Checkmark 
Does your pharmacy have systems in place for handling complaints and investigating sterility failures and adverse events? Checkmark 
Is every step of the compounding process from prescribing to compounding and labeling through dispensing reviewed and verified by a licensed pharmacist Checkmark 

For more information, visit www.mcguffpharmacy.com.

 

Tags:  compounding pharmacy 

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Can Tumeric Reduce the Spread of Breast Cancer?

Posted By Administration, Thursday, March 10, 2011
Updated: Friday, April 18, 2014

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by Nalini Chilkov, LAC, OMD

Recent studies from the University of California, San Diego, published in the British Journal, NATURE, have discovered a molecule called RANKL, found in aggressive breast cancer cells that predicts more deadly, lethal and life threatening disease. The findings from these recent studies suggests that drugs that block RANKL may be effective in preventing both the early stages of breast cancer and the advanced progression of the disease. Research has also shown that curcumin, the active ingredient in the common spice, turmeric, has properties that also reduce the expression of these deadly molecules within cancer cells and can potentially slow the spread of breast cancer.

Breast Cancer is not one disease. There are actually many breast cancers. When a woman is diagnosed with breast cancer, the tumor cells in her body must be analyzed in order to understand the nature of her unique disease.  Some cancer cells are more aggressive and fast growing. Some cancer cells are sleepy, slow growing and less dangerous.

It is the presence of these more aggressive cancer cells that predicts that the breast cancer will spread to other parts of the body through a process called metastasis. Metastasis kills. Cancer patients rarely die from the primary tumor, the site where the cancer originates in the body. Breast cancer patients typically die from cancer that has spread or metastasized to other parts of the body, debilitating the function of vital organs such as the liver, lungs or brain. When breast cancer cells are aggressive and able to spread throughout the body, long term survival is threatened. Identifying agents that stop or slow the spread of disease through these mechanisms can stop or slow the spread of cancer and save lives.This new research demonstrates that when a protein molecule called RANKL (Receptor Activated Nuclear Factor Kappa Ligand) is present in breast cancer cells in high amounts, these tumor cells are more activated, more aggressive and more likely to spread, more likely to kill. RANKL is produced by regulatory T-Cells that modulate our immune response.  High levels of these T-cells means high levels of RANKL, high levels of inflammation and aggressive high risk disease.

Blocking tumor promoting RANKL can block the spread of breast cancer cells to other parts of the body.  A new drug, denusomab, has recently been released by Amgen that performs this function. However, this  new drug is not widely available to patients for all possible applications, requires insurance company approval and is very expensive. Therefore few patients will be able to have access to and benefit from this new therapy in the near future. The good news is that there is alternative cancer answer available now without a prescription, the natural substance curcumin, derived from turmeric that can lower inflammation, lower RANKL, lower risk.

Dr. Bharat Aggarwal, Ph.D. Professor, Department of Experimental Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX is one of many respected researchers and experts who has published many studies on the effects of curcumin on cancer cells. According to Dr. Aggarwal

Curcumin has a very special nature which will work both for cancer prevention as well as for cancer therapy.

Turmeric (Curcuma longa) is one of the most potent Cancer Fighting Foods. Curcumin, the active ingredient in this common medicinal and culinary herb has been widely studied. It is recognized as a potent cell protectant, anti-oxidant and anti-inflammatory agent. Turmeric has been used for centuries to support cancer patients in Traditional Chinese Herbal Medicine and Indian Ayurvedic Medicine. Now modern science demonstrates why it works. Curcumin has been shown to influence many cellular factors, including lowering RANKL.

Curcumin has been shown to decrease RANKL in tumor cells. Curcumin can block RANKL as well as other inflammatory and tumor promoting molecules in cells (COX-2, LOX-5, MMP2,TNFa, NFKbEGFR, HER2, bFGF, TGF-B1, and VEGF.)  Turmeric is found in many herbal formulas for the prevention and treatment of cancer.

The active medicinal principle, curcumin, when taken orally, is best absorbed when taken with oil in traditional Indian curries. To use botanical medicine for the prevention and treatment of any serious health condition, the herb must be of pharmaceutical quality and taken in the proper doses. As with any potent botanical medicine, the use of curcumin as an anti-inflammatory and anti-tumor agent should be used under the supervision and guidance of a knowledgeable health care professional. Countries such as India in which tumeric is frequently consumed in the daily diet have lower rates of many cancers including prostate cancer, breast cancer and colon cancer. Tumeric can be safely added to your food as a cooking spice to add anti-inflammatory, anti-oxidant and anti-cancer properties to your daily diet.

Tags:  breast cancer  cancer  tumeric 

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Fall and Winter Power Vegetables

Posted By Administration, Monday, March 7, 2011
Updated: Friday, April 18, 2014

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by Andrea Purcell, ND

The vegetables found under the ground and the heartier ones above ground are packed with vitamins and minerals and perfect for grating, roasting, steaming & mashing this time of year.

The below ground varieties include: Beets, Sweet Potatoes, & Carrots

The above ground varieties include Kale, Brussels sprouts, & Winter squash.

Lets tackle the above grounders first:

Kale and Brussels Sprouts are in the same famous family known as cruciferous. This famous family of vegetables has gained A LOT of press for its anti-cancer benefits. In fact half of the studies on brussels sprouts revolve around its cancer fighting properties. They are high in Vitamin A, C and folic Acid.

Kale is a coarser green and many people have no idea how to prepare it. Once you figure it out you can enjoy one of the healthiest, nutrient greens on the planet. Kale has Vitamins A, C, B6, and minerals of calcium and iron. Did you know that when prepared properly we would get more calcium out of kale than spinach? When preparing cut off the stem part about 1.5 inches and then chop. Try sautéing in a bit of olive oil and water.

Winter Squash comes in a number of varieties, such a butternut, kombucha, and acorn; there are multi-striped varieties as well. The toughest thing about squash is the preparation, the peeling, de-seeding, and chopping. If you have a man, put him to use in this department. Otherwise I suggest cutting in half and placing open side down on a baking sheet and roasting in the oven for 45 minutes. Remove from oven and let cool; the skin will be A LOT easier to remove. Once cooked squash can be mashed or added into soups. Any vegetables orange or yellow in color contain Beta-carotene, and vitamin C, these are antioxidant and anti-inflammatory. Winter squashes also contain B-vitamins, and folic acid.

Check out my latest You Tube cooking video on Sautéed Brussels and Kale, I also have one on making Kale chips. You can access my You Tube channel through the www.AskDrPurcell.com site.

Now for the below grounders:

Carrots and Sweet potatoes are little darlings of the culinary world because of their natural sweetness. In fact many people who don’t like vegetables will eat them. Due to their orange color and carotenoid content leading to anti-oxidant protection within the eye. They are high in Beta Carotene, which is converted inside our bodies to Vitamin A that helps boost the immune system, and protect our skin.

Beets are amazing grated fresh into salads, and roasted. Boiled beets are less appealing.

Beets are high in fiber and can assist with constipation. They are also high in iron and folic acid the two main causes of anemia. If you’re anemic eat your beets! They also contain choline, an important detoxifier for our livers. Beets can be roasted with sweet potatoes, or roasted and then added to chilled salads. Once cooked, beets can be marinated in any dressing and will absorb those flavors bringing a lot of sweet, tangy goodness to the table.

Tags:  food and drink  vegetarianism 

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Maximizing Health and Well-Being While Flying

Posted By Administration, Friday, March 4, 2011
Updated: Friday, April 18, 2014

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by Zina Kroner, DO

 As a nutritionally-oriented internist, I have seen air travel take quite a toll on the health and well-being of many of my friends and patients. With the excitement of traveling to a new destination, the new food, the change in schedule, the stress, the hassle; it is easy to neglect one’s health. My patients are frequently asking me for health travel advice. While practicing in a city where both business and leisure travel are staples in the lives of many of my patients, I have developed a nutritional and lifestyle plan to help optimize health while traveling.  

Drink 2 large glasses of water on an empty stomach in the morning of travel. This will hydrate you effectively. Have a high protein breakfast.  
 
Stress plays a significant role in air travel. Aside from a healthy diet, restorative sleep, regular exercise, and the addition of key nutritional supplements to the regime are helpful. One mineral that helps to combat stress is magnesium. It is one of the first nutrients to be depleted in the setting of stress. Your adrenal glands depend on magnesium, as do over 300 different enzyme reactions in the body. I recommend my patients take 100mg of magnesium-taurate the morning of the flight, and then another 100mg just before the flight.  
 
It is not uncommon for travelers to contract a respiratory infection, the flu, or other infection while flying. The poor air circulation in the cabin compounded by the proximity to other passengers who may potentially be sick poses a double threat. Those with weak sinuses are at a heightened risk, as well, due to the periodic changes in air pressure. Washing hands and using hand sanitizers in the plane may be of benefit. Hydration and optimal nutrition are integral components, as well. I recommend my patients take several key nutrients to help boost the immune system in the setting of travel. I recommend taking oleuropin before the flight, which is the active ingredient in the olive leaf that has potent antibacterial, antifungal, and antiviral properties. In addition, beta 1,3 glucans and the prickly pear are cutting edge nutrients that I recommend that have been studied for their anti-microbial effects. Vitamin C and a combination of immune boosting mushrooms, such as cordyceps, reishi, and maitake, may help to prevent colds and other respiratory ailments in flight.
 
Boosting the immune system by addressing the gut is essential. It is an established fact that over sixty percent of the immune system is in the gut, referred to as the gut associated lymphoid tissue (GALT). In addition to a healthy diet, intake of a probiotic (beneficial gastrointestinal flora) is imperative to optimizing function. I strongly recommend taking a probiotic a week before the date of travel and to continue for a week thereafter.  
Constipation is common in the setting of travel.  The change in food, regime, stress level, and diet are contributors to this phenomenon. Probiotics can help deal with this. Magnesium plays a crucial role as well, being that it is a muscle relaxor that can relax the muscles of the colon wall and therefore improve regularity. Hydration, exercise and healthy fiber intake are important as well.
 
It is not uncommon to get a muscle cramp during the flight. Magnesium, a natural muscle relaxer, can help to prevent this. Be careful, because what feels like a cramp may actually be a blood clot. I highly recommend taking natural supplements that improve circulation before the flight. Natural vitamin E and omega-3 fish oil have been shown to optimize the cardiovascular system. Their mild blood thinning effect may help to prevent a clot. I also recommend the use of nattokinase for clot prevention. There is a lot of research supporting nattokinase’s role as an anti-clotting agent. It is an enzyme extracted from natto, which is derived from fermented soybeans.  
 
To make it more user-friendly, I have put together all the supplements described above into prearranged packets. I have blended the highest quality nutrients into the “Flight Pack,” the only physician-grade supplement pack on the market used to optimize health and well-being while flying. I hope you find them helpful. Take one packet with a meal before your flight. Each Flight Pack contains 8 supplements. If it is okay with your physician, you can take this packet daily while traveling. Do not take if you are pregnant, are taking a blood thinner, have kidney or liver disease, or a bleeding disorder.  Living smarter, living longer… (The product can be ordered online at www.advanced-medicine.com.)

 

Tags:  health  prevention  technology 

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Controlling Inflammation: Five Natural Ways to Put Out the Fire

Posted By Administration, Friday, February 25, 2011
Updated: Friday, April 18, 2014

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by Nalini Chilkov, LAC, OMD

The relationship between cancer and inflammation is well established. There is a strong association between chronic, ongoing inflammation in the body and the occurrence of cancer. It is most obviously demonstrated with the increased chance (five to seven times higher than the general population) for people with chronic inflammatory diseases.

For example chronic acid reflux and heartburn which inflames the stomach and esophagus increases risk of stomach and esophageal cancer.  Acid reflux may be caused by infection with H. Pyolori which can be treated with antibiotics as well as natural medicines.

  • Chronic infection of the liver with Hepatitis virus B and C increases risk of liver cancer. 
  • Chronic autoimmune inflammation of the colon or lower intestine, Ulcerative Colitis and Crohn's Disease, increases risk for colon cancer.
  • Chronic inflammation of the lungs due to exposure to  inhaled chemical irritants including chemicals found in cigarette smoke  or volatile inhaled chemicals from resins and varnishes or  inhaled particles such as asbestos increase risk of lung cancer.
  • Chronic inflammation of the skin due to repeated sunburns increases risk of skin cancer.

Inflammation fuels cancer in several ways: 

  • Inflammatory chemicals release free radicals or free roving electrons that damage cells and may initiate damage to the genetic material in our cells, our DNA thus leading to cellular mutations, loss of normal cell functions and cancer.
  • Inflammatory chemicals stimulate the production of new capillaries, tiny blood vessels that feed cancerous growths.
  • Many cancer cells will spread and metastasize in clumps that contain both  inflammatory white blood cells of the activated immune system, called lymphocytes and  sticky  blood cells called platelets, which allow the cells to attach to new organs and tissues. This allows cancer cells spread by travelling to and establishing growth in new locations.

Common Triggers of Inflammation:

  • chronic bacterial, viral or parasitic infections
  • chemical irritants such as formaldehyde or toluene found in many cosmetics or benzene found in oven cleaners,  detergents, furniture polishes and nail polish removers
  • Inhaled particles  from fiberglass, silica or asbestos found in building materials and insulation
  • Ionizing radiation from sun exposure or frequent medical scans and xrays

Once the immune system has become activated and inflammation unfolds, the inflamed cells are further damaged by oxidative stress... the presence of roving free electrons that can damage cellular genetic material, our DNA. Damaged DNA is a primary cause of cancer as the expression of genes becomes altered.  Protecting cells from this damage is crucial in preventing and controlling cancer.

Recognizing that inflammation is occurring and is ongoing and poorly managed is the first step.  The second step is to take action

Here are Five Ways to Reduce Inflammation Naturally

1/Eat an Anti-Inflammatory Diet
An anti-inflammatory diet is organic and free of chemical additives and artificial colorings and flavorings and preservatives.  Eat whole, fresh, unprocessed foods that are not charred or deep fried. Eat a wide variety of colorful fruits and vegetables.  Eat healthy fats and oils, emphasizing Omega 3 fats found in cold water fish such as salmon and cod and sardines. Include other healthy oils such as walnuts, almonds,  avocadoes, olives and flax seeds.  Eat animal products from grass fed rather than grain fed (conventionally raised) animals.  Emphasize a plant based diet over a diet derived primarily from animal products. Avoid refined sugars and flours and corn syrup.  Eat plenty of fiber from whole grains, fruits and vegetables and beans.  Drink plenty of fluids everyday.

2/Use Anti-Inflammatory Herbs to Manage Inflammation
Common Herbs which reduce inflammation by lowering inflammatory and damaging molecules such COX2 and LOX5 in our cells include: Tumeric, Ginger root, Boswellia, Resveratrol, Milk Thistle and Cat’s Claw.

3/Avoid chemical exposures:  Eat an organic, chemical free diet as noted above.  Drink filtered water.  Use only cosmetics that are free of irritating and carcinogenic additives.  Identify chemical exposures in the home (cleaning supplies, garden supplies) and the workplace (chemical exposures, fumes, inhalants, radiation).

4/Identify and Treat Chronic Infections: Do you have persistent heartburn?  Do you have chronic loose stool or diarrhea or gas and bloating?  Have you been exposed to hepatitis or parasites while travelling internationally? Do you have a chronic post nasal drip or cough?  See your health care provider to determine the cause and get proper treatment and follow up. Once the infection is resolved take measures to boost your immunity to prevent future infections. Eat fermented foods or use probiotic supplements which contain healthy organisms that are part of natural immunity in our digestive tract and intestines.

5/Keep your body lean.  Keep your weight under control. Reduce your Body Fat.  Build Muscle. Excess body fat is a factory for inflammatory molecules.  All overweight and over fat people have much higher levels of inflammation than people who are lean.  Eat a balanced diet, get regular cardiovascular and weight bearing exercise.  Get enough sleep and manage your stress.  All of these factors will contribute to normal body weight, reduced fat and increased lean muscle.

References:
Ed Friedlander, “Inflammation and Repair,” www.pathguy.com/lectures/inflamma.htm (accessed fall 2006).
Emily Shacter and Sigmund A. Weitzman, ”Chronic Inflammation and Cancer,” Oncology 16, no. 2 (February 2002). www.cancernetwork.com/journals/oncology/o0202d.htm (accessed fall 2006).
National Cancer Institute Division of Cancer Biology, “Executive Summary of Inflammation and Cancer Think Tank.” http://dcb.nci.nih.gov/thinktank/Executive_Summary_of_Inflammation_and_
Cancer_Think_Tank.cfm (accessed fall 2006).
Haiyan Xu et al., “Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance,” J. Clin. Invest. 112 (2003): 1821-30. Also available at www.ncbi.nlm.nih.
gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=14679177 (accessed fall 2006).
American Heart Association, Inc., “Inflammation, Heart Disease and Stroke: The Role of
Schindler, Thomas, et al. 2006. Relationship Between Increasing Body Weight, Insulin Resistance, Inflammation, Adipocytokine Leptin, and Coronary Circulatory Function. JACC 47:1188-95.

Tags:  inflammation 

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Alternative Versus Integrative Appraoches to Cancer Treatment

Posted By Administration, Monday, February 21, 2011
Updated: Friday, April 18, 2014

If you watched Dateline's interview with Suzanne Somers and are wondering about ACAM's position on alternative approaches to cancer treatment, this video outlines the basic differences between integrative and alternative medicine.  

Visit msnbc.com for breaking news, world news, and news about the economy

 

 

Tags:  cancer  integrative medicine 

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Zinc found to be Effective in Treating Colds

Posted By Administration, Wednesday, February 16, 2011
Updated: Friday, April 18, 2014

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An evaluation of 15 studies concludes that zinc lozenges, tablets or syrup can help cut the duration of cold symptoms by a day and reduce their severity. But the debate on the subject is far from over.

People who begin using zinc lozenges, tablets or syrup at the first signs of a cold are more likely to get well faster, researchers reported Tuesday. But the new findings probably won't be the last word on the issue, which has been the subject of debate since the idea was first proposed in 1984.

Since that time, 18 studies have examined zinc in preventing or treating colds. Some found zinc supplements were modestly helpful, others failed to turn up any benefits.

One analysis of 14 studies, published in 2007, concluded that many of the studies were too flawed to draw any conclusions.

In the latest report, published by the Cochrane Library, an international network of experts who conduct systematic reviews of research, scientists in India evaluated 15 studies, including four published since 2000.

Two of the studies evaluated focused on zinc's effectiveness in preventing colds and the rest on its ability to shorten the duration of colds. The 15 studies involved 1,360 participants ranging in age from 1 to 65 with good overall health.

Pooling the data, researchers found that people who took zinc within 24 hours of the start of symptoms were over their colds about one day sooner than people who took placebos. The analysis also found that the severity of cold symptoms was somewhat milder among people who took zinc.

Whether these results will be considered meaningful depends on whom you ask, said Dr. Kay Dickersin, a professor of epidemiology at Johns Hopkins University's Bloomberg School of Public Health and director of the U.S. Cochrane Center, one of the 12 centers around the world that facilitate the work of the Cochrane reviews. Dickersin was not involved in the research.

"I might say, 'A day less of symptoms is good; I'll do it.' But you might say, 'A day is nothing; it's not worth driving to the drugstore,' " she said.

Moreover, since the study designs varied widely, it's impossible to make recommendations on what doses are optimal, what formulations are best and how long to use the products, said the authors of the analysis, Meenu Singh and Rashmi R. Das of the Postgraduate Institute of Medical Education and Research in Chandigarh, India.

"I think there is a need for more research so we can get a sense of how well zinc works or if it even does work," Dickersin said.

Zinc lozenges and syrup, commonly available in drugstores, are typically taken every two to three hours during waking hours for at least five days. Most products recommend a standard daily dose for cold treatment is about 30 milligrams of syrup per day or about 60 milligrams in lozenges.

When a zinc acetate formulation is taken in a high enough dose and started early in the onset of a cold, it's likely to be effective, said Dr. Ananda Prasad, an expert on zinc at Wayne State University in Detroit who conducted two studies, both of which showed a positive effect.

"In our studies, we only included patients who had [begun treatment] within 24 hours" of the start of symptoms, he said. "If you don't take zinc within 24 hours, it does not have much effect."

But an examination of only the most scientifically rigorous of the zinc studies shows it probably doesn't shorten colds, said Dr. Terence M. Davidson, the director of the UC San Diego Nasal Dysfunction Clinic.

"The more rigorously scientific studies, where you took a group of people and gave half of them zinc and half a placebo and inoculated their nose with a cold virus, found there were no differences," Davidson said. "I think enough research has been done to show if there is some benefit, it's not going to be very significant."

There may also be risks from some of these products, said Davidson, who was the first to identify harmful side effects from zinc nasal spray.

In 2009, the Food and Drug Administration warned consumers to stop using three zinc-containing Zicam nasal products after receiving 130 reports about loss of smell associated with the products. The Cochrane Library analysis did not investigate zinc nasal sprays.

Researchers don't know why zinc may affect the common cold. It could be that zinc prevents rhinoviruses from attacking nasal cells, slows the replication of the virus or prevents histamine release (which causes sneezing, runny nose and rash).

In the United States, colds contribute to 75 to 100 million visits to doctors each year at a cost of about $7.7 billion. Colds are among the most common reasons for absenteeism from work and school.

"Any medication that is only partially effective in the treatment and prevention of the common cold could markedly reduce morbidity and economic losses due to this illness," Singh and Das wrote.

Source: Roan, Shari. February 16, 2011. The Los Angeles Times. Zinc found to be effective in treating colds. http://www.latimes.com/health/la-he-zinc-colds-20110216,0,1557679.story

Tags:  treatment  zinc 

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Sublingual Desensitization for a Sniff-Free Spring

Posted By Administration, Wednesday, February 16, 2011
Updated: Friday, April 18, 2014

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by Allan Magaziner, DO

It’s nothing to sneeze at: 54 million Americans suffer from seasonal allergies. Until now, many have either wearily resigned themselves to the watery eyes, runny nose, sneezing, wheezing and hives associated with the condition, or have opted to try to combat these symptoms with allergy shots that can be costly and inconvenient. That’s been the bad news. The good news is that a recent study of more than 60 patients allergic to pollen, dust mites and cat allergens has shown that an approach known as sublingual desensitization is indeed a safe and effective alternative to traditional immunotherapy injections. The study findings have prompted researchers to strongly recommend its use, especially in children. In the study, the practice was shown to significantly reduce the symptoms of hay fever and nasal allergies, as well as the need for medication, compared to placebo.

The study finally validates what we’ve been practicing at the Magaziner Center for Wellness with great success for more than 24 years. During this time, we’ve found sublingual desensitization (which is defined as immunotherapy using drops or pills) to be:

  • Safer
  • Less invasive
  • More convenient – as it can be self-administered by the patient
  • Without risk of anaphylactic shock, a potential side effect of immunotherapy injections.
  • Less taxing mentally and physically

This last bullet has been an important one for our patients who are children whose parents wisely sought a natural therapy. Sublingual desensitization is great for kids – it’s the difference between taking a drop or a pill orally versus being stuck with a needle. And, let’s face it, how many children do you know that aren’t a little upset at the sight of a needle?

Like all treatments at the Magaziner Center for Wellness, our patients first undergo a thorough evaluation. We test patients’ reactions to common, as well as unexpected, allergens, including:

  • Food
  • Smoke
  • Cat/dog dander
  • Pollens (grass, trees and weeds)
  • Dust/dust mites
  • Chemicals (perfumes, paint, carpets, etc.)
  • Mold

Why? Because, simply put, allergies are additive. If a person suffers from seasonal allergies, what he or she eats and breathes throughout the year affects his or her reaction during the documented allergy season. In fact, we have found that food allergies and food sensitivities have more to do with chronic complaints than almost any other factors.

After patients’ reactions are tested, we use injection therapy to place tiny amounts of the allergen into the bloodstream to assess clinical symptoms and behavioral reactions (i.e., change in frequency of headaches, even handwriting samples). When we get to the point that triggers a response, we give successive dosages until the symptoms that have been created disappear. Once the level is identified, we make up a vial of antigens that patients place as drops under their tongue on a daily basis.

In the simplest terms, we are naturally treating the immune system and getting it to respond appropriately to the allergens. This takes time, of course, so it is recommended that anyone who suffers from seasonal allergies receive treatment in mid-March so that the immune system’s response can be built well in advance of the blossoming of trees and flowers between April and October.

Tags:  allergies  prevention 

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New Light Shed Upon "Environmentally Friendly" LEDs

Posted By Administration, Tuesday, February 15, 2011
Updated: Friday, April 18, 2014

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LED lights have been marketed as environmentally preferable alternatives to traditional light bulbs, but many contain lead, arsenic and a dozen other potentially hazardous substances, according to new research out of UC Irvine.

"LEDs are touted as the next generation of lighting," says Oladele Ogunseitan, chairman of UCI's Department of Population Health & Disease Prevention, in a university statement about his published research. "But as we try to find better products that do not deplete energy resources or contribute to global warming, we have to be vigilant about the toxicity hazards of those marketed as replacements." 

A light-emitting diode (LED) is a semiconductor light source that for years has been used as indicator lamps for aviation, automobiles and traffic signals. Amid concerns about global warming and the need for devices that are safer and use less energy, LEDs have increasingly replaced traditional bulbs that contain mercury. An expansion into the household market is currently under way.

For the research, Ogunseitan and fellow scientists at UCI and UC Davis crunched multicolored lightbulbs sold in Christmas strands; red, yellow and green traffic lights; and automobile headlights and brake lights. They then measured the contents and found differing levels of toxic materials, including lead and arsenic. 

Low-intensity red lights contained up to eight times the amount of lead allowed under California law. High-intensity, brighter bulbs had more contaminants than lower ones. White bulbs contained the least lead but had high levels of nickel.

Referring to the holiday lights in the January 2011 issue of Environmental Science & Technology, the team wrote, "We find the low-intensity red LEDs exhibit significant cancer and non-cancer potentials due to the high content of arsenic and lead." 

Results from the larger lighting products will be published later, but as Ogunseitan indicates, "It's more of the same."

Toxins like those Ogunseitan and his team found in LEDs have been linked to different cancers, neurological damage, kidney disease, hypertension, skin rashes and other illnesses. The copper used in some LEDs also poses an ecological threat to fish, rivers and lakes.

As of now, LED products are not classified as hazardous waste. Ogunseitan believes his research exposes a need for mandatory product-replacement testing, something that was never done as manufacturers put LEDs in products that replaced incandescent bulbs. 

As precautions, Ogunseitan advises refraining from throwing LEDs in landfills. He also recommends that crews dispatched to clean up vehicle collisions wear protective gear and that homeowners don gloves and masks when handling broken LED lights. 

You won't be overcome by cancer if you breathe the contents of a broken or cracked LED light, he notes. It'll just be one more toxin your body is exposed to on the road to the Big C.

Source: February 15, 2011. OC Weekly Blog. Coker, Mike. LED Lights, Like Incandescent Bulbs They Replace, Contain Toxins: UC Irvine Research. http://blogs.ocweekly.com/navelgazing/2011/02/oladele_ogunseitan_uci_led_lig.php

Tags:  technology 

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NIH Study Finds Two Pesticides Associated with Parkinson's Disease

Posted By Administration, Monday, February 14, 2011
Updated: Friday, April 18, 2014

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New research shows a link between use of two pesticides, rotenone and paraquat, and Parkinson's disease. People who used either pesticide developed Parkinson’s disease approximately 2.5 times more often than non-users.

The study was a collaborative effort conducted by researchers at the National Institute of Environmental Health Sciences (NIEHS), which is part of the National Institutes of Health, and the Parkinson's Institute and Clinical Center in Sunnyvale, Calif.

"Rotenone directly inhibits the function of the mitochondria, the structure responsible for making energy in the cell," said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author of the paper appearing online in the journal Environmental Health Perspectives. "Paraquat increases production of certain oxygen derivatives that may harm cellular structures. People who used these pesticides or others with a similar mechanism of action were more likely to develop Parkinson's disease.

The authors studied 110 people with Parkinson’s disease and 358 matched controls from the Farming and Movement Evaluation (FAME) Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/fame/index.cfm) to investigate the relationship between Parkinson’s disease and exposure to pesticides or other agents that are toxic to nervous tissue. FAME is a case-control study that is part of the larger Agricultural Health Study (http://www.niehs.nih.gov/research/atniehs/labs/epi/studies/ahs/index.cfm), a study of farming and health in approximately 90,000 licensed pesticide applicators and their spouses. The investigators diagnosed Parkinson's disease by agreement of movement disorder specialists and assessed the lifelong use of pesticides using detailed interviews.

There are no home garden or residential uses for either paraquat or rotenone currently registered. Paraquat use has long been restricted to certified applicators, largely due to concerns based on studies of animal models of Parkinson's disease. Use of rotenone as a pesticide to kill invasive fish species is currently the only allowable use of this pesticide.

"These findings help us to understand the biologic changes underlying Parkinson’s disease. This may have important implications for the treatment and ultimately the prevention of Parkinson's disease," said Caroline Tanner, M.D., Ph.D., clinical research director of the Parkinson’s Institute and Clinical Center, and lead author of the article.

The NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit www.niehs.nih.gov. Subscribe to one or more of the NIEHS news lists (www.niehs.nih.gov/news/releases/newslist/index.cfm) to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visitwww.nih.gov.


Reference: Tanner CM, Kamel F, Ross GW, Hoppin JA, Goldman SM, Korell M, Marras C, Bhudhikanok GS, Kasten M, Chade AR, Comyns K, Richards MB, Meng C, Priestly B, Fernandez HH, Cambi F, Umbach DM, Blair A, Sandler DP, Langston JW. 2011. Rotenone, paraquat and Parkinson’s disease. Environ Health Perspect; doi:10.1289/ehp.1002839 [Online 26 January 2011].

Source: National Institutes of Health (NIH). February 11, 2011. NIH study finds two pesticides associated with Parkinson's Disease. http://www.nih.gov/news/health/feb2011/niehs-11.htm?

Tags:  NIH  parkinson's disease  toxins 

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A Not-So-Sweet Loss for Organic Sugar

Posted By Administration, Tuesday, February 8, 2011
Updated: Friday, April 18, 2014

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The US Department of Agriculture last Friday gave farmers the go-ahead to resume planting Roundup Ready sugarbeets—claiming it’s the only way to avoid a nationwide shortage of sugar!

Hot on the heels of the deregulation of genetically engineered (GE) alfalfa, the USDA said it would once again allow the GE sugarbeet to be planted, contrary to the order of district court judge Jeffrey S. White, who said a full environmental impact statement (EIS) needed to be done first. As the Wall Street Journal points out, an EIS of the type ordered by the judge is usually thousands of pages long and takes years to conduct. That would have kept the genetically modified sugarbeets out of the hands of farmers at least through 2012.

This would allow farmers to begin planting GE sugarbeets this spring. But the environmental and organic seed groups that originally sued the USDA said Friday they would ask Judge White to block this latest move by the USDA.

Processors say there aren’t enough non-GE sugarbeet seeds around for farmers to plant this spring. A study conducted for the sugar industry predicted that US sugar production would plunge 20% if the judge’s ban stays in place, and it appears this study alarmed food companies enough that they were able the pressure USDA into acting now. (For more on sugar and sweeteners, see our article elsewhere in this issue.)

In this case, the sugarbeets are being “partially deregulated”: USDA is permitting farmers to plant genetically modified sugarbeets this year only if they adhere to rules designed to prevent the plant’s wind-blown pollen from reaching organic fields, where its biotechnology traits could spread—though if the rules themselves prove ineffective, organic sugarbeets will be contaminated.

That contamination is what is most worrisome. The Organic Consumers Association had this to say about the deregulation of alfalfa: “[It is] guaranteed to spread its mutant genes and seeds across the nation; guaranteed to contaminate the alfalfa fed to organic animals; guaranteed to lead to massive poisoning of farm workers and destruction of the essential soil food web by the toxic herbicide, Roundup; and guaranteed to produce Roundup-resistant superweeds….” Health advocates have the same concerns about sugarbeets.

If you haven’t already done so, please visit the Aliance for Natural Health's Action Alert page where you can write to President Obama, Congress, and the USDA, and tell them to reverse this terrible decision. Please contact them today!


Tags:  diet  food and drink 

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Vitamin D Insufficiency

Posted By Administration, Friday, February 4, 2011
Updated: Friday, April 18, 2014

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Tom D. Thacher, MD and Bart L. Clarke, MD

The past decade has seen renewed interest in the sunshine vitamin, vitamin D, because new data suggest that its benefits extend beyond healthy bones. Accompanying this renewed interest has been a proliferation of published studies related to the effects of vitamin D in many varying clinical conditions. This article discusses the definition of vitamin D insufficiency, identifies the sources of variation in vitamin D status, reviews the evidence for the clinical benefits of vitamin D, and recognizes indications for vitamin D testing.

Representative studies were selected to highlight some of the limitations of current knowledge related to vitamin D insufficiency and the clinical benefits of vitamin D. We selected studies with the strongest level of evidence for clinical decision making related to vitamin D and health outcomes from our personal libraries of the vitamin D literature and from a search of the PubMed database using the term vitamin D in combination with the following terms related to the potential nonskeletal benefits of vitamin D: mortality, cardiovascular, diabetes mellitus, cancer, multiple sclerosis, allergy, asthma, infection, depression, psychiatric, and pain. The level of evidence was assessed with the following hierarchy: meta-analyses of randomized controlled trials (RCTs), RCTs, nonrandomized intervention studies, meta-analyses of observational studies (cohort and case-control studies), and observational studies.

The road to the discovery of vitamin D began with recognition of the childhood bone disease of rickets. The first formal medical treatise on rickets was published by Francis Glisson in 1650, when it was identified as a new disease that was more frequent in the rich than in the poor. During the industrial revolution of the 1800s, the prevalence of rickets increased dramatically, ranging from 40% to 60% among children in crowded and polluted urban areas. In 1822, Sniadecki was the first to recognize and report the association of rickets with a lack of sunlight exposure. By the mid-1800s, cod liver oil had been established as an effective treatment for rickets. The work of Mellanby and McCollum led to the discovery of vitamin D as the agent in cod liver oil that had antirachitic properties. This discovery eventually led to the fortification of milk and other foods with vitamin D in the 1930s, and as a result rickets all but disappeared in North America and Europe.

VITAMIN D METABOLISM

The terminology related to the biochemistry of vitamin D can be confusing. Vitamin D has 2 forms and several metabolites. The 2 forms are vitamin D2 and vitamin D3, also calledergocalciferol and cholecalciferol, respectively. Vitamin D3 is produced in the skin in response to ultraviolet B radiation from sunlight or can be obtained from the diet (ie, animal sources such as deep sea fatty fish, egg yolks, or liver) or from supplements. Few foods naturally have substantial vitamin D content, and dietary vitamin D is obtained primarily through fortified foods or supplements. Vitamin D2, which is found in some plants in the diet and is produced commercially by irradiation of yeast, is used for fortification and supplementation. Both vitamin D2 and vitamin D3 can be used for supplementation.

FIGURE

FIGURE.

Vitamin D metabolism. Ca = calcium; 1,25(OH)2D = 1,25-dihydroxyvitamin D; 25(OH)D = 25-hydroxyvitamin D; PTH = parathyroid hormone.

 

 

 

Both forms of vitamin D undergo identical metabolism (Figure). Some evidence indicates that vitamin D2 may be metabolized more rapidly than vitamin D3, but with regular daily intake they can be considered bioequivalent. Both forms of vitamin D are converted to 25-hydroxyvitamin [25(OH)D] in the liver, and the serum level of 25(OH) D is measured to determine the adequacy of vitamin D status. In the kidney, 25(OH)D is hydroxylated to 1,25-dihydroxyvitamin D [1,25(OH)2D], which is the only biologically active form of vitamin D. Acting principally on the duodenum, 1,25(OH)2D increases calcium absorption. It also acts on bone cells, both osteoblasts and osteoclasts, to mobilize calcium.

The characteristics of 1,25(OH)2D are those of a hormone, and consequently vitamin D is a prohormone rather than a true vitamin. The structure of 1,25(OH)2D is similar to that of other steroid hormones. As long as sunlight exposure is adequate, 1,25(OH)2D can be produced by the body without the requirement for ingestion in the diet. Like other hormones, 1,25(OH)2D circulates at picogram concentrations that are 1000 times less than those of the precursor 25(OH)D. Based on the need for increased calcium absorption, the synthesis of 1,25(OH)2D is tightly regulated and stimulated primarily by serum parathyroid hormone (PTH), as well as low serum calcium or phosphorus levels, and inhibited by circulating FGF23 produced by osteocytes. Although produced in the kidney, 1,25(OH)2D acts at a distance in the intestinal cell to increase calcium absorption or in the bone to stimulate differentiation and activation of osteoblasts and osteoclasts.

 

 


 

ASSESSING VITAMIN D STATUS

Determination of vitamin D status is not based on measurement of serum 1,25(OH)2D concentrations. Vitamin D status is assessed by measuring the prohormone 25(OH) D, which is an indicator of supply rather than function. The most stable and plentiful metabolite of vitamin D in human serum, 25(OH)D has a half-life of about 3 weeks, making it the most suitable indicator of vitamin D status. In the past, vitamin D deficiency was identified by the presence of bone disease, either rickets or osteomalacia. Bone disease caused by vitamin D deficiency is associated with serum 25(OH)D values below 10 ng/mL (to convert to nmol/L, multiply by 2.496). More recently, the term vitamin D insufficiency has been used to describe suboptimal levels of serum 25(OH)D that may be associated with other disease outcomes. Precisely defining vitamin D deficiency or insufficiency on the basis of 25(OH)D values is still a matter of much debate. A useful but rather simplistic classification of vitamin D status is shown in the Table. A cutoff value of 30 ng/mL is sometimes used for optimal vitamin status. On the basis of measured concentrations of 25(OH)D, many patients are given a diagnosis of vitamin D deficiency or insufficiency when most have no evidence of disease.

TABLE

 

 

TABLE.

Classification of Vitamin D Status by 25(OH)D Concentrationa,b

 

 

As discussed in detail in recent reviews, investigators have considered various functional measures to assess the adequacy of vitamin D status. One functional definition of optimal vitamin D status is the 25(OH)D level that maximally suppresses PTH secretion, because the major stimulus for PTH secretion is a low level of serum ionized calcium. In adults, multiple cross-sectional examinations of the relationship between serum PTH and 25(OH)D levels demonstrate a plateau in suppression of PTH when the 25(OH)D level reaches approximately 30 ng/mL. This is the rationale for selecting 30 ng/mL as the cutoff value for defining optimal vitamin D status. However, this definition represents an average value at a population level but does not account for the wide variation in the 25(OH) D level that represents adequacy at an individual level. Many patients have very low 25(OH)D values without evidence of increased production of PTH, and conversely, 25(OH)D levels greater than 30 ng/mL do not guarantee PTH suppression. Another limitation of this definition is that, in children, an elevated PTH level does not indicate inadequate vitamin D status and has been associated with increased calcium absorption. In puberty, the PTH concentration increases, which may stimulate increased periosteal bone formation and increased bone accrual. In fact, preliminary evidence suggests that, with adequate calcium intake, a high-normal PTH level and low-normal 25(OH)D level may result in greater bone size and mass during puberty.

Another method used in some research studies for defining optimal vitamin D status is the 25(OH)D level at which there is no incremental increase in 1,25(OH)2D levels after administration of vitamin D, because the level of 1,25(OH)2D is adequate to meet demand. Similar to the findings related to PTH in adults, an incremental increase in the level of 1,25(OH)2D was observed after administration of vitamin D in children when values of 25(OH)D were less than 25 to 30 ng/mL. In situations of very low calcium intakes, some evidence suggests that the demand for 1,25(OH)2D may be greater. Thus, vitamin D requirements may vary based on customary calcium intake.

Another functional measure of vitamin D status is the 25(OH)D level that results in maximal intestinal calcium absorption. By combining the results of 3 studies in adults, Heaney concluded that optimal calcium absorption occurred at 25(OH)D levels of 32 ng/mL or greater. In contrast, another study found no association between 25(OH)D levels and calcium absorption in healthy women. Fractional calcium absorption was high (>50%) in Nigerian children with presumed dietary calcium deficiency rickets and low dietary calcium intakes despite low normal serum 25(OH)D concentrations. After vitamin D administration and a marked increase in 25(OH) D and 1,25(OH)2D concentrations, fractional calcium absorption did not increase any further. In these studies in children, fractional calcium absorption was not related to serum 1,25(OH)2D levels either before or after vitamin D administration. In a study of adults attending an osteoporosis clinic, concentrations of 1,25(OH)2D and intestinal calcium absorption did not appear to decline until 25(OH) D concentrations fell to 4 ng/mL or less, a level that is generally considered to be indicative of severe vitamin D deficiency.

More recently, the criterion for optimal vitamin D status has moved away from being defined as the 25(OH) D concentration needed to achieve skeletal health to that which demonstrates optimal benefits on nonskeletal health outcomes. The evidence related to these outcomes will be considered later in this review.

SOURCES OF VARIATION IN VITAMIN D STATUS

Factors known to influence 25(OH)D levels include race, vitamin D intake, sun exposure, adiposity, age, and physical activity. Even when all the factors known to influence 25(OH)D concentrations are taken into account, most of the individual variation of 25(OH)D values is difficult to explain. Consequently, it is difficult to assess the risk of clinical or biochemical consequences of vitamin D insufficiency in a patient on the basis of concentrations of 25(OH) D alone. The duration of vitamin D insufficiency, the responsiveness of the vitamin D receptor, dietary calcium intake, and individual calcium requirements likely modify the clinical consequences of vitamin D deficiency or insufficiency based on levels of 25(OH)D.

A single exposure to summer sun in a bathing suit for 20 minutes produces the equivalent of 15,000 to 20,000 IU of vitamin D3. In a study of Hawaiian surfers with sun exposure of at least 15 hours per week for the preceding 3 months, 25(OH)D levels ranged from 11 up to 71 ng/mL, demonstrating wide individual variation. Outdoor sun exposure and time spent outdoors are better predictors of serum 25(OH)D values than dietary vitamin D intake.

The 25(OH)D level achieved with the same oral dose of vitamin D varies widely by individual. The level of 25(OH)D that results in clinical consequences probably varies with calcium intake, race, age, body fat, and individual genetic factors, all of which may influence calcium homeostasis. Genetic variation represented by polymorphisms of certain genes in the vitamin D metabolic pathway explains some of the interindividual variability of 25(OH)D concentrations, particularly polymorphisms of the enzyme 7-dehydrocholesterol reductase in the skin, cytochrome P450 25-hydroxylase in the liver, and vitamin D–binding protein in the circulation. The functional effect of a particular level of 25(OH)D depends on the uptake of 25(OH)D by target cells and the efficiency of 1α-hydroxylation to produce 1,25(OH)2D.

MEASUREMENT OF 25(OH)D LEVELS

Some controversy exists regarding the best method for measuring 25(OH)D levels. Radioimmunoassay has been the most common method reported in the literature and was the method used in some of the large-scale population studies of vitamin D, such as the National Health and Nutrition Examination Survey (NHANES) and the Women's Health Initiative (WHI).

The accuracy of measurement varies widely between individual laboratories and between different assay methods. In one study, identical serum samples were provided to 6 different laboratories, and the chemiluminescent assay tended to return higher values for 25(OH)D. Competitive protein-binding assays are also known to generally yield higher 25(OH)D values. When serum samples were spiked with an additional 20 ng/mL of 25(OH)D, the increment in 25(OH)D level was less than 20 ng/mL in all the laboratories, except the one using high-performance liquid chromatography. Antibodies used in some radioimmunoassays do not detect both 25(OH)D2 and 25(OH)D3. The use of a standard cutoff value for adequate vitamin D status is problematic if applied to all laboratories and all methods. A single serum sample could be assessed as showing adequate vitamin D status in one laboratory and an insufficient level in another, with differences of up to 17 ng/mL.

More recently, large medical laboratories have begun using liquid chromatography–tandem mass spectrometry, which identifies the 25-hydroxylated forms of both vitamin D2and D3. The total 25(OH)D, which is the sum of 25(OH)D2 and 25(OH)D3, is used to evaluate vitamin D status. Since 2003, there has been more than a 15-fold increase in the volume of 25(OH)D measurements at Mayo Clinic in Rochester, MN (Singh R., personal communication), reflecting the increasing attention clinicians are giving to vitamin D status.

CLINICAL MANIFESTATIONS OF VITAMIN D DEFICIENCY

Nutritional Rickets

The classical manifestation of vitamin D deficiency is nutritional rickets, which results from inadequate mineralization of growing bone. Consequently, rickets is a disease of children. Far from being eradicated, nutritional rickets continues to occur throughout the world, with reports from at least 60 countries in the past 20 years. In a review of published cases of rickets in the United States, most occurred in children younger than 30 months. The vast majority of cases in the United States occurred in African American infants who were fed with breast milk rather than formula. Florid rickets manifests with leg deformities; enlargement of the growth plates of the wrists, ankles, and costochondral junctions; and rib cage deformities. Subtle symptoms that should raise the clinical suspicion of rickets in children include bone pain in the legs, delayed age of standing or walking, frequent falling, and delayed growth. Hypocalcemic seizures in the first year of life may be the initial manifestation of rickets.

Radiography of the long bones at the knees and the wrists is necessary to confirm the diagnosis of rickets. Radiography demonstrates impaired mineralization of the growth plates, evident by widening of the growth plate and fraying of the margin of the metaphyses. Biochemical features most consistently include hypophosphatemia and an elevated alkaline phosphatase level. As a result of vitamin D deficiency, serum concentrations of 25(OH)D are very low in patients with rickets, usually less than 5 ng/mL. However, concentrations of 25(OH)D may not be markedly reduced if rickets results from calcium deficiency or if the child has recently received vitamin D or sun exposure. In some tropical countries, where sun exposure is plentiful, calcium deficiency is more important than vitamin D deficiency as a cause of rickets. However, even in the United States, only 22% of children with nutritional rickets had deficient levels of 25(OH)D, indicating that calcium deficiency as a cause of rickets needs to be considered domestically as well.

Osteomalacia

Osteomalacia refers to the failure of organic osteoid formed by osteoblasts to become mineralized with calcium and phosphorus. Although histological osteomalacia is characteristic of rickets, the term osteomalacia is generally used to describe the bone disease caused by vitamin D deficiency in adults, who no longer have growing bones. The clinical manifestations of these 2 conditions are different.

Bone pain is a characteristic feature of osteomalacia, and it can be confused with arthritis or fibromyalgia. Bone pain due to osteomalacia primarily affects the bones between the joints, whereas arthritis usually causes predominantly joint pain, and fibromyalgia causes more diffuse muscle and soft tissue pain; however, it can be difficult to distinguish between these disorders. Proximal muscle weakness and gait instability are often present. Because the growth plates have closed in adults, the radiographic features differ from those typical of rickets. Radiography may reveal pseudofractures of the pelvis, femurs, metatarsals, or lateral margins of the scapulae. The biochemical features of osteomalacia are similar to those of rickets, with increased serum alkaline phosphatase and PTH values, and low calcium, phosphorus, and 25(OH)D values in most cases. A review of all the archived cases of bone biopsy–proven osteomalacia seen by the Bone Histomorphometry Laboratory at Mayo Clinic concluded that radiographic examination as well as serum calcium, phosphorus, and alkaline phosphatase assays are adequate screening tests in patients who have a clinical presentation suggestive of osteomalacia, but that 25(OH)D values may be normal.

In a cross-sectional study of iliac bone biopsy specimens obtained at autopsy, an excess accumulation of osteoid, which corresponds with histological osteomalacia, was found only in patients with 25(OH)D values less than 25 ng/mL. However, even patients with very low values of 25(OH)D did not consistently have evidence of osteomalacia.

POTENTIAL BENEFITS OF VITAMIN D

Apart from the deficiency diseases of rickets and osteomalacia, recent evidence suggests other skeletal and nonskeletal benefits of vitamin D. In evaluating the evidence, it is important to recognize the limitations inherent in the study design and methodology. Important issues that apply to vitamin D research include the following:

  1. Was the study design observational, which can only demonstrate associations and is subject to confounding, or was it an RCT that generally balances unmeasured confounding variables?

  2. How was the intake of vitamin D measured? Was the serum 25(OH)D value considered a proxy measure of vitamin D intake?

  3. What outcome was measured to assess the benefit of vitamin D? Was it the achieved 25(OH)D level or a specific clinical outcome that matters to the patient? Was assessment of the outcome the primary aim of the study?

  4. Is 25(OH)D the most appropriate biomarker of vitamin D status in all situations?

 

In the following section, representative studies of the available evidence related to the skeletal and nonskeletal effects of vitamin D are reviewed.

Skeletal Benefits

Bone Density. In addition to the treatment and prevention of vitamin D–deficiency rickets in children, vitamin D has been associated with other beneficial skeletal effects. A retrospective cohort study of pubertal girls demonstrated increased bone mineral density (BMD) of the femoral neck, but not of the spine or radius, among those who received supplemental vitamin D in infancy. Evidence of a positive association between BMD and serum 25(OH)D concentrations in adolescents is fair, but the evidence for a positive association in infants is inconsistent. Serum 25(OH)D concentration was related to hip BMD in community-dwelling women and men aged at least 20 years who participated in the US NHANES III survey. Higher calcium intake was significantly associated with higher BMD only for women with 25(OH)D values less than 20 ng/mL. One of the limitations of a cross-sectional study like the NHANES survey is that it can demonstrate only associations, not cause-and-effect relationships. Another confounding factor may be associated with low vitamin D intake and low bone density. For example, healthier people who exercise more outside in the sun may have greater bone density because of their exercise and higher 25(OH)D levels because of sun exposure. The WHI calcium and vitamin D supplementation trial showed that hip bone density was 1.06% higher in women receiving calcium and vitamin D supplementation vs placebo at 9 years, but that their lumbar spine and total body bone density did not differ significantly from those receiving placebo during this interval.

Fractures and Falls. On the basis of RCTs, the strongest evidence for the benefit of vitamin D relates to the prevention of fractures and falls. In a meta-analysis of 12 RCTs, a reduced nonvertebral fracture risk was demonstrated only for doses of vitamin D greater than 400 IU/d (relative risk [RR], 0.80; 95% confidence level [CI], 0.72-0.89). Similarly, a meta-analysis of 8 RCTs demonstrated that vitamin D reduced the risk of falls (RR, 0.78; 95% CI, 0.64-0.94), but only if the dose was 700 IU/d or greater and the 25(OH)D concentration was at least 25 ng/mL. The benefit of vitamin D could have been limited to those with unrecognized osteomalacia, which is associated with proximal muscle weakness and gait instability. These high-quality studies provide clear evidence that a minimum dose of 800 IU/d of vitamin D will reduce the risk of falls and fractures in older adults. However, a recent RCT of a 500,000 IU annual dose of vitamin D in women of advanced age increased the median 25(OH)D concentration from 20 ng/mL to 48 ng/mL one month later but resulted in an increased risk of falls and fractures in the group receiving this regimen.

Nonskeletal Benefits

Interest in the nonskeletal effects of vitamin D has been increasing since the discovery of vitamin D receptors and the 1α-hydroxylase enzyme in multiple tissues, including cells of the pancreas, immune system, macrophages, vascular endothelium, stomach, epidermis, colon, and placenta. In these tissues, 25(OH)D can be converted to 1,25(OH)2D locally, without altering serum 1,25(OH)2D concentrations. Through these paracrine effects, 1,25(OH)2D influences the expression of genes in local tissues. However, the evidence for the nonskeletal benefits of vitamin D is not as strong as the evidence for the skeletal effects.

Lower Mortality Rate. In a prospective observational study of adults older than 65 years participating in NHANES III, the risk of death was 45% lower in those with 25(OH)D values greater than 40 ng/mL compared with those with values less than 10 ng/mL (hazard ratio [HR], 0.55; 95% CI, 0.34-0.88). However, this may simply reflect the fact that people with underlying illness or immobility (who are more likely to die) tend to have lower 25(OH)D levels, in part as a result of having spent less time outdoors or of having less adequate nutrition. Because vitamin D is sequestered in adipose tissue, obesity is also associated with lower 25(OH)D levels. However, observational studies cannot prove whether low 25(OH)D status is the cause of greater mortality or just a marker of other underlying risk factors.

In contrast, a meta-analysis of 18 RCTs of vitamin D supplementation in postmenopausal women of advanced age, with dosages ranging from 300 to 2000 IU/d, reported a 7% lower risk of death in those receiving a vitamin D supplement (RR, 0.93; 95% CI, 0.87-0.99). This highlights the difference often found between RCTs and observational studies. The effect sizes found in observational studies are often attenuated or absent in RCTs. The situation with vitamin D is analogous to that of hormone replacement therapy (HRT) in postmenopausal women. The beneficial effects of HRT were demonstrated for multiple health outcomes in observational studies, but the WHI RCT in older postmenopausal women failed to confirm the beneficial effects of HRT on dementia and cardiovascular disease. In the observational trials, healthier women were more likely to use estrogen replacement and had fewer adverse health outcomes, indicating a “healthy user” bias. Only an RCT definitively demonstrated that the risks of first-time use of HRT outweighed the benefits in women older than 60 years.

Despite the slight reduction in mortality associated with vitamin D supplementation, the primary aim of the RCTs included in the meta-analysis was not to assess mortality. Not all trials of vitamin D reported mortality outcomes, so those trials could not be included in the meta-analysis. Trials that showed a mortality effect would be more likely to report this outcome, leading to a high likelihood of reporting bias that could render the slight mortality reduction statistically insignificant.

Lower Cardiovascular Mortality. The reduced mortality in the aforementioned observational study mirrored in large part the reduced cardiovascular mortality in those with 25(OH)D values greater than 40 ng/mL compared with those with values less than 10 ng/mL (HR, 0.42; 95% CI, 0.21-0.85). In another observational cohort study, patients who had angiography and 25(OH)D measurements were followed up for 8 years. Those from the highest 25(OH)D quartile (median, 28 ng/mL) had a lower mortality (HR, 0.45; 95% CI, 0.32-0.64) than those from the lowest quartile (median, 8 ng/mL). Although these observational studies do not demonstrate that low 25(OH)D values accelerate cardiovascular mortality, low 25(OH)D concentrations were associated with serum markers of inflammation that are indicators of cardiac risk.

Recently, concern has been expressed that vitamin D could potentially accelerate vascular disease. In a study of African Americans with type 2 diabetes mellitus, 25(OH)D levels correlated with increased calcified plaque in the aorta and carotids, but not in the coronary arteries. Vascular disease associated with chronic kidney disease, especially that associated with very low bone turnover, may also be accelerated with supplementation with standard doses of vitamin D. Furthermore, concern has been raised recently that other disorders characterized by vascular inflammation, such as diabetes mellitus, rheumatoid arthritis, or systemic lupus erythematosus, may not benefit from standard recommended doses of vitamin D supplementation.

Vitamin D may affect other cardiovascular and metabolic disease risks. In an observational study of adolescents in NHANES III, those with the lowest 25(OH)D values (<15 ng/mL) had more than a 2-fold greater odds of having an elevated blood pressure compared with the group of adolescents with higher 25(OH)D levels (>26 ng/mL) (odds ratio [OR], 2.4; 95% CI, 1.3-4.2).

The NHANES III data in adults indicated that those with 25(OH)D levels of less than 21 ng/mL had an increased risk of hypertension, diabetes, obesity, and high triglyceride levels—all metabolic manifestations associated with increased cardiovascular mortality. Although obesity is associated with lower serum 25(OH)D levels because of the sequestration of vitamin D in adipose tissue, it is likely not the consequence of low 25(OH)D levels. Additionally, the 25(OH)D level may be a marker of other factors associated with obesity, such as physical inactivity and reduced outdoor sun exposure.

Reduced Risk of Diabetes Mellitus. A meta-analysis of 5 observational studies of vitamin D supplementation in childhood reported a nearly 30% reduction in the risk of type 1 diabetes in children who had ever received vitamin D supplements (OR, 0.71; 95% CI, 0.60-0.84). Unfortunately, most studies had no information about vitamin D dosage or adherence. Because these were observational studies, and vitamin D was not randomly assigned to children, it is possible that characteristics of families who provided supplemental vitamin D to their children contributed to the decreased risk of type 1 diabetes in children receiving supplements.

Vitamin D receptors are present in pancreatic β cells, and vitamin D may augment insulin secretion and insulin sensitivity. Adolescents in NHANES III with serum 25(OH)D levels of less than 15 ng/mL were more likely to have elevated blood glucose levels than those with the highest 25(OH)D values (>26 ng/mL) (OR, 2.5; 95% CI, 1.0-6.4). The observational Nurses Health Study found that vitamin D supplementation and calcium supplementation were both associated with a reduction in risk of type 2 diabetes. Current data related to vitamin D and the risk of type 2 diabetes are limited by inadequate adjustment for confounding variables, post hoc analyses, and inability to identify the separate effects of calcium and vitamin D. Because milk is the major source of both vitamin D and calcium in the diet, it is difficult to identify the independent effects of dietary calcium and vitamin D on the basis of intake or 25(OH)D levels. Skim milk intake is also inversely associated with obesity, which could account for an association between the intake of dietary calcium and vitamin D and a reduced risk of type 2 diabetes.

Reduced Risk of Cancer. Vitamin D is known to promote cellular differentiation, inhibit cellular proliferation, and reduce the growth of certain tumors in laboratory animals. A meta-analysis of case-control studies of those with and without colon cancer found that, for each 20 ng/mL increase in serum 25(OH)D levels, the odds of colon cancer were reduced by more than 40% (OR, 0.57; 95% CI, 0.43-0.76). Other studies have shown that dietary calcium intake is also associated with reduced colon cancer risk and adenoma formation. Because milk intake is a major determinant of serum 25(OH)D levels, it is difficult to separate the effect of vitamin D from that of calcium intake.

In the case of colon cancer, one large RCT was performed to evaluate the effect of combined supplementation with calcium and vitamin D on the risk of colon cancer. In the WHI trial, supplementation with calcium and vitamin D had no significant effect on the risk of colorectal cancer during 8 years of follow-up. Several limitations of this study may have contributed to this lack of effect. Colorectal cancer is a long latency disease, and 8 years may not have been sufficient time to observe the effect of calcium and vitamin D. Another criticism is that the relatively low dose of 400 IU of vitamin D may have not been protective or sufficient to increase serum 25(OH)D levels adequately. Concentrations of 25(OH)D were measured at baseline but not during follow-up. Declining adherence over time would have further reduced the effective doses of calcium and vitamin D.

Breast cancer has also been associated with vitamin D insufficiency. A meta-analysis combining 7 observational studies reported a lower risk of breast cancer among women in the highest compared with the lowest quartile of 25(OH) D values (OR, 0.55; 95% CI, 0.38-0.80). As with colon cancer, calcium intake was also associated with a reduced risk of breast cancer. Because obesity is associated with an increased risk of breast cancer and low 25(OH)D levels, it is a confounding factor in the association between breast cancer risk and vitamin D.

As with colon cancer, the WHI RCT of a combined regimen of calcium and vitamin D showed no benefit of supplementation on the risk of breast cancer, again highlighting the different conclusions of observational studies and RCTs. The limitations of the breast cancer study are similar to those of the study focused on colon cancer. This study demonstrated the potential confounding effects of physical activity and obesity. Baseline 25(OH)D levels were greater among women with lower body mass index and more recreational physical activity. When controlling for body mass index and physical activity, serum 25(OH)D concentration was not associated with breast cancer risk.

In a meta-analysis of 11 observational studies, prostate cancer was not associated with serum 25(OH)D levels. The evidence regarding an association between pancreatic cancer and 25(OH)D levels is conflicting. A multinational cohort study found no protective association between greater 25(OH)D values and gastric, esophageal, endometrial, ovarian, kidney, non-Hodgkin lymphoma, and pancreatic cancers. Drake et al recently showed that event-free survival and overall survival were reduced in vitamin D–insufficient patients newly diagnosed as having diffuse large B-cell lymphoma and T-cell lymphoma during 34.8 months of follow-up.

To date, studies have not shown impressive effects of vitamin D treatment on malignancies.

Reduced Risk of Multiple Sclerosis. The incidence of multiple sclerosis increases with increasing latitude, corresponding with reduced ultraviolet B sun exposure and lower serum levels of 25(OH)D. A case-control study demonstrated that the odds of having multiple sclerosis were lower in the group with the highest 25(OH)D levels. However, the association was found only in white patients [OR, 0.59; 95% CI, 0.36-0.97 for a 20 ng/mL increase in 25(OH)D], not in African American patients. It is difficult to exclude the possibility that other confounding exposures associated with increasing latitude and greater indoor activity during winter months contribute to the risk of multiple sclerosis. Little evidence supports a therapeutic role for vitamin D in the treatment of multiple sclerosis.

Reduced Risk of Allergy and Asthma. Several lines of evidence demonstrate the effects of vitamin D on proinflammatory cytokines, regulatory T cells, and immune responses, with conflicting interpretation of the effects of vitamin D on allergic diseases. In a cross-sectional study of Costa Rican children, low 25(OH)D levels were associated with elevated IgE and eosinophil counts, as well as with increased asthma-related hospitalizations and use of anti-inflammatory medication. However, an association does not prove causation, and alternative explanations can account for this association. For example, children with more severe asthma may spend more time indoors and have less sun exposure.

Low maternal vitamin D intake in pregnancy has been associated with an increased likelihood of childhood wheezing at ages 3 and 5 years. In contrast, maternal 25(OH)D levels of greater than 30 ng/mL in pregnancy have been associated with childhood eczema at age 9 months and asthma at age 9 years. Vitamin D supplementation in infancy has been associated with increased atopy and allergic rhinitis in adulthood. Increasing 25(OH)D levels were associated with increasing risk of allergic rhinitis among adults in NHANES III. The conflicting data indicate the need for RCTs to demonstrate the effect of vitamin D on the prevention and control of allergic diseases.

Reduced Risk of Infection. Vitamin D is required for the expression of cathelicidin by macrophages, which is involved in bacterial killing. A meta-analysis of 7 observational studies noted a reduced risk of active tuberculosis in those with the highest vs the lowest values of 25(OH)D (OR, 0.68; 95% CI, 0.43-0.93). However, an RCT in a West African population with baseline mean 25(OH)D values of 31 ng/mL showed no effect of 100,000 IU of supplemental vitamin D given at the beginning and at 3 and 8 months of tuberculosis treatment on the rate of sputum conversion or resolution of markers of clinical severity. However, this dose of vitamin D may have been insufficient because the increase in 25(OH)D concentration during treatment did not differ between the supplement and placebo groups.

In observational data from NHANES III, persons with 25(OH)D values lower than 10 ng/mL were more likely to have had a recent upper respiratory tract infection than those with higher 25(OH)D values in all 4 seasons of the year. This association was even stronger in those with asthma or chronic obstructive pulmonary disease. Whether this association is explained by the fact that people who remain indoors are more likely to catch colds remains unclear.

A case-control study reported that mean 25(OH)D values were lower in children with bronchiolitis or pneumonia admitted to the pediatric intensive care unit than in healthy control children or in children with pneumonia admitted to the general pediatric ward.

Reduced Risk of Mental Illness. A cohort of Finnish children who received supplemental vitamin D in their first year of life had a lower risk of developing schizophrenia. However, the significance of this association is unclear because it was unrelated to adherence to vitamin D supplementation, was only evident in males, and was not found with any other mental illness.

To examine the effect of vitamin D on depression, overweight and obese patients were randomized to receive 20,000 or 40,000 IU of vitamin D or placebo weekly for 1 year. At baseline, those with 25(OH)D concentrations lower than 16 ng/mL had greater Beck Depression Inventory scores, indicating that they were more depressed, than those with higher 25(OH)D levels. The 2 groups receiving vitamin D supplementation had significant improvement in their scores, whereas the placebo group did not.

Less Musculoskeletal Pain. A small descriptive study reported that most patients (93%) with persistent musculoskeletal pain had 25(OH)D values of 20 ng/mL or less. In one RCT, patients with diffuse musculoskeletal pain or osteoarthritis and 25(OH)D values lower than 20 ng/mL were randomized to receive vitamin D or placebo for 3 months. Those given vitamin D had no improvement in their pain compared with baseline or compared with placebo-treated patients. In another double-blind RCT, primary care patients with 25(OH)D levels of 10 to 25 ng/mL were randomized to receive 50,000 IU of vitamin D or placebo weekly for 8 weeks. The treated group showed significantly greater improvement in fibromyalgia assessment scores than the placebo group. Patients with 25(OH)D values lower than 10 ng/mL were treated in an unblinded fashion with 50,000 IU of vitamin D weekly for 8 weeks but had no symptom improvement.

Reduced Risk of Renal Disease. In a subgroup analysis of the NHANES III data set, low 25(OH)D values were associated with a greater risk of kidney failure in African American but not in white participants. However, the opposite trend was observed in whites.

INDICATIONS FOR VITAMIN D TESTING

Measurement of serum 25(OH)D levels is indicated in select circumstances. If clinical symptoms of rickets in children or osteomalacia in adults are present, measurement of 25(OH)D levels will confirm vitamin D deficiency. Such testing would be appropriate in adults or children with bone pain, elevated serum alkaline phosphatase or PTH levels, and low serum calcium or phosphorus levels. Persons of advanced age, those with osteoporosis, or those at increased risk of falls or fractures may also benefit from measurement of 25(OH)D levels. However, one could argue that providing at-risk groups with routine supplementation of adequate doses of vitamin D may make testing for vitamin D insufficiency unnecessary. When to test and how to treat adults with vitamin D deficiency have recently been reviewed in this journal. No evidence shows benefit for screening 25(OH)D levels in the asymptomatic population.

CONCLUSION

Critically evaluating the evidence regarding the purported benefit of vitamin D on a multitude of health outcomes is difficult. The bulk of current data is based on observational, epidemiological studies, which are useful for generating hypotheses but not for proving causality. It is particularly difficult to tease out the effects of confounding variables that relate both to health outcomes and to vitamin D status, such as physical activity, milk intake, and adiposity. Few of the observational associations have been confirmed by RCTs, and many of the interventional studies of vitamin D also included calcium supplementation. Future clinical trials, including a National Institutes of Health–funded 5-year 20,000-participant prospective RCT comparing the effect of supplementation with 2000 IU/d of vitamin D3 or placebo, will help clarify the benefits and risks of vitamin D supplementation in many of the disorders discussed in this review.

On the basis of the current data, it seems prudent for persons older than 60 years to take a vitamin D supplement of 800 to 2000 IU/d to reduce the risk of falls and fractures. These recommendations are consistent with the recently released report of the Institute of Medicine, which recommended that healthy adults take 600 IU/d to maintain skeletal health and also concluded that information about the health benefits beyond bone health could not be considered reliable. Dark-skinned infants who are exclusively breast-fed are at greater risk of rickets and should receive 400 IU/d of supplemental vitamin D. Vitamin D supplementation in these ranges is likely to prevent bone loss, may improve bone density, may reduce fractures, and appears to reduce falls. Although vitamin D intoxication has been associated only with intakes of 50,000 to 1 million IU/d over the course of months or years, the potential risks of kidney stones, vascular disease, and fractures with high-dose vitamin D regimens are unclear. Until more data from RCTs are available, a healthy dose of skepticism should be maintained regarding the other health claims for vitamin D.

REFERENCES

  1. Harbour R, Miller J. A new system for grading recommendations in evidence based guidelines. BMJ. 2001;323(7308):334-336. 
     
  2. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89(11):5387-5391.
     
  3. Trang HM, Cole DE, Rubin LA, Pierratos A, Siu S, Vieth R. Evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than does vitamin D2. Am J Clin Nutr. 1998;68(4):854-858. 
     
  4. Holick MF, Biancuzzo RM, Chen TC, et al. Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. J Clin Endocrinol Metab. 2008;93(3):677-681. 
     
  5. Thacher TD, Obadofin MO, O'Brien KO, Abrams SA. The effect of vitamin D2 and vitamin D3 on intestinal calcium absorption in Nigerian children with rickets. J Clin Endocrinol Metab. 2009;94(9):3314-3321. 
     
  6. Plum LA, DeLuca HF. The functional metabolism and molecular biology of vitamin D action. In: Holick MF, ed. Vitamin D: Physiology, Molecular Biology, and Clinical Applications. 2nd ed. New York, NY: Humana Press; 2010:61-97.
  7. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-281. 
     
  8. Kennel KA, Drake MT, Hurley DL. Vitamin D deficiency in adults: when to test and how to treat. Mayo Clin Proc. 2010;85(8):752-757. 
     
  9. Prentice A, Goldberg GR, Schoenmakers I. Vitamin D across the lifecycle: physiology and biomarkers. Am J Clin Nutr. 2008;88(2):500S-506S.
     
  10. Chapuy MC, Preziosi P, Maamer M, et al. Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int. 1997;7(5):439-443. 
     
  11. Abrams SA, Griffin IJ, Hawthorne KM, Gunn SK, Gundberg CM, Carpenter TO. Relationships among vitamin D levels, parathyroid hormone, and calcium absorption in young adolescents. J Clin Endocrinol Metab. 2005;90(10):5576-5581.
     
  12. Tylavsky FA, Ryder KM, Li R, et al. Preliminary findings: 25(OH)D levels and PTH are indicators of rapid bone accrual in pubertal children. J Am Coll Nutr.2007;26(5):462-470. 
     
  13. Peacock M, Selby PL, Francis RM, Brown WB, Hordon L. Vitamin D deficiency, insufficiency, sufficiency and intoxication: What do they mean? In: Norman AW,Schaefer K, Grigoleit H-G, Herrath DV, eds. Vitamin D: Chemical, Biochemical and Clinical Update. Berlin, Germany: Walter de Gruyter; 1985:569-570.
  14. Thacher TD, Fischer PR, Isichei CO, Pettifor JM. Early response to vitamin D2 in children with calcium deficiency rickets. J Pediatr. 2006;149(6):840-844.
     
  15. Docio S, Riancho JA, Perez A, Olmos JM, Amado JA, Gonzalez-Macias J.Seasonal deficiency of vitamin D in children: a potential target for osteoporosis-preventing strategies? J Bone Miner Res. 1998;13(4):544-548. 
     
  16. Steingrimsdottir L, Gunnarsson O, Indridason OS, Franzson L, Sigurdsson G. Relationship between serum parathyroid hormone levels, vitamin D sufficiency, and calcium intake. JAMA. 2005;294(18):2336-2341. 
     
  17. Thacher TD, Fischer PR, Obadofin MO, Levine MA, Singh RJ, Pettifor JM.Comparison of metabolism of vitamins D(2) and D(3) in children with nutritional rickets. J Bone Miner Res. 2010;25(9):1988-1995. 
     
  18. Heaney RP. Functional indices of vitamin D status and ramifications of vitamin D deficiency. Am J Clin Nutr. 2004;80(6 suppl):1706S-1709S. 
     
  19. Aloia JF, Chen DG, Yeh JK, Chen H. Serum vitamin D metabolites and intestinal calcium absorption efficiency in women. Am J Clin Nutr. 2010;92(4):835-840.
     
  20. Graff M, Thacher TD, Fischer PR, et al. Calcium absorption in Nigerian children with rickets. Am J Clin Nutr. 2004;80(5):1415-1421. 
     
  21. Need AG, O'Loughlin PD, Morris HA, Coates PS, Horowitz M, Nordin BE.Vitamin D metabolites and calcium absorption in severe vitamin D deficiency. J Bone Miner Res. 2008;23(11):1859-1863. 
     
  22. Hollis BW, Wagner CL, Drezner MK, Binkley NC. Circulating vitamin D3 and 25-hydroxyvitamin D in humans: an important tool to define adequate nutritional vitamin D status. J Steroid Biochem Mol Biol. 2007;103(3-5):631-634. 
     
  23. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Am J Clin Nutr. 2003;77(1):204-210. 
     
  24. Aloia JF, Patel M, Dimaano R, et al. Vitamin D intake to attain a desired serum 25-hydroxyvitamin D concentration. Am J Clin Nutr. 2008;87(6):1952-1958.
     
  25. Ahn J, Yu K, Stolzenberg-Solomon R, et al. Genome-wide association study of circulating vitamin D levels. Hum Mol Genet. 2010;19(13):2739-2745.
     
  26. Binkley N, Krueger D, Cowgill CS, et al. Assay variation confounds the diagnosis of hypovitaminosis D: a call for standardization. J Clin Endocrinol Metab.2004;89(7):3152-3157. 
     
  27. Granado-Lorencio F, Mosteiro JS, Herrero-Barbudo C, Navarro ED,Blanco-Navarro I, Perez-Sacristan B. 25-OH-vitamin D assay variation and subject management in clinical practice. Clin Biochem. 2010;43(4-5):531-533. 
     
  28. Singh RJ. Quantitation of 25-OH-vitamin D (25OHD) using liquid tandem mass spectrometry (LC-MS-MS). Methods Mol Biol. 2010;603:509-517. 
     
  29. Thacher TD, Fischer PR, Strand MA, Pettifor JM. Nutritional rickets around the world: causes and future directions. Ann Trop Paediatr. 2006;26(1):1-16. 
     
  30. Weisberg P, Scanlon KS, Li R, Cogswell ME. Nutritional rickets among children in the United States: review of cases reported between 1986 and 2003. Am J Clin Nutr. 2004;80(6 suppl):1697S-1705S. 
     
  31.  Thacher TD, Fischer PR, Pettifor JM, Lawson JO, Manaster BJ, Reading JC.Radiographic scoring method for the assessment of the severity of nutritional rickets. J Trop Pediatr. 2000;46(3):132-139. 
     
  32. Fischer PR, Rahman A, Cimma JP, et al. Nutritional rickets without vitamin D deficiency in Bangladesh. J Trop Pediatr. 1999;45(5):291-293.
     
  33. Thacher TD, Fischer PR, Pettifor JM, et al. A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children. N Engl J Med.1999;341(8):563-568. 
     
  34. DeLucia MC, Mitnick ME, Carpenter TO. Nutritional rickets with normal circulating 25-hydroxyvitamin D: a call for reexamining the role of dietary calcium intake in North American infants. J Clin Endocrinol Metab. 2003;88(8):3539-3545.
     
  35. Bingham CT, Fitzpatrick LA. Noninvasive testing in the diagnosis of osteomalacia. Am J Med. 1993;95(5):519-523. 
     
  36. Priemel M, von Domarus C, Klatte TO, et al. Bone mineralization defects and vitamin D deficiency: histomorphometric analysis of iliac crest bone biopsies and circulating 25-hydroxyvitamin D in 675 patients. J Bone Miner Res.2010;25(2):305-312. 
     
  37. Wagner CL, Greer FR. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics. 2008;122(5):1142-1152.
     
  38. Zamora SA, Rizzoli R, Belli DC, Slosman DO, Bonjour JP. Vitamin D supplementation during infancy is associated with higher bone mineral mass in prepubertal girls. J Clin Endocrinol Metab. 1999;84(12):4541-4544.
     
  39. Cranney A, Horsley T, O'Donnell S, et al. Effectiveness and safety of vitamin D in relation to bone health. Evidence Report/Technology Assessment No 158. Published August 2007. AHRQ Publication No 07-E013. Rockville, MD: Agency for Healthcare Research and Quality.
  40. Bischoff-Ferrari HA, Kiel DP, Dawson-Hughes B, et al. Dietary calcium and serum 25-hydroxyvitamin D status in relation to BMD among U.S. adults. J Bone Miner Res. 2009;24(5):935-942. 
     
  41. Jackson RD, LaCroix AZ, Gass M, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med. 2006;354(7):669-683.
     
  42. Bischoff-Ferrari HA, Willett WC, Wong JB, et al. Prevention of nonvertebral fractures with oral vitamin D and dose dependency: a meta-analysis of randomized controlled trials. Arch Intern Med. 2009;169(6):551-561. 
     
  43. Bischoff-Ferrari HA, Dawson-Hughes B, Staehelin HB, et al. Fall prevention with supplemental and active forms of vitamin D: a meta-analysis of randomised controlled trials. BMJ. 2009;339:b3692. 
     
  44. Sanders KM, Stuart AL, Williamson EJ, et al. Annual high-dose oral vitamin D and falls and fractures in older women: a randomized controlled trial. JAMA.2010;303(18):1815-1822. 
     
  45. Ginde AA, Scragg R, Schwartz RS, Camargo CA Jr.. Prospective study of serum 25-hydroxyvitamin D level, cardiovascular disease mortality, and all-cause mortality in older U.S. adults. J Am Geriatr Soc. 2009;57(9):1595-1603. 
     
  46. Autier P, Gandini S. Vitamin D supplementation and total mortality: a meta-analysis of randomized controlled trials. Arch Intern Med. 2007;167(16):1730-1737.
     
  47. Lawlor DA, Davey Smith G, Kundu D, Bruckdorfer KR, Ebrahim S. Those confounded vitamins: what can we learn from the differences between observational versus randomised trial evidence? Lancet. 2004;363(9422):1724-1727. 
     
  48. Grady D, Rubin SM, Petitti DB, et al. Hormone therapy to prevent disease and prolong life in postmenopausal women. Ann Intern Med. 1992;117(12):1016-1037.
  49. Grodstein F, Manson JE, Stampfer MJ. Postmenopausal hormone use and secondary prevention of coronary events in the nurses' health study: a prospective, observational study. Ann Intern Med. 2001;135(1):1-8. 
  50. Kawas C, Resnick S, Morrison A, et al. A prospective study of estrogen replacement therapy and the risk of developing Alzheimer's disease: the Baltimore Longitudinal Study of Aging. Neurology. 1997;48(6):1517-1521.
  51. Shumaker SA, Legault C, Rapp SR, et al. Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women: the Women's Health Initiative Memory Study: a randomized controlled trial. JAMA.2003;289(20):2651-2662. 
  52. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women's Health Initiative randomized controlled trial. JAMA. 2002;288(3):321-333.
  53. Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008;168(12):1340-1349.
  54. Freedman BI, Wagenknecht LE, Hairston KG, et al. Vitamin D, adiposity, and calcified atherosclerotic plaque in African-Americans. J Clin Endocrinol Metab.2010;95(3):1076-1083. 
  55. Reis JP, von Muhlen D, Miller ER III., Michos ED, Appel LJ. Vitamin D status and cardiometabolic risk factors in the United States adolescent population.Pediatrics. 2009;124(3):e371-e379. 
  56. Martins D, Wolf M, Pan D, et al. Prevalence of cardiovascular risk factors and the serum levels of 25-hydroxyvitamin D in the United States: data from the Third National Health and Nutrition Examination Survey. Arch Intern Med.2007;167(11):1159-1165. 
  57. Zipitis CS, Akobeng AK. Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis. Arch Dis Child.2008;93(6):512-517. 
  58. Pittas AG, Dawson-Hughes B, Li T, et al. Vitamin D and calcium intake in relation to type 2 diabetes in women. Diabetes Care. 2006;29(3):650-656.
  59. Pittas AG, Lau J, Hu FB, Dawson-Hughes B. The role of vitamin D and calcium in type 2 diabetes: a systematic review and meta-analysis. J Clin Endocrinol Metab.2007;92(6):2017-2029. 
  60. Yin L, Grandi N, Raum E, Haug U, Arndt V, Brenner H. Meta-analysis: longitudinal studies of serum vitamin D and colorectal cancer risk. Aliment Pharmacol Ther. 2009;30(2):113-125. 
  61. Jenab M, Bueno-de-Mesquita HB, Ferrari P, et al. Association between pre-diagnostic circulating vitamin D concentration and risk of colorectal cancer in European populations: a nested case-control study. BMJ. 2010;340:b5500.
  62. Pufulete M. Intake of dairy products and risk of colorectal neoplasia. Nutr Res Rev. 2008;21(1):56-67. 
  63. Wactawski-Wende J, Kotchen JM, Anderson GL, et al. Calcium plus vitamin D supplementation and the risk of colorectal cancer. N Engl J Med.2006;354(7):684-696. 
  64. Chen P, Hu P, Xie D, Qin Y, Wang F, Wang H. Meta-analysis of vitamin D, calcium and the prevention of breast cancer. Breast Cancer Res Treat.2010;121(2):469-477. 
  65. Chlebowski RT, Johnson KC, Kooperberg C, et al. Calcium plus vitamin D supplementation and the risk of breast cancer. J Natl Cancer Inst.2008;100(22):1581-1591. 
  66. Gandini S, Boniol M, Haukka J, et al. Meta-analysis of observational studies of serum 25-hydroxyvitamin D levels and colorectal, breast and prostate cancer and colorectal adenoma [published online ahead of print July 21, 2010]. Int J Cancer.doi: 10.1002/ijc.25439.
  67. Stolzenberg-Solomon RZ. Vitamin D and pancreatic cancer. Ann Epidemiol.2009;19(2):89-95. 
  68. Helzlsouer KJ, VDPP Steering Committee. Overview of the cohort consortium vitamin D pooling project of rarer cancers. Am J Epidemiol. 2010;172(1):4-9.
  69. Drake MT, Maurer MJ, Link BK, et al. Vitamin D Insufficiency and Prognosis in Non-Hodgkin's Lymphoma. J Clin Oncol. 2010;28(27):4191-4198.
  70. Krishnan AV, Trump DL, Johnson CS, Feldman D. The role of vitamin D in cancer prevention and treatment. Endocrinol Metab Clin North Am.2010;39(2):401-418. 
  71. Munger KL, Levin LI, Hollis BW, Howard NS, Ascherio A. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA.2006;296(23):2832-2838. 
  72. Ascherio A, Munger KL, Simon KC. Vitamin D and multiple sclerosis. Lancet Neurol. 2010;9(6):599-612. 
  73. Litonjua AA. Childhood asthma may be a consequence of vitamin D deficiency.Curr Opin Allergy Clin Immunol. 2009;9(3):202-207. 
  74. Wjst M, Dold S. Genes, factor X, and allergens: what causes allergic diseases?Allergy. 1999;54(7):757-759. 
  75. Brehm JM, Celedon JC, Soto-Quiros ME, et al. Serum vitamin D levels and markers of severity of childhood asthma in Costa Rica. Am J Respir Crit Care Med.2009;179(9):765-771. 
  76. Camargo CA Jr., Rifas-Shiman SL, Litonjua AA, et al. Maternal intake of vitamin D during pregnancy and risk of recurrent wheeze in children at 3 y of age. Am J Clin Nutr. 2007;85(3):788-795. 
  77. Devereux G, Litonjua AA, Turner SW, et al. Maternal vitamin D intake during pregnancy and early childhood wheezing. Am J Clin Nutr. 2007;85(3):853-859.
  78. Gale CR, Robinson SM, Harvey NC, et al. Maternal vitamin D status during pregnancy and child outcomes. Eur J Clin Nutr. 2008;62(1):68-77. 
  79. Hypponen E, Sovio U, Wjst M, et al. Infant vitamin D supplementation and allergic conditions in adulthood: northern Finland birth cohort 1966. Ann N Y Acad Sci. 2004;1037:84-95. 
  80. Wjst M, Hypponen E. Vitamin D serum levels and allergic rhinitis. Allergy.2007;62(9):1085-1086. 
  81. Liu PT, Stenger S, Li H, et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science. 2006;311(5768):1770-1773.
  82. Nnoaham KE, Clarke A. Low serum vitamin D levels and tuberculosis: a systematic review and meta-analysis. Int J Epidemiol. 2008;37(1):113-119.
  83. Wejse C, Gomes VF, Rabna P, et al. Vitamin D as supplementary treatment for tuberculosis: a double-blind, randomized, placebo-controlled trial. Am J Respir Crit Care Med. 2009;179(9):843-850. 
  84. Ginde AA, Mansbach JM, Camargo CA Jr.. Association between serum 25-hydroxyvitamin D level and upper respiratory tract infection in the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2009;169(4):384-390.
  85. McNally JD, Leis K, Matheson LA, Karuananyake C, Sankaran K,Rosenberg AM. Vitamin D deficiency in young children with severe acute lower respiratory infection. Pediatr Pulmonol. 2009;44(10):981-988. 
  86. McGrath J, Saari K, Hakko H, et al. Vitamin D supplementation during the first year of life and risk of schizophrenia: a Finnish birth cohort study. Schizophr Res.2004;67(2-3):237-245. 
  87. Jorde R, Sneve M, Figenschau Y, Svartberg J, Waterloo K. Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial. J Intern Med. 2008;264(6):599-609. 
  88. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc.2003;78(12):1463-1470. 
  89. Warner AE, Arnspiger SA. Diffuse musculoskeletal pain is not associated with low vitamin D levels or improved by treatment with vitamin D. J Clin Rheumatol.2008;14(1):12-16. 
  90. Arvold DS, Odean MJ, Dornfeld MP, et al. Correlation of symptoms with vitamin D deficiency and symptom response to cholecalciferol treatment: a randomized controlled trial. Endocr Pract. 2009;15(3):203-212. 
  91. Melamed ML, Astor B, Michos ED, Hostetter TH, Powe NR, Muntner P. 25-hydroxyvitamin D levels, race, and the progression of kidney disease. J Am Soc Nephrol. 2009;20(12):2631-2639. 
  92. Manson JE, Buring JE. Brigham and Women's Hospital. Vitamin D and Omega-3 Trial (VITAL). In: ClinicalTrials.gov [Internet]. Bethesda, MD: National Library of Medicine (US). 2010-[cited 2010 Dec 2]. Available fromhttp://clinicaltrials.gov/show/NCT01169259. NLM Identifier: NCT01169259.
  93. Institute of Medicine. Dietary reference intakes for calcium and vitamin D.Washington, DC, November 30, 2010. http://templatelab.com/Dietary-Reference-Intakes-for-Calcium-and-Vitamin-D/. Accessed November 30, 2010

Source: Mayo Clin Proc. 2011 Jan;86(1):50-60. Thacher TD, Clarke BL. Department of Family Medicine, Mayo Clinic, Rochester, MN 55905, USA. thacher.thomas@mayo.edu. http://www.mayoclinicproceedings.com/content/86/1/50.long

Tags:  vitamin D 

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Steelers Linebacker James Harrison Swears by his Hyperbaric Chamber

Posted By Administration, Wednesday, February 2, 2011
Updated: Friday, April 18, 2014

Watch this clip from ESPN featuring Pittsburgh Steelers Linebacker James Harrison and his use of a Portable Hyperbaric Chamber - Vitaeris 320 manufactured by OxyHealth.

 

For more information on the OxyHealth Vitaeris 320 hyperbaric chamber please contact:
Benjamin Galbraith
+1.562.728.3257

 

Tags:  chamber  hyperbaric 

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Cancer Causing Chemicals: Dangerous Exposures Everyday

Posted By Administration, Thursday, January 27, 2011
Updated: Friday, April 18, 2014

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by Nalini Chilkov, LAC, OMD

More than 80,000 chemicals now in use have never been fully assessed for toxic impacts on human health and the environment. Many of these chemicals are linked to increased incidence of cancer. Watch this shocking and disturbing video by expert Linda Greer, the Director of the Health Program at NRDC, the Natural Resources Defense Council, one of the most effective environmental protection groups. She clearly states that there is a lack of government oversight by the, EPA, the U.S. Environmental Protection Agency, the very department that is supposed to be protecting us, but protects corporate interests instead, putting our lives and our children’s health and wellbeing at risk.

The chemical industry should have to demonstrate that a chemical isn’t dangerous before it’s used in everyday products. But the Toxic Substances Control Act (TSCA) has no such requirements.  These regulations have not been updated since 1976.  It’s time to require that all chemicals be tested for safety and grant the EPA the authority to protect the public from toxic chemicals. But chemicals are “innocent until proven guilty”. This means chemicals are in use that have no proven safety record. Watch the video

 

The Breast Cancer Fund has a comprehensive report on the link between environmental toxic chemicals and breast cancer. The President's Cancer Panel released a report in April 2010  detailing the link between cancer and toxic exposures including chemicals used in industry, in the military and in medicine.  The report states that “the link between exposure and cancer is strong” and  ”the risk of cancer increases with more exposure”. Children, the unborn fetus and pregnant women are at greatest risk.

If you wish to be informed about the chemicals in products that you use at home and work, visit the website of the Environmental Working Group. They also have another website devoted to the many unregulated toxic chemicals found in personal care products such as shampoos, lotions, toothpaste and cosmetics.  Another educational site that shows you how to  feed your family safe and healthy food and reduce your chemical exposures at home is Organic Authority.

Dr. Sanjay Gupta, MD, a medical doctor and medical journalist produced a television series "Toxic America" which reveals the most common chemicals that are linked to a multiplicity of health problems, including many cancers that are ubiquitous in our daily lives.  This report brings to light the many chemicals that find their way into the womb and into newborns who are come into life on day one with high levels of toxic chemicals in their tiny and developing bodies and then nurse on toxin laden breast milk increasing their body burden of dangerous chemicals.

Tags:  cancer  toxins 

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The Good Bugs

Posted By Administration, Monday, January 24, 2011
Updated: Friday, April 18, 2014

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by Joel Lopez, MD, CNS

Probiotics, we hear all about them now, on TV, radio and print ads! It’s great, considering that just a few years ago, most people didn’t know what they were.

Probiotics, otherwise known as “good germs”, are part of the normal flora of our intestinal tract. They begin to inhabit our intestinal tract as soon as we’re born (by vaginal delivery, rather than caesarian delivery). They are nourished by eating healthy foods from infancy, starting by drinking mother’s milk (rather than cow’s milk or soy milk). As we age and are exposed to poor diet, antibiotics, chlorinated water, steroids and environmental pollutants (xenoestrogens), their numbers begin to decline. When their numbers decline, pathogenic yeast begin to overgrow (as well as bacteria), causing symptoms in both men and (more obviously in) women (such as vaginal discharge).

Known functions of probiotics include:

  1. The manufacture of B vitamins (such as folic acid, biotin, B3 and B6).
  2. The manufacture of the enzyme “lactase”.
  3. Produce antibacterial substances.
  4. Produce anti-carcinogenic compounds.
  5. Help reduce high cholesterol levels.
  6. Improve the efficiency of the digestive tract.
  7. Help recycle hormones such as estrogen.
  8. Protect against radiation.
  9. Deactivate certain toxins, among many others.

The primary bacteria inhabiting the small intestine is Lactobacillus acidophilus while that of the colon is Bifidobacterium bifidum. It is essential that these organisms be replaced when taking antibiotics of any kind.

In today’s world, it’s a good idea to incorporate probiotics in a wellness program because of the antibiotics that we’re unknowingly exposed to (from food and perhaps, our water supply). There are different brands available. Some need to be refrigerated while others do not. They come in various forms such as powders, liquid, capsules or “pearls”. To find out which brands are better, check out a study done by Consumer Labs. In the study, they found out that claims made by some companies such as number of viable organisms in their product somehow vary from the actual live cells. Factors such as improper storage and handling as well as shelf life affect these numbers. Therefore, it’s always important to do your own research.

Tags:  bugs 

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Depression, Drugs and Interaction Dangers

Posted By Administration, Thursday, January 13, 2011
Updated: Friday, April 18, 2014

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by Ali Meschi, PhD, CNC

Complexity and the roots of depression have always been a major and complex health issue.  Depression contains other health issues such as behavioral, psychological, social, cultural, religious and the spiritual aspects of ones life.  Because of the complexity aspects of depression, it should always be treated with one and the “Whole Person” ideology in mind.

The depression epidemic has gotten worse since the September 11th tragedy and all that followed.  The stress of the tragedy has put a lot of old wounds of mind back in the front seat, dominating the daily activity in every aspect of everyone’s life, not only in the United States, but also throughout the world.

Dr. Jane Mak, a Neuropsychologist and clinical psychologist has stated that many of her past patients including children, have been back for visits to seek resolution to their flared up old wounds.

Today, four out of every six Americans are having difficulty concentrating on their jobs.  Three out of 4 patients take some form of supplements totally unsupervised.  Many take the supplements with or without their physician’s knowledge and sometimes in combination with prescription drug/s, presenting safety issues.

Despite the various aches and pains, irritability, difficulty concentrating, fatigue, digestive problems, anxiety, guilt and much more, Depression is not a disease by medical evidence.  Depression is not more than a “trapped inward feeling”, with no two people experiencing exactly the same symptoms.

Depression may have underlying factors such as Thyroid Disease, Cardiovascular or Endocrine System problems, deficiency and or imbalances of certain nutrients, digestion, food sensitivities, artificial lighting, inactivity, numerous toxic environment chemicals found in the household.  Heavy metal poisoning, adrenal, ovarian or testical problems, immune deregulation, anemia, blood sugar fluctuations, prolonged physical illness and many more symptoms can cause Depression.

True “healing” cannot be achieved by simply “relieving” the pain and symptoms.  Studies have shown that if the cause and effect relationship between depression and functional decline is not understood properly, depression can become a killer disease.

Contrary to today’s only approach of treatment, stopping the pain, we must hear the message (the symptom) and understand the message (the symptom) that the body is trying to tell us.  The message is simple, something is wrong somewhere.  I recommend we stop shooting the messenger (pain) and start being a good listener to our body’s warning signs.  My simple message to you, do not self-treat!

 


I often see patients who have decided to self-prescribe medications or supplements for various problems, depression included. Not only do they mask the real problem, not listening to their body and its symptoms, they run the risk of having dangerous drug interactions.  If you are currently on any medication or supplements, please take the time to read the following Drug/s Interaction Dangers.  It could save your life.

Food(s) / Supplement(s) / Drug(s) Interaction Dangers

Add-on Interactions:

“Add-on” interactions are the most common type and can be the most dangerous, even fatal.  These occur between drugs that have similar effects, either depressant + depressant or stimulant + stimulant.

Depressants include: alcohol, antianxiety agents, tranquilizers, anticonvulsants, antihistamines, certain high blood pressure drugs, muscle relaxants, narcotics and the popular pain reliever propoxyphene (e.g., Darvon).

Stimulants include: antidepressants (MAO inhibitor type drugs and tricyclics family drugs), appetite suppressants, some asthma drugs, caffeine, nasal decongestants, methylphenidate (Ritalin) and pemoline (Cylert).  You should always ask your doctor and/or pharmacist about these types of interactions before you take any medication.

Amine-containing foods + MAO inhibitors:

MAO inhibitors are used in some cases of clinical depression.  This can be a life threatening combination that may result in a dangerous rise in blood pressure, with severe headache, fever, visual disturbances, and confusion, possibly followed by brain hemorrhage/stroke.

Caution: Avoid amine-containing foods, even for several weeks after stopping MAO-inhibitor type antidepressant drugs.

Amine-Containing foods include: avocados, baked potatoes, bananas, bean pods, beer, bologna, caviar, cheese, chicken liver, canned figs, instant soup mixes, meat tenderizers, nuts, pepperoni, pickled herring, raspberries, salami, sauerkraut, summer sausage, sour cream, soy sauce, wines, yogurt, yeast and other aged or fermented foods.

MAOI’s include: isocarboxazid (Marplan), phenelzine (Nardil), tranylcypromine (Parnate)

Tricyclics include: amitriptyline (Elavil, Enddep), desipramine (Norpramin, Pertofrane), imipramine (Janimine, Tofranil), nortriptyline (Aventryl, Pamelor), Doxepin (Adapin).

Both types of antidepressant drugs MAOIs and Tricyclics require close monitoring to determine proper dosage.  The drugs must be taken for at least three weeks before mood improves.  And the side effects associated with these two families (Gambini’s and Kapone’s) can be severe and debilitating.

Trycyclics can induce dry mouth, constipation, weight gain, blurred vision, heart attacks, stroke, high or low blood pressure, heart block, seizure, hallucinations, delusions, confusion, disorientation, in coordination, tingling, abnormal involuntary movements, anxiety, insomnia, nightmares, dizziness, ocular pressure, rashes, bone marrow depression, elevation or lowering of blood sugar, edema, hair loss and more.

MAOI’s can provoke the same side effects plus an increased risk of hypertension and hepatitis.
 

Tags:  depression  side effects 

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Medical Aromatherapy

Posted By Administration, Monday, January 10, 2011
Updated: Friday, April 18, 2014

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by Joel Lopez, MD, CNS

Medical aromatherapy or the use of essential oils for therapeutic purposes, is one of the oldest forms of medicine and cosmetics known to man. According to Egyptian hieroglyphics and Chinese medical manuscripts, physicians and priests were using essential oils thousands of years before Christ to heal the sick. What are essential oils anyway? Essential oils are the subtle, aromatic and volatile liquids extracted from the flowers, seeds, stems, leaves, bark and roots of herbs, shrubs and trees. The extraction process is done primarily through distillation. Some of the oils that have been used since Biblical times include frankincense, myrrh and cinnamon. Modern clinical research has been confirming the medicinal properties of these oils. For instance, frankincense has been found to have superior immune stimulating properties while cinnamon has blood sugar regulating properties.

Are all essential oils equal? Unfortunately, that’s not the case. For example, the majority of the rose oils come from Bulgaria. In order to keep up with demand from the perfume or cosmetic industry, they have to produce large volumes and in the process compromise quality by using solvent extraction instead of steam distillation.

Some of the modern applications of oils include eugenol (from clove), which is used in the dental industry and thymol (from thyme) which is used as an antiseptic. For one of the best sources of essential oils, check out www.cleanbodycare.com.

 

Tags:  aromatherapy 

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Vitamin D and Your Health: Just How Critical is this "Sunshine Vitamin"?

Posted By Administration, Friday, January 7, 2011
Updated: Friday, April 18, 2014

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By John C. Pittman, MD, and Mark N. Mead, MSc

If you’re like millions of Americans who regularly tune into the news, you probably heard about the vitamin D report issued in November 2010 by the Institute of Medicine’s Food & Nutrition Board (FNB), a committee of 14 medical scientists appointed to assess current data of health outcomes associated with these two nutrients. The FNB report concluded that most North Americans get enough of this “sunshine vitamin” through their diets, and moreover that consuming extra vitamin D is unlikely to help protect the public from cancer, heart disease, diabetes, or other chronic diseases.  Among the report’s other conclusions:

• Raise the recommended daily amount of vitamin D to 600 international units (IU), up from the 200 IU level that had been recommended in 1997.  People over age 70 are advised to get 800 IU daily.  Our response:  Most experts agree that it is virtually impossible to significantly raise your vitamin D levels when supplementing at only 600 to 800 IU/day. Michael Holick, MD, PhD, director of the General Clinical Research Center at Boston University Medical Center and author of numerous scientific reports on vitamin D, has recommended that all adults supplement with 2000 IU daily. Holick himself takes 3000 IU per day and has many patients taking at least that much. Robert Heaney, a professor of medicine at Creighton University in Omaha who has long studied vitamin D’s health benefits, says people should consider taking up to 4,000 IUs a day.

• The risk of harm increases at daily vitamin D intake levels greater than 4000 IU. Our response:  This would suggest that a daily intake of 10,000 IU/day would cause toxicity in humans; however, the FNB report provided no evidence to support this position, citing only one poorly conducted study indicating 20,000 IU/day may cause mild elevations in serum calcium but not clinical toxicity.  Several leading vitamin D researchers have proposed that the new upper tolerable limit should be 10,000 IU, based on extensive observations of adults taking this dose or higher.

• Regarding the serum 25-hydroxyvitamin-D level—the primary indicator of vitamin D status—the FNB report deemed that a level of 20 ng/mL is sufficient for all persons.  Our response:  The most widely used benchmark for sufficiency has been 32 ng/mL, and many experts suggest that higher levels may be needed for specific health outcomes.

The FNB report made headlines across the country, and prompted many people to either cut back on their vitamin D dose or stop supplementing altogether.  However, we see several serious limitations in the FNB’s approach and conclusions.  First, the guidelines are based on the minimum amount of vitamin D needed to ensure bone health and do not address the amount that may affect other health outcomes, such as the prevention of cancer and heart disease, or improvement in muscle and joint health.  Ostensibly, the FNB committee believed that evidence was insufficient to determine the role of vitamin D in the prevention of these other chronic diseases and health outcomes.  However, many leading vitamin D authorities throughout the world would take issue with this perspective.

For example, a comprehensive evidence-based review, published in the November-December 2009 Journal of the American Board of Family Medicine, concluded that, “Low vitamin D levels are associated with increased overall and cardiovascular mortality, cancer incidence and mortality, and autoimmune diseases such as multiple sclerosis.”  Even more recently, an international committee of 25 experts from various medical disciplines proposed clinical guidelines for vitamin D intake.  Their focus was on the vitamin D needs of adult patients with or at risk for fractures, falls, cardiovascular or autoimmune diseases, and cancer.  The expert panel reached strong agreement about the need for vitamin D supplementation in these specific groups of patients and the need for assessing their 25(OH)D serum levels “for optimal clinical care.”  A target range of “at least 30 to 40 ng/mL” was recommended—about twice the level proposed by the FNB report.  These recommendations were published in the September 2010 issue of Autoimmunity Reviews.

 

 

 


Against this backdrop, it’s also important to realize that the FNB’s guidelines have nothing to do with the requirements for optimal functioning and overall health.  Physicians who carefully observe what happens with their individual patients are better able to discern the effects of different doses of vitamin D in the context of specific health situations.  For someone with low blood levels of vitamin D, an initially high supplemental dose—on the order of 5000 to 10,000 IU per day—may result in better mood, increased muscle strength, relief of joint aches, and other clinical benefits.  But one size does not fit all; the same dose of vitamin D is not appropriate for everyone.  This is why individual testing and expert supervision are so important when trying to pinpoint the optimal dose for you personally.

The Sunshine Deficiency

Vitamin D has emerged in recent years as a nutrient with astounding potential for promoting human health. The vitamin’s most recognized function is the enhancement of calcium absorption and bone mineral metabolism. In 2007, the Dietary Supplement Education Alliance estimated that appropriate use of calcium with vitamin D by older adults for five years could lead to the elimination of approximately 776,000 hospitalizations and nursing stays linked to hip fractures, resulting in an annual savings of $16.1 billion. In other words, supplements such as calcium and vitamin D serve as a potent form of “biological insurance” that can help keep the human frame intact. As we explain in a moment, however, the benefits of improving your vitamin D status extend far beyond healthy bones.

Vitamin D is classified as a vitamin, but it’s really a hormone your body generates in response to sunlight. Fair-skinned people can generate 20,000 IU of vitamin D through 20-30 minutes of mid-day sun exposure; in contrast, dark-skinned individuals may require at least four times this level of exposure to attain the same output. (Note that these levels far surpass any amount obtainable through diet alone, which helps explain why the US recommended dietary allowance of vitamin D is set at a mere 200-400 IU for people aged 1-70 years.) 

Your body’s production of vitamin D depends on the amount of skin surface exposed and the quality of sunlight.  Direct-overhead sun exposure provides the strongest stimulus for the skin’s synthesis of vitamin D.  In temperate regions, almost all of this “human photosynthesis” occurs in summertime, because the angle of sunlight largely determines the intensity of ultraviolet radiation, hence the rate of vitamin D production.

Given these facts, it comes as no surprise that most cases of vitamin D deficiency are due to a sunlight deficit, not a dietary one. If you were to totally avoid the sun and regularly took two standard multivitamins every day for several years, each containing 400 IU of vitamin D as your sole source of vitamin D, you would eventually become vitamin D deficient. (Remember, most people meet 90% of their vitamin D needs from very casual sun exposure, like the sunlight that strikes your face, arms and hands when stepping outside for a few minutes in the middle of the day.)

These days, due to fears of developing skin cancer, many people get too little sunshine.  This results in a low or suboptimal blood level of 25-hydroxyvitamin D—the sole measure of one’s vitamin D status.  If this level is low—say, below 50 nanomoles per liter (nmol/L) — research indicates that you may be more prone to developing a host of health problems.  The classical disorder linked with vitamin D deficiency is known as osteomalacia, a painful softening of the bones. In children, the deficiency causes the shafts of leg bones to irreversibly bow or bend, resulting in the grotesque disfigurement known as rickets.  Sunbathing or taking cod liver oil (which contains vitamin D) were eventually found to prevent rickets, which is now extremely rare, thanks mainly to the practice of fortifying dairy products with vitamin D.

But lack of vitamin D can also lead to various other health problems, including osteoporosis, osteopenia, heart disease, hypertension, diabetes, osteoarthritis, joint problems, muscle weakness, chronic muscle pain, fibromyalgia, multiple sclerosis, Type 1 diabetes, depression, mental illness and yes, many types of cancer as well. Let’s take a quick look at what science is telling us about the connections between vitamin D and these various disorders.

Osteoporosis and Osteopenia.  When you’re lacking in vitamin D, you’re more prone to developing osteoporosis, osteopenia, and osteomalacia (as mentioned above), and your risk of experiencing a fracture increases.  Achievement of optimal blood vitamin D levels is essential for boosting bone mineral density and maximizing bone strength, which is why elderly people with osteoporosis—particularly those being treated with bisphosphonates—are advised to boost their intake to at a range of 800 to 2000 IU, along with calcium.  Again, however, if your vitamin D status is poor initially, it’s important to supplement at a higher dosage level in order to truly improve the blood levels of 25(OH)D. Daily supplementation at the right level—again, relative to the blood test result—is especially important for older adults because aging is linked with a reduced capacity to synthesize vitamin D in the skin upon sun exposure.

Cardiovascular Disease and High Blood Pressure. Vitamin D deficiency has been linked with a greater risk of cardiovascular disease and high blood pressure. For example, a meta-analysis of 18 studies found that the lower the serum vitamin D level, the higher the risk of high blood pressure, as reported in the 28 December 2010 Journal of Hypertension. In addition, we know that vitamin D can impact several key mechanisms involved in heart disease, such as inhibiting inflammation as well as vascular muscle proliferation and vascular calcification. To date, however, studies evaluating vitamin D supplementation have not consistently shown a benefit, possibly due to suboptimal levels of vitamin D (no studies have yet looked at doses higher than 2000 IU, even in deficient individuals) or a lack of consideration for other factors that impact cardiovascular health.

Cancer. People living in colder climates not only experience more bone thinning with age but also have higher rates of various cancers. These individuals tend to spend more time indoors, so they get less sun exposure. It’s also interesting to note that cancer mortality rates tend to be lowest in the summer, when vitamin D levels are highest. Laboratory studies indicate that high-dose vitamin D may help block the growth of cancers of the breast, colon, rectum, prostate, lung and head/neck region, as well as lymphoma, leukemia and multiple myeloma. Generally, the lower one’s overall sun exposure and vitamin D intake, the greater the risk of developing and dying from cancer. In a five-year clinical trial conducted out of Creighton University in Nebraska, women who regularly took 2000 IU of vitamin D3 showed a 77% reduction in overall cancer rates compared to women taking a placebo pill, as reported in the June 2007 issue of the American Journal of Clinical Nutrition. This 2000 IU level of vitamin D3 has also been shown to reduce PSA levels in men with prostate cancer.  

One other key application concerns cancer treatment. Vitamin D has a synergistic effect against malignant disease when combined with several kinds of anti-cancer drugs, including the taxanes (Taxol and Taxotere), platinum compounds (e.g., cisplatin), dexamethasone, tamoxifen, and mitoxantrone.  Soy isoflavones, too, seem to synergize with vitamin D in combating cancer. Finally, there’s good evidence that vitamin D can be very effective in slowing down the breakdown of bone and lessening bone pain in patients with advanced cancers. 

Obesity and Metabolic Syndrome. Vitamin D is fat-soluble and therefore stored in fatty tissue. This explains why obese people have a greater capacity to store the vitamin; however, obese people have been shown to produce about half the vitamin D produced by people of a normal weight when exposed to the same amount of sunshine.   Moreover, the vitamin D in those who are lean is more available for the body's metabolic needs than in those who are obese. In a 2007 report for Clinical Nutrition, about half of all morbidly obese individuals were found to be vitamin D deficient. Those with the lowest levels of vitamin D had the greatest risk for the so-called metabolic syndrome. (The latter condition includes the presence or more of the following factors: excess abdominal fat, elevated triglyceride levels, low HDL cholesterol, elevated blood pressure, and elevated fasting glucose and insulin levels.)

Autoimmune Diseases. Lack of vitamin D has been linked with multiple sclerosis, rheumatoid arthritis, type I diabetes, lupus, and Crohn’s disease.  For example, babies deficient in vitamin D may have a greatly increased risk of developing type I diabetes by age 30 compared to those who are not deficient. Animal studies suggest that a vitamin D supplement will greatly impede the development of type I diabetes in susceptible individuals. A 2009 report in Arthritis Research & Therapy concluded that vitamin D deficiency is highly prevalent in patients with lupus and rheumatoid arthritis.  However, whether supplementation can help patients with these disorders remains to be proven.

Colds and Flus. Sharply reduced levels of vitamin D, due to the low intensity of solar UV radiation, may have some connection to the increased occurrence of colds and the flu in winter. Scientists have found that people with low vitamin D levels are less capable of fighting off infections, and that supplementing with vitamin D boosts resistance to colds and the flu. In a randomized controlled trial conducted in Japan, researchers gave 1,200 IU/day of vitamin D3 for six months to Japanese 10 year-olds and compared them to children receiving a placebo. As reported in the May 2010 American Journal of Clinical Nutrition, there was a 42% reduction in the incidence of influenza A, along with an 83% reduction in asthma attacks in the vitamin D group compared to the placebo group.  Had those researchers followed the new FNB recommendations and used 400 IU instead of 1,200 IU, it is unlikely that the children would have experienced any benefit at all.

The problems just mentioned are only the tip of the proverbial iceberg.  Low levels of vitamin D also have been linked with mood disorders (e.g., depression), mental illness, autism, muscle weakness, periodontal disease, unexplained bone and muscle pain, infertility, preeclampsia, cystic fibrosis, psoriasis, and age-related cognitive decline.  In some cases, clinical benefits have been seen following vitamin D supplementation—for example, reductions in depressive moods in adults, and improvements in muscle strength and function in children with autism. 

How Much Is Needed?

These days, most of us just don’t get out in the sun as much as our ancestors did. We spend far more time indoors, and yet the sunshine that comes through glass windows will not stimulate vitamin D synthesis. Even if we did get outdoors on a regular basis, we’d then have to reckon with problems associated with getting too much sun—problems such as sunburn, premature aging of the skin, and a heightened risk of skin cancer, especially in fair-skinned people. Older individuals and obese people have more difficulty synthesizing vitamin D, so they would need to be out in the sun longer, thus further increasing the skin cancer risk.

Aside from sunshine, we can get additional vitamin D from foods like fatty fish and fortified milk.  Unfortunately, most fortified dairy products contain synthetic vitamin D, which confers fewer biological benefits than vitamin D3. Moreover, relying on fatty fish may not be a suitable way to get your vitamin D, because you’d have to eat a large amount of fish every day. For many people, vitamin D-rich cod liver oil is a great source, one that has been used in northern regions for well over a century.

This brings us back to vitamin D supplements. Vitamin D in its natural form is called vitamin D3 or cholecalciferol. This form of vitamin D generally has more drawn-out effects and need not be taken daily; in contrast, synthetic forms such as calcitriol need to be taken daily for optimal effectiveness.  Also whereas vitamin D is relatively cheap, calcitriol can be quite expensive – and your insurance company may or may not provide coverage. 

So how much do we really need?  Many of the leading vitamin D authorities say that, if you rarely if ever get any mid-day summertime sun exposure, most adults can benefit by supplementing in the range of  2,000 and 5,000 IU per day.  A recent clinical trial by Dr. Reinhold Vieth confirmed that the 5000 IU amount was safe even for elderly people. For people who do get exposed to 15 or 20 minutes of mid-day sunshine in the spring, summer and fall, the recommended amount is about 2,000 IU per day.  You can also take your week’s worth of vitamin D (say 15,000 to 20,000 IU) all on the same day, once a week.  This makes it much easier to take the vitamin, but there are those individuals who may still have problems absorbing this much Vitamin D at one time, in which case daily dosing is still better. 

The only caveat of taking higher doses of vitamin D is that some individuals may be prone to a condition known as hypercalcemia (excessive calcium in the blood). Symptoms of hypercalcemia include weakness, fatigue, somnolence, headache, anorexia, dry mouth, metallic taste, nausea, vomiting, cramps, diarrhea, muscle pain, bone pain and irritability. If you have cancer and certain other conditions, your physician should monitor you for hypercalcemia in order to safeguard against this problem. If you do happen to become hypercalcemic, your physician will have you discontinue the vitamin D and then check your blood calcium level daily until it has normalized, and then twice weekly on a lower dose of vitamin D.

John Cannell, MD, founding director of the Vitamin D Council, notes that thousands of individuals reading the Council’s newsletter routinely have taken 5,000 IU/day for up to eight years. “Not only have they reported no significant side effects, indeed, they have reported greatly improved health in multiple organ systems,” Dr. Cannell states. “My advice: especially for pregnant women, continue taking 5,000 IU/day until your 25(OH)D is between 50 ng/ml and 80 ng/ml—the vitamin D blood levels obtained by humans who live and work in the sun and the mid-point of the current reference ranges at all American laboratories.” The FNB recommendations are a major disappointment to Cannell and many other proponents of higher vitamin D intake. Given the low cost of vitamin D, as well as the large body of evidence for safety and benefit at intakes well above these recommendations, why not take a chance of achieving those benefits?

John C. Pittman, MD, is the Medical Director of the Carolina Center for Integrative Medicine in Raleigh, NC, and is certified by the American Board of Clinical Metal Toxicology.  Mark N. Mead, MSc, serves as the Center’s Nutrition Educator and Integrative Medicine Research Consultant.

For more information, please visit thier website:  www.carolinacenter.com

 

Tags:  vitamin D 

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Recovery from Autism: The Power and Promise of Integrative Medicine

Posted By Administration, Monday, January 3, 2011
Updated: Friday, April 18, 2014

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by John C. Pittman, MD, and Mark N. Mead, MSc

Are mercury, lead, and other toxic metals likely culprits in classic autism, ADHD, Asperger Syndrome, and other Autism Spectrum Disorders (ASDs)?  Can yeast overgrowth and intestinal imbalances have a substantial impact on many ASDs?  Do kids with ASDs often suffer from an inability to detoxify toxic compounds?  Can these children benefit from therapies aimed at removing these toxic factors and correcting the underlying biological problems?

The answer to all these questions, based on our clinical experiences and training at the Autism Research Institute, is a resounding yes. But if this is the case, why is there so much disagreement among pediatricians and public health scientists?  The reason: Much of the population-based research to date has focused on the more superficial aspects of ASDs, and in doing so has helped engender the misunderstanding that such toxic factors as mercury and fungal toxins are of little relevance to the child with autism.

Of Detox Defects and Vulnerable Brains

A recent study, published in a 2010 issue of Acta Neurobiologiae Experimentalis, found that individuals diagnosed with ASD had blood mercury levels that were approximately double those observed in non-ASD individuals.  However, closer examination of the data revealed a threshold blood mercury level below which no autism was seen.  Specifically, the total blood mercury level did not increase the odds of having autism until it was greater than 26 nmol/L (>5.2 μg/L). Individuals with a blood level higher than 26 nmol/L were three times more likely to be diagnosed with autism than individuals whose blood level was lower than 26 nmol/L.

These findings, which come from the Institute of Chronic Illnesses, Inc., in Silver Spring, Maryland, are consistent with multiple studies showing increased levels of mercury in the teeth and brains of children diagnosed with an ASD relative to non-ASD kids.  Several studies also found increased mercury in the urine and fecal samples following chelation therapy, as well as associated urinary porphyrins among ASD individuals relative to the control groups.  Moreover, a 2009 report in the Journal of Toxicology demonstrated a strong relationship between the severity of autism and the relative body burden of toxic metals.

 


 

Now, some scientists may reasonably argue that blood mercury levels are not consistently linked with ASDs, and they would be correct.  However, blood mercury levels do not reflect chronic exposures or tissue levels—only acute exposures, for example, from industrial accidents, eating mercury-laden fish, or off-gassing from dental amalgams. The metals that accumulate from pre- and post-natal exposure are not reliably detected by a blood test, only by a combination of urinary porphyrins and urinary mercury following administration of metal-binding agents. Doctors who have studied heavy metal toxicology understand this.

Also seemingly paradoxical is the finding of lower hair levels of mercury in very young children with ASDs. This suggests that ASD kids are unable to excrete the mercury that has accumulated in their bodies. Indeed, we find that virtually all children with autism show measurable defects in their detoxifying capacity. These defects render the children unable to eliminate or neutralize many brain-toxic factors such as lead, mercury, and pesticides—and more prone to the brain-injuring effects of inflammation and oxidative stress. Many of these kids also have immune system imbalances that keep ther brains inflammed as well as rendering them even more susceptible to harmful bacteria and other microbes and their toxins.

The implications of this complex profile of susceptibility are profound. These children are like the proverbial “canaries in the coal mine”—far more vulnerable to the pollutants that other children’s bodies handle with ease. If you’re not taking into account the detoxification and immunologic problems commonly found in autistic children, then population-based comparisons of exposure levels have less relevance.

Deficiencies in key nutrients and metabolites that support detoxification pathways also are extremely common among children with ASDs.  For example, many of these kids show low glutathione or its metabolites in their blood and urine. Since glutathione is the core detoxifying molecule in our cells, this deficiency greatly limits the child’s ability to process and eliminate mercury and other toxicants from the blood.  Those children who are genetically less capable of detoxification, or whose detox mechanisms are overwhelmed with other toxins, are far more prone to toxic overload—and thus to the neurologic and behavioral problems linked with ASDs.

Developmental Delay or True Treatment Effect?

Another common criticism you will hear of doctors who are using this innovative approach is that autism is a condition of developmental delay, and that at least some of these children—possibly 5 to 19 percent—will go on to develop and function fairly well. Without conducting randomized controlled trials, these critics say, you never can know whether the development and improvement of symptoms would have occurred anyway with time, or whether the improvement could simply be attributed to behavioral and occupational therapy.

Going further, the critics contend that the single-person level of observation can be very deceiving, and that you can easily be fooled into believing that what you are observing is a real benefit versus something that might have happened by chance.

Here’s the main problem with this view, and perhaps the most profound myth-busting truth of all. You cannot be fooled by what you’re seeing when improvements occur on the integrative treatment program, and then those same improvements vanish if the child goes off the program.  If your child quickly gets worse every time they go off their program, and then improves again every time they go back on, this is clearly due to the treatment.  This is what separates clinical trials from case-by-case observations in the clinical setting, and it is incredibly important in the context of ASDs, since every case is so different and requires a high degree of individual tailoring based on testing results.

Let’s take the example of intestinal candidiasis, or yeast overgrowth.  When children with ASDs are treated for an obvious yeast overgrowth, at some point they begin to show a dramatic improvement in their behavior—showing great eye contact, communicating well or even animatedly, becoming more peaceful and attentive. When they go off the anti-yeast treatment, their behavior can spin wildly out of control again.

Another example:  Many children are sensitive to gluten. Take them off gluten-containing foods for three weeks, then reintroduce those foods and watch what happens.  Very often there will be some improvement in behavior during the time off gluten, but if the child has an underlying intestinal infection or yeast overgrowth situation, that must be resolved first.

Our approach at the Carolina Center for Integrative Medicine addresses the problems that are common to virtually all children with ASDs, including detoxification weaknesses, toxic overload, nutritional deficiencies, and intestinal imbalances such as yeast overgrowth. Various nutrient deficiencies have been documented in children with ASDs, and targeted nutritional strategies are often very helpful and again make other strategies more effective. In addition, we help identify certain “trigger” foods, such as casein-containing dairy products, wheat and other gluten sources, sugar, chocolate, preservatives, and food colorings.

As implied in the mention of gluten and yeast (see above), proper sequencing of the treatments is part of the art of medicine when it comes to helping kids with ASDs. For example, the full benefits from heavy metal detoxification and hyperbaric therapy (pressurized oxygen) are only likely to occur when the GI tract problems are addressed first. Children undergoing this integrative approach may show rapid improvement in language and social skills, as well as better sleep, moods, and overall disposition.

The medical-scientific community is beginning to wake up to the power of this perspective. In November 2009, the American Academy of Pediatrics, Autism Speaks, and the North America Society for Pediatric Gastroenterology, Hepatology and Nutrition, hosted a symposium of researchers and physicians to address GI problems seen in children with ASDs. The symposium was intended to raise awareness among specialists about GI disorders in autism and to educate doctors about new treatment strategies for ASDs.

Overcoming Autism:  A Success Story

When it comes to harnessing the power of this integrative approach, one of the keys to therapeutic success is catching ASDs at an early age, when there is still sufficient neuro-plasticity or brain plasticity.  The term plasticity refers to the central nervous system’s ability to change neurons and neuronal pathways, and ultimately to re-organize entire neural networks.  A good example of this early-life therapeutic advantage is the story Mike Simpson, now age 5, who was diagnosed in November 2006 with autism.  At the time of his diagnosis, several physicians had told Mike’s parents, John and Suki Simpson, that no treatment options existed and that recovery was impossible.

Mike’s pediatrician referred the parents to the state’s behavioral intervention program.  Although they found the program somewhat helpful, it clearly was only a start, and his behavior remained that of a child with classic autistic disorder.  “At the time, Mike did not respond to his own name,” Suki Simpson recalls.  “He was unable to sit in a chair or by a table, and he could not focus on any activity for any extended period of time.”  Due to these limitations, it seemed unlikely that he could reasonably benefit from the behavioral program.

In his first year of life, Mike appeared to be deaf because he would not respond to his name, nor did he react to loud noises, such as the doorbell ringing or a car horn honking.  Testing revealed that his hearing was fine.  In fact, as the parents later learned, Mike was quite sensitive to sound—but was not responding because he was tuning the sound out due to the pain it caused.  This phenomenon is fairly typical among children with autism.

One glance at Mike’s diet at the time might have provided some insight into his behavioral issues.  From the moment he began eating solid foods, according to the Simpson parents, he seemed to constantly crave carbohydrate items such as crackers, pizza, chicken nuggets and Cheerios.  His diet as a whole was quite limited, and he invariably shunned new foods.  The parents began to wonder whether his diet might have something to do with the abnormal behaviors he was exhibiting.

“We began to speculate about how nutrition could be impacting Mike’s body and mind,” says John Simpson. “Perhaps his limited diet was giving him headaches, or perhaps he lacked the nutrition needed for normal brain function.  Perhaps he was unable to sleep because his stomach was upset, or he was not eating well because the food did not taste good to him.  These kinds of questions prompted us to begin looking into alternative approaches to autism.”  As the parents looked further, they came to believe that a “leaky gut” and possibly other digestive problems, along with poor nutrition, could be fueling Mike’s abnormal behaviors.

When Mike turned age two in the spring of 2007, the parents placed him on a gluten-free, casein-free (GFCF) diet—a diet free of cow’s milk, wheat and most other grain products.  “Immediately, we saw several of his behaviors improve,” Suki Simpson says.  “Soon afterward, we added digestive enzymes as supplements to his diet six months later.  This led to small but continual improvements in his focus and communication, including his very first ‘Mama.’  That was immensely exciting.  We realized then that there had to be an underlying biological reason for his behavioral symptoms.”

In December 2007, after an Internet search of physicians listed in the Defeat Autism Now! (DAN!) directory, the parents sought my expertise and scheduled an office visit with me at the Raleigh-based Carolina Center for Integrative Medicine.  (Much of the Carolina Center’s approach to autism is adapted from the DAN! program. To help decide which supplements and which parts of the program to emphasize, we recommend individualized, in-depth clinical and laboratory testing.)

After an extensive evaluation that included laboratory testing to look for signs or markers of hidden infection, I determined that Mike had an overgrowth of Candida yeast and bacteria in his intestines.  The first treatment priority was to reduce the yeast levels in order to improve his digestive function health.  In addition to pharmaceutical and herbal anti-fungals, Mike received specific supplements aimed at killing disease-causing organisms, as well as replacing those microbes with beneficial bacteria. 

Our second effort was targeted towards vitamins and other nutrients his body lacked, and were intended to help him feel and function normally.  At the same time, the parents also elected to have him start hyperbaric therapy, involving the use of pressurized oxygen to activate neurons in his brain.  Children undergoing hyperbaric therapy often show rapid progression in language skills and the expansion of their vocabulary, as well as a range of behavioral improvements.  Later in his treatment, Mike received an antiviral medication called Valtrex, which is thought to work as a brain anti-inflammatory agent.  Recent research, all published in peer-review medical journals, has highlighted the benefits of this integrative medical approach.  For some excellent summaries of this research, see the August and December 2002 issues of Alternative Medicine Review, as well as the February 2008 Journal of Alternative & Complementary Medicine.

The multi-pronged treatment—including anti-microbial therapy, physiological rehabilitation, and nutritional and behavioral interventions—led to rapid and dramatic improvements.  Within four months, Mike not only knew his own name and made good eye contact, he also began speaking the name of everyone with whom he was coming into contact on a daily basis.  He could speak in full sentences and quickly developed a huge vocabulary.  He could count to 40, and his ability to recite the alphabet, identify letters, and put letters together was that of a first grader.  To his parents’ delight, Mike became very sociable, talkative and interactive, singing songs and playing games like tag and Hide-and-Seek.  He made friends easily at school, and it was very clear to his teachers that he had a keen ability to learn. 

“If we had not seen it happen before our own eyes, we would not have believed it to be possible,” says Suki Simpson.  “Recovery from autism is possible.  In the beginning, teaching Mike was like driving down a dead end street. Today, we are cruising along a highway with interaction in both directions.”  Suki adds that Mike has been thriving both socially and intellectually in a mainstream classroom at their local elementary school.  “He has lots of friends,” she says.  “And he talks with them and us all the time.  We couldn’t be happier with his complete turnaround, and for that, we give credit to the Carolina Center’s approach.”

In short, there is now light at the end of the tunnel.  At this writing, we have seen hundreds of children with ASDs go from having all types of aberrant behaviors to becoming playful, sociable, and communicative.  Many of them have gone from extreme isolation to being mainstreamed in a normal school, performing just as well as their peers, sometimes even ending up at the top of their class. Yes, behavioral interventions such as speech therapy, occupational therapy, and Applied Behavior Analysis still have an integral role to play, but very often the results they achieve are limited.  By addressing the underlying biological issues, autism and other ASDs can be greatly improved. And in some cases, as we saw with young Mike Simpson, autism and ASD symptoms may disappear altogether.

John C. Pittman, MD, is the Medical Director of the Carolina Center for Integrative Medicine in Raleigh, NC, and is certified by the American Board of Clinical Metal Toxicology.  Mark N. Mead, MSc, serves as the Center’s Nutrition Educator and Integrative Medicine Research Consultant.

For more information, please visit our website:  www.carolinacenter.com

Key scientific references:

Rossignol DA.  Novel and emerging treatments for autism spectrum disorders: a systematic review.  Ann Clin Psychiatry. 2009;21(4):213-36.

Bradstreet JJ, Smith S, Baral M, Rossignol DA.  Biomarker-guided interventions of clinically relevant conditions associated with autism spectrum disorders and attention deficit hyperactivity disorder.  Altern Med Rev. 2010;15(1):15-32.

Landrigan PJ.  What causes autism? Exploring the environmental contribution. Curr Opin Pediatr. 2010; 22(2):219-25.

Adams JB, Baral M, Geis E, Mitchell J, et al.  The severity of autism is associated with toxic metal body burden and red blood cell glutathione levels.  J Toxicol. 2009;2009:532640.

Adams JB, Baral M, Geis E, Mitchell J, et al.  Safety and efficacy of oral DMSA therapy for children with autism spectrum disorders: Part A--medical results. BMC Clin Pharmacol. 2009;9:16.

O'Hara NH, Szakacs GM.  The recovery of a child with autism spectrum disorder through biomedical interventions.  Altern Ther Health Med. 2008;14(6):42-4.

Kidd PM. An approach to the nutritional management of autism.
Altern Ther Health Med. 2003;9(5):22-31

Kidd PM.  Autism, an extreme challenge to integrative medicine. Part 2: medical management.  Altern Med Rev. 2002;7(6):472-99.

Kidd PM.  Autism, an extreme challenge to integrative medicine. Part: 1: The knowledge base.  Altern Med Rev. 2002;7(4):292-316.

Tags:  autism  integrative medicine 

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How Carbohydrates Elevate Cholesterol

Posted By Administration, Wednesday, December 29, 2010
Updated: Friday, April 18, 2014

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by Zina Kroner, DO

Yes, carbs can indeed elevate cholesterol.  This sentence is not a typo.  
 
The Scenario
 
Assume that you have an unfavorable cholesterol profile (low HDL, high triglycerides and low LDL).  The typical scenario is as follows: You have high cholesterol, you pursue a million dollar workup with your cardiologist, including a stress test, EKG, blood work, etc, and the ultimate recommendation is to follow the Dean Ornish Diet.  This diet was based on a five year intervention study called the Lifestyle Heart Trial which followed 48 men with heart disease and told them to exercise, manage stress, stop smoking, get psychological help, and go on a high fiber, low fat and low calorie diet.  Of the 48 men, 20 actually completed the study, where all the recommendations were adhered to.  
 
The results showed that there was actually some reversal of heart disease!  The bottom line that was extracted from this study was that a low fat diet helps to reverse heart disease.  Seldom were the other factors addressed.  Since then, most patients have been advised by their cardiologists and internists to stay on a diet of this nature.  
 
Thereafter, many have tried to comply with the low fat diet and noticed that cholesterol was not dropping.  Hmmm…  Let’s look at the science to figure this out.
 
I am going to break this one down to the nitty gritty details, so beware.  
 
How Carbs Actually Elevate Cholesterol
 
You are eating your whole grain toast or dairy item in the morning with fruits, pasta for lunch and a rice dish with a protein for dinner.  Your desserts are always fresh or dried fruits.  You are drinking juices with your meals.  Once the digestive juices are appropriately secreted and the food is churned, the necessary nutrients are absorbed through the intestinal walls.  Glucose (derived from carbs), amino acids (derived from proteins), and fatty acids ( derived from fats) are passed through a corridor (the portal vein) and enter the liver.  
 
The pancreas is paying very close attention to the molecules passing through this corridor into the liver.  
It gets quite excited when it sees glucose and quickly shows its affection by secreting insulin. Insulin does several things:


 
It stimulates the production of cholesterol. Many of you have heard of statin drugs. They work by inhibiting an enzyme called HMGcoA reductase. Insulin stimulates this enzyme!  How can it be possible for your cholesterol to go down if the foods that you are eating stimulate the very enzyme that cholesterol reducing drugs are trying to decrease?
 
Insulin slows down an amino acid called carnitine.  Carnitine is important because it functions to shepherd the fatty acids into the part of the cell where they will be converted into usable energy. Insulin can therefore harbor weight gain by not allowing the fatty acids to be converted into energy effectively, via the mechanism of carnitine.
 
Insulin causes cells in the liver, muscles and fat to take up glucose. In the liver, the glucose is stored as glycogen.  Here is the interesting part… There is not that much glycogen in the liver, so whatever sugar the liver is unable to hold is spilled over to another processing system. The glucose is packaged neatly into triglycerides. Yes, the ones associated directly with cardiovascular disease. This was the bottom line, ladies and gents. VLDL (very low density lipoprotein ) is then stimulated by the liver and LDL, the bad cholesterol) is made. Whew!
 
When there is not much glucose in he body, as in the case in a lower-carb diet, there is no signal to release the insulin. Insulin is absent (or low), glucose is not taken up by the cells and triglycerides are not manufactured from the spillover of glucose. Therefore, the above process is not as robust. With low insulin levels, the body begins to use fat as an energy source since it does not have the glucose. Using fat as an energy source is one of the mechanisms of weight loss.  Let’s pause for the  “ahaa” moment.  
 
So there it is, eat low carb and see the weight come off and cholesterol decrease.  A common mistake is that patients eat BOTH low and high carb simultaneously. They also focus on meats that are not lean. They come into my office telling me about all the healthy proteins they have been eating. Only problem is that they are having tons of rice or pasta along with a small amount of fatty protein. Taking the above mechanism of action into consideration, this is truly counterintuitive,.  
 
Please reread the mechanism several times. Once you understand it, you will be able to intelligently change your diet.  Being informed is crucial. 

Tags:  cholesterol  food and drink 

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Controversy Over Fish Oil's Cardioprotective Effects

Posted By Administration, Thursday, December 23, 2010
Updated: Friday, April 18, 2014

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by Ronald L. Hoffman, MD, CNS

Although diets rich in marine lipids and fish-oil supplements have staked a claim to heart disease prevention, controversy remains. A recent study examining the role of omega-3-enriched margarine as a functional food for secondary prevention of heart attacks yielded negative results;1 publication of the study spawned skeptical and even derisive headlines in the popular press: Omega-3 Fats Offer No Protection Against Heart Disease—Study and Low Doses of Omega-3s Don't Help with Heart Disease: Say it Ain't So, Fish Oil!.

Are the results of this study (perhaps somewhat prematurely titled "The Alpha Omega Trial") definitive? How do clinicians reconcile these negative findings with the vast body of references that support the cardiovascular benefits of fish consumption and omega-3 supplementation? And most important, what are the implications for consumers and for potential advocacy by health-care professionals?

The current regulatory climate for fish-oil claims underscores this uncertainty. Lovaza (omega-3-acid ethyl esters), the only FDA-approved fish-oil supplement, is indicated only for its pharmacologic effect of lowering elevated triglycerides. FDA labeling specifically qualifies that "The effect of Lovaza on cardiovascular mortality and morbidity in patients with elevated triglyceride levels has not been determined."2

No comparable approval, either explicit or tacit, exists in the United States for the application of fish-oil supplements to primary or secondary prevention of cardiovascular disease (CVD). But a considerable proportion of the population consumes these supplements, and a high percentage of health-care providers embrace such recommendations—if not for their patients, then for themselves and their families.

While the exact proportions are not known, a recent investigation showed that 62% of U.S. doctors surveyed agreed that one of their roles as a health-care professional is to provide information to patients about appropriate dietary supplements.The most popular supplements among cardiologists were multivitamins, omega-3s/fish oil, and vitamin C.

Even regulatory language governing claims for cardioprotection via consumption of omega-3-rich foods remains highly circumscribed. In September 2004, the FDA announced permission for "qualified health claims on omega-3 fatty acids" to the effect that, "Supportive but not conclusive research shows that consumption of eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA] omega-3 fatty acids may reduce the risk of coronary heart disease."4

 


Compounding the controversy are international discrepancies vis a vis the prescription of fish-oil supplements. A front-page article in The New York Times pointed out that while 57% of family clinicians in Washington State acknowledged fish oil's potential benefits in preventing a second heart attack, only 17% identified themselves as frequent prescribers of fish oil.5 

The situation in the United States stood in contrast with that in Europe where, according to Dr. Massimo Santini, chief of cardiology at Rome's San Filippo Neri hospital, a doctor's failure to prescribe fish oil to a heart patient "would be considered tantamount to malpractice."5

The article concluded that in the United States, "community doctors do not learn how to use [fish oil]," while insurers will not pay for cardiovascular prevention via fish-oil supplementation because it is not specifically approved by the FDA for that indication.5

In its scientific statement on fish consumption, fish oil, omega-3 fatty acids, and CVD, the American Heart Association (AHA) acknowledges that: "[Randomized controlled trials] have demonstrated that omega-3 fatty acid supplements can reduce cardiac events (e.g., death, nonfatal MI, nonfatal stroke) and decrease progression of atherosclerosis in coronary patients. However, additional studies are needed to confirm and further define the health benefits of omega-3 fatty acid supplements for both primary and secondary prevention."6

After some equivocation to the effect that dietary approaches to omega-3 supplementation are preferable, the AHA allows that certain individuals, whose dietary preferences preclude adequate intake from natural sources, "in consultation with their physician, could consider supplements for coronary heart disease [CHD] risk reduction."6

What lines of evidence support fish-oil supplementation for cardiovascular prevention? Early impetus came from epidemiologic studies. As early as 1944, Sinclair noted the decreased prevalence of CVD in Arctic Eskimos who subsisted largely on omega-3-rich fish and aquatic mammals.7 In the 1970s, Danish researchers noted improved cardiovascular profiles and lower MI mortality among Greenland Eskimos consuming a low-carbohydrate, fat-rich diet when compared with subjects consuming a Western diet on the Danish mainland.8

Three large randomized trials have documented the effects of omega-3 polyunsaturated fatty acid (PUFA) in primary and especially in secondary prevention of CHD.9 More than twenty years ago, the Diet and Reinfarction Trial demonstrated a 29% reduction in mortality—almost entirely attributable to decreased cardiovascular death—in subjects consuming high amounts of omega-3 from fish sources or supplements.10The reduction in cardiovascular events was particularly impressive in individuals consuming fish-oil capsules.

A subsequent prevention trial corroborated the benefits of fish-oil supplementation for secondary prevention in MI survivors, namely with one Lovaza capsule per day delivering 
850 mg of EPA/DHA in a 1.2:1 ratio. Researchers demonstrated a 21% and a 30% reduction, respectively, in total death and cardiovascular death over the one-year duration of the study.11 These results were driven by an impressive 46% reduction in sudden cardiac death. Reductions in major clinical events continued to be demonstrated at 3.5-year follow-up.12

Additional evidence for the protective effects of omega-3 supplementation comes from the Japan EPA Lipid Intervention Study, published in 2007. In a mixed trial of primary and secondary prevention, 18,645 patients with hypercholesterolemia (70% women) were randomized to statin alone or statin and highly purified EPA 1,800 mg/day. At the end of the five-year study, those randomized to statin plus EPA had a 19% reduction in major cardiovascular events.13

How do clinicians reconcile these results with those of the Alpha Omega Trial, which demonstrated no secondary prevention benefits of supplementation with an omega-3-enriched margarine spread?

Researchers leading the Alpha Omega Trial assigned 4,837 MI survivors to one of four experimental groups. For 40 months, participants consumed either (1) placebo margarine, (2) margarine with a combined total of 400 mg of EPA/DHA, (3) margarine with 2 g of alpha-linolenic acid (ALA), a plant-derived precursor to EPA/DHA, or (4) a margarine containing a combination of EPA/DHA and ALA. State-of-the-art antihypertensive, antithrombotic, and lipid-modifying therapy was implemented in all four groups.

The results showed that neither the EPA/DHA nor the ALA (nor a combination of both) proved more beneficial than placebo. Does this constitute a repudiation of the omega-3 CVD prevention hypothesis?

Critics of the Alpha Omega Trial were quick to point out specific objections to its methodology. First, aggressive pharmacologic management may have masked some of the advantages conferred by fish oil. Additionally, it was thought that the results did not disqualify a putative benefit of omega-3-enriched margarines in primary prevention.

Some have claimed that the choice of a margarine-like spread as a delivery system might have compromised the efficacy of the active omega-3 component. The caloric load provided by daily consumption of 18.8 g of omega-6-rich vehicle and the attendant consumption of multiple slices of high glycemic index bread on which the margarine-like substance was spread, might have acted as confounders.

But most important, the low-dose of EPA/DHA (400 mg) employed in the trial is well below the threshold noted in some studies to influence cardiovascular outcome. The study might best be viewed as merely contravening the hoped-for cardio-protective role of a specific functional food—with inherent limitations to palatability attributable to fish oil's inability to being disguised in neutral vehicles. Therefore, it would be an overstatement to claim, as some have, that the Alpha Omega Trial is the death knell for omega-3 supplementation in CVD.

How then are omega-3 PUFAs thought to influence CVD progression and reduce mortality? Several pathways have been investigated.

Hypolipidemic. It is well established that omega-3s reduce lipid levels, and this is the basis for the approved indication for use of Lovaza in hypertriglyceridemia. It is generally acknowledged that doses >3-4 g/day are required. The mechanism of omega-3's triglyceride reduction relates to its favorable effects on reducing hepatic production and secretion of very-low-density lipoprotein (VLDL) and VLDL apo B particles, its favorable effects on plasma lipolytic activity through lipoprotein lipase-mediated clearance, and its ability to stimulate beta-oxidation of other fatty acids in the liver.14

Generally, omega-3s produce no significant improvements in LDL, except in patients with elevated triglycerides, in whom modest improvements in LDL and HDL are sometimes seen. Even when absolute LDL levels are not significantly impacted by fish-oil supplementation (or even when they increase, as has occasionally been reported), there is evidence that omega-3s may shift particle size to a more benign, "fluffier" LDL, thus favorably impacting the atherogenic profile.

Antithrombotic. Fish oils produce platelet inhibition and reduce fibrinogen. Although some experts contend that higher doses (>3-4 g/day) are required, others argue for a lower threshold. Epidemiologic evidence of fish oil's anti-clotting effects comes from several studies that link higher intake of fish oil to a reduction in ischemic strokes with coincident increased risk of hemorrhagic strokes. This leads to a net gain in protection, since ischemic strokes outnumber hemorrhagic strokes by 85% to 15%.

Antihypertensive. Fish oil is thought to exert an antihypertensive effect in several ways. It supports flow-mediated vasodilation, enhances vascular reactivity, and may balance autonomic tone by reducing adrenergic drive.

An analysis of randomized trials revealed that consumption of approximately 4.0 g/day of omega-3 fatty acid was associated with a significant 1.7- and 1.5-mm Hg reduction in systolic and diastolic BP, respectively; these reductions were more pronounced in older patients and in individuals with higher BP. Evidence suggests that lowering systolic BP by as little as 2 mm Hg can yield reductions of 4% in CAD mortality.15

Adiponectin. A hormone produced by fat cells, adiponectin plays a role in regulating lipids and glucose. Low levels of this hormone are associated with obesity, and higher levels have been shown to confer protection against heart disease. When administered to obese individuals, 1.8 g/day of EPA increased the level of adiponectin.16 

Insulin regulator. To date, research in the area of insulin regulation has been inconclusive. While numerous studies support a role for EPA/DHA in attenuating insulin resistance, and omega-3 deficiency has been associated with the metabolic syndrome, the Agency for Healthcare Research and Quality reports, "Among 18 studies of type 2 diabetes or the metabolic syndrome, omega-3 fatty acids . . . had no effect on fasting blood sugar, or glycosylated hemoglobin, by meta-analysis. Omega-3 fatty acids had no effect on plasma insulin or insulin resistance in type 2 diabetics or patients with the metabolic syndrome, by qualitative analysis of four studies."17

Antiarrhythmic. The principle cause of sudden cardiac death (SCD) is sustained ventricular arrhythmia. Considerable evidence supports an antiarrhythmic role for omega 3s, probably via autonomic pathways. Studies show that EPA/DHA enhances sympatho-vagal tone, leading to slower heart rates and fewer arrhythmias, and in some studies, reduced incidence of SCD. Omega 3s have also been shown to favorably impact heart rate variability, a marker of autonomic adaptability.

Knowledge of fish oil's beneficial effects on arrhythmias recently prompted a trial of omega-3 supplementation in patients with implantable cardioverter defibrillators (ICDs). The results—which showed a higher incidence of ICD discharges in consumers of fish-oil supplements—and the consequent negative publicity have dampened enthusiasm over fish oil for this indication.

Some studies have shown impressive results for fish oil in prophylaxis of atrial fibrillation, particularly in patients at risk after coronary artery bypass grafting.18

Anti-inflammatory. Omega-3 fatty acids act as eicosanoid precursors to reduce inflammation. This may impact cardiovascular risk in several ways.

First, chronic inflammation is thought to play a critical role in endothelial damage that leads to compromised vascular reactivity and atherosclerotic changes. Additionally, inflammation promotes unstable plaque, a harbinger of thrombotic events.

Next, it is now commonly acknowledged that elevated high-sensitivity C-reactive protein (hs-CRP), a selective marker of intra-arterial inflammation, is a robust risk factor for CVD. Research on the potential for fish oil to lower this cardiospecific parameter has produced mixed results. One study found that atorvastatin (Lipitor), but not fish oil, reduced hs-CRP in obese, at-risk subjects.19 In other research, omega-3 supplements did not reduce hs-CRP in healthy subjects.20 Another set of findings showed that EPA/DHA reduced hs-CRP in patients on dialysis, a population known to be at higher risk for inflammation and CVD.21

Finally, fish oil has a less equivocal effect on other inflammatory mediators, specifically such cytokines as tumor necrosis factor-alpha, elevations of which are hallmarks of chronic congestive heart failure (CHF). Studies show improvement in cytokine levels in CHF patients taking EPA/DHA, with corresponding improvements in clinical outcomes.9

Prevention of restenosis. Accelerated restenosis following angioplasty or stenting is one of the thorniest problems in medicine, associated with numerous failed strategies. Because of fish oil's acknowledged antiatherosclerotic effects, it became a likely candidate for restenosis prevention. Early meta-analyses showed modest benefit and provided reason to be hopeful.22 Unfortunately, the Coronary Angioplasty Restenosis Trial demonstrated no reduction in restenosis rates with 5 g/day of Omacor, a precursor to Lovaza.23

Other benefits. Ancillary benefits of fish-oil supplementation are thought to be considerable. Therapeutic effects have been investigated, with various degrees of evidence, in such diverse conditions as bipolar disorder, depression, dementia, psychosis, certain cancers (including breast, colon, and prostate) cancer cachexia, rheumatoid arthritis, cystic fibrosis, inflammatory bowel disease, dysmenorrhea, IgA nephropathy, systemic lupus, asthma, chronic obstructive pulmonary disease, psoriasis, eczema, dry eye, macular degeneration, pre-eclampsia, and prevention of organ-transplant rejection.24

With regard to fish oil's role in secondary prevention of CVD, studies suggest potential amelioration of depression in heart attack survivors who take omega-3s. Depression is a known comorbidity following MI. It is also a negative prognostic, so, if proven, fish oil's antidepressant effects would be a valuable ancillary benefit.

A recent trial compared fish oil plus sertraline with sertraline alone in a group of post-MI patients. Mood improved in all the patients, but no difference was seen in depression scores between fish-oil-supplemented patients vs. controls.

"Whether higher doses of EPA, DHA, or sertraline, a longer duration of treatment, or the use of omega-3 as monotherapy can improve depression in patients with stable heart disease remains to be determined," the authors concluded.25

ADVERSE EFFECTS AND CONTRAINDICATIONS

The most commonly observed adverse effects of omega-3 PUFA supplementation are nausea, GI upset, and "fishy" burp. These problems can sometimes be ameliorated through the use of flavored, emulsified omega-3 formulations that are palatable even to children. Alternatively, enteric-coated forms of fish oil are designed to dissolve distal to the stomach, reducing the potential for oily reflux.

Because of fish oil's antiplatelet effects, concerns have been raised over the possibility that higher intakes will lead to an increase hemorrhagic complications. However, a comprehensive review concluded that no increased risk of clinically significant bleeding was noted with omega-3 PUFA doses of up to 7 g of combined DHA and EPA per day, even when coupled with antiplatelet therapy or warfarin.26 Results may vary in clinical practice, and such clotting disorders as Von Willebrand disease or thrombocytopenia may pose relative contraindications to high-dose fish-oil supplementation.

A recent study explored fish-oil supplements' synergy with aspirin and clopidogrel in post-stenosis patients. Resistance to platelet inhibition was overcome with no concomitant increase in adverse hemorrhagic events.27

To prevent excessive perioperative bleeding, patients undergoing elective surgery are typically advised to forgo fish-oil supplementation for several weeks, but some studies actually support a role for fish oil in improving surgical outcomes. Some researchers have credited fish oil with offering circulatory benefits, or alternatively with modulating immunity, perhaps by blunting the exaggerated cytokine response to surgery.28

Lately, concerns have been raised over fish oil's potential to down-regulate immunity in detrimental ways. One study observed that fish oil decreased resistance to influenza virus in a murine model,29 but the observation has not been extended to humans.

FISH-OIL SUPPLEMENTS ON THE MARKET

Fish-oil supplements come in a variety of forms. Cod-liver oil is the original article, but its disadvantages relative to omega-3 capsules include low ratio of EPA/DHA to overall calories, greater risk of mercury and PCB contamination, and potential for vitamin A and D toxicity with high levels of supplementation.

Most fish-oil capsules are free of significant mercury and PCB contamination, and industry standards for monitoring and disclosure are relatively stringent. Disparities exist, however, in the amount of active EPA and DHA delivered per capsule, and some ultra-discounted brands may be of dubious benefit due to the sheer number of capsules required to achieve clinically meaningful supplementation.

Manufacturers sometimes use the term "pharmaceutical grade" to imply greater potency or purity, but the claim is not regulated and almost meaningless. Also, controversy persists over relative advantages of two competing technologies for enhancing the EPA/DHA concentration: triglyceride substitution vs. ethyl esterification (used in Lovaza). Each camp claims superior bioavailability, but evidence remains inconclusive.

Finally, new formulation technology permits the offering of EPA/DHA in variable ratios designed to target specific clinical goals. EPA and DHA may have differing effects on desirable cardioprotective endpoints. The precise "optimal" ratio of EPA/DHA for heart disease prevention, if such a thing exists, has not yet been determined.

Uncertainty remains among health-care professionals as to the potential therapeutic application of fish-oil supplements in heart disease. A wide range of mechanistic, epidemiologic, and controlled-trial evidence substantiates a role for omega-3 fatty-acid supplementation in both primary and secondary cardiovascular prevention. An extensive margin of safety has been confirmed in most settings. More work remains to be done in studying the effects of fish oil in specific subpopulations and circumstances as well as in clarifying optimal dosage regimens and EPA/DHA ratios. Only then can specific guidelines for administration of omega-3 supplements coalesce into consistent and clear recommendations from health-care professionals.

Dr. Hoffman is founder and medical director of the Hoffman Center in New York City. The author has no relationships to disclose relating to the content of this article.

REFERENCES

1. Kromhout D, Giltay EJ, Geleijnse JM; Alpha Omega Trial Group. n-3 fatty acids and cardiovascular events after myocardial infarction. N Engl J Med. 2010;363:2015-2026.

2. GlaxoSmithKline. Lovaza prescribing information. Available at us.gsk.com/products/assets/us_lovaza.pdf.

3. Natural Products Insider. Cardiologists recommend dietary supplements for a healthy heart. Available at multivu.prnewswire.com/mnr/lifesupplemented/36723/.

4. U.S. Food and Drug Administration. FDA announces qualified health claims for omega-3 fatty acids. Available at www.fda.gov/NewsEvents
/Newsroom/PressAnnouncements/2004/ucm108351.htm#.

5. Rosenthal E. In Europe it's fish oil after heart attacks, but not in U.S. The New York Times. October 3, 2006: A1. Available at www.nytimes
.com/2006/10/03/health/03fish.html.

6. Kris-Etherton PM, Harris WS, Appel LJ; American Heart Association. Nutrition Committee. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002;106:2747-2757. Available at circ
.ahajournals.org/cgi/content/full/106/21/2747.

7. Sinclair HM. The diet of Canadian Indians and Eskimos. Proc Nutr Soc. 1953;12:69-82.

8. Dyerberg J, Bang HO, Hjorne N. Fatty acid composition of the plasma lipids in Greenland Eskimos. Am J Clin Nutr. 1975;28:958-966. Available at www.ajcn.org/cgi/reprint/28/9/958.pdf.

9. Lavie CJ, Milani RV, Mehra MR, Ventura HO. Omega-3 polyunsaturated fatty acids and cardiovascular diseases. J Am Coll Cardiol. 2009;54:585-594.

10. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet. 1989;2:757-761.

11. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico. Lancet. 1999;354:447-455.

12. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002;105(16):1897-1903. Available at circ.ahajournals.org/cgi/content/full/105/16/1897.

13. Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis.Lancet. 2007;369:1090-1098.

14. Jacobson TA. Role of n-3 fatty acids in the treatment of hypertriglyceridemia and cardiovascular disease. Am J Clin Nutr. 2008;87:1981S-1990S. Available at www.ajcn.org/cgi/content/full/87/6/1981S.

15. Geleijnse JM, Giltay EJ, Grobbee DE, et al. Blood pressure response to fish oil supplementation: metaregression analysis of randomized trials. 
J Hypertens. 2002;20:1493-1499.

16. Itoh M, Suganami T, Satoh N, et al. Increased adiponectin secretion by highly purified eicosapentaenoic acid in rodent models of obesity and human obese subjects. Arterioscler Thromb Vasc Biol. 2007;27:1918-1925. Available at atvb.ahajournals.org/cgi/content/full/27/9/1918.

17. MacLean CH, Mojica WA, Morton SC, et al. Effects of omega-3 fatty acids on lipids and glycemic control in type II diabetes and the metabolic syndrome and on inflammatory bowel disease, rheumatoid arthritis, renal disease, systemic lupus erythematosus, and osteoporosis. Evid Rep Technol Assess (Summ). 2004;89:1-4. Available at www.ahrq.gov/downloads/pub/evidence/pdf/o3lipid/o3lipid.pdf.

18. Calò L, Bianconi L, Colivicchi F, et al. N-3 Fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery: a randomized, controlled trial. J Am Coll Cardiol. 2005;45:1723-1728.

19. Chan DC, Watts GF, Barrett PH, et al. Effect of atorvastatin and fish oil on plasma high-sensitivity C-reactive protein concentrations in individuals with visceral obesity. Clin Chem. 2002;48:877-883. Available at www.clinchem.org/cgi/content/full/48/6/877.

20. Geelen A, Brouwer IA, Schouten EG, et al. Intake of n-3 fatty acids from fish does not lower serum concentrations of C-reactive protein in healthy subjects. Eur J Clin Nutr. 2004;58:1440-1442. Available at www.nature.com/ejcn/journal/v58/n10/full/1601986a.html.

21. Saifullah A, Watkins BA, Saha C, et al. Oral fish oil supplementation raises blood omega-3 levels and lowers C-reactive protein in haemodialysis patients—a pilot study. Nephrol Dial Transplant. 2007;22):3561-3567. Available at ndt.oxfordjournals.org/content/22/12/3561.long.

22. O'Connor GT, Malenka DJ, Olmstead EM, et al. A meta-analysis of randomized trials of fish oil in prevention of restenosis following coronary angioplasty. Am J Prev Med. 1992;8:186-192.

23. Johansen O, Brekke M, Seljeflot I, et al. N-3 fatty acids do not prevent restenosis after coronary angioplasty: results from the CART study. Coronary Angioplasty Restenosis Trial. J Am Coll Cardiol.1999;33:1619-1626.

24. National Library of Medicine. Fish Oil. Available at www.nlm.nih.gov/medlineplus/druginfo/natural/993.html.

25. Carney RM, Freedland KE, Rubin EH, et al. Omega-3 augmentation of sertraline in treatment of depression in patients with coronary heart disease: a randomized controlled trial. JAMA. 2009;302:1651-1657. Available at jama.ama-assn.org/cgi/content/full/302/15/1651.

26. Harris WS. Expert opinion: omega-3 fatty acids and bleeding-cause for concern? Am J Cardiol.2007;99:44C-46C.

27. Gajos G, Rostoff P, Undas A, Piwowarska W. Effects of polyunsaturated omega-3 fatty acids on responsiveness to dual antiplatelet therapy in patients undergoing percutaneous coronary intervention: the OMEGA-PCI (OMEGA-3 fatty acids after PCI to modify responsiveness to dual antiplatelet therapy) study.J Am Coll Cardiol. 2010;55:1671-1678.

28. Tsekos E, Reuter C, Stehle P, Boeden G. Perioperative administration of parenteral fish oil supplements in a routine clinical setting improves patient outcome after major abdominal surgery. Clin Nutr.2004;23:325-330.

29. Schwerbrock NM, Karlsson EA, Shi Q, et al. Fish oil-fed mice have impaired resistance to influenza infection. J Nutr. 2009;139:1588-1594. Available at www.ncbi.nlm.nih.gov/pmc/articles/PMC2709305/.

All electronic documents accessed November 15, 2010.

Tags:  fish oil  heart  prevention 

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Insights on Stress

Posted By Administration, Monday, December 20, 2010
Updated: Friday, April 18, 2014

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by Andrea Purcell, ND

The 2 running themes at the office this week seem to have been the stomach bug; which is making its way around Southern California, and Stress. My advice for the former is to wash your hands, and choose restaurants carefully when eating out.

Today’s discussion will be on the latter since Stress seems to be all around us, permeating some days more than others. It directly affects our health, (blood pressure being the quickest marker of it), our ability to restore and replenish (when it affects our sleep), and it robs us of being nourished through our daily interactions.

Below are 3 examples of how we must remain in the present, see the opportunity in adversity, and how nurturing ourselves through coping mechanisms can reduce our stress.

REMAIN IN THE PRESENT:

When we put ourselves on autopilot, motoring through life, day after day, the divine aspects of life lose their luster.

Our life becomes something we just do, instead of the wave of possibility that each new dawn can bring. One of my patients this week was mentioning how she initially came to the clinic. She had run into one of her friends at the car wash that she hadn’t seen in a while. They got to talking and she said to him, “there must be some reason why we were meant to meet.” He replied, “I bet your right, so let's just start talking and see where it leads.” They spoke about their lives, their challenges, their spouses, their health and so on. By the end of the conversation she heard how Naturopathic Medicine had helped him and confided that she too had been in search of a doctor or clinic that could help her get to the cause of her health issues as well, which in turn led her to my office. And so it goes….

The purpose of this example is not to say everyone needs a Naturopathic Doctor, it is to merely suggest that opportunities are within the people that we meet every day. When we are stressed we tend to withdraw and be focused on how we can just make it through the day. When this happens we tend to miss the “life-rafts” that get thrown our way.

Open yourself to the possibility within each interaction, sometimes the reason is revealed right away and sometimes it reveals itself over time, there are so many cross links within the divine plan.

 

 


OPPORTUNITY IN ADVERSITY:

Our life experiences change us and can spur us on in directions we never dreamed prior to their occurrence.

I don’t really know why but the end of one year and the beginning of another energetically seem to be filled with more births and deaths than usual. The ultimate cliché of when one life ends another begins, and so it is within the cycles of nature and time. I do know that when things are bad they never stay bad, and when things are good they never stay good, that is the organic nature of life; which can easily be seen within the real-estate market.

A patient of mine, who is a nurse, recently lost her mother to the complications of conventional medicine. (Not her cancer or her cardiovascular disease.) Through this experience, which left her disheartened with the conventional standards of care, she has changed her focus from dermatology to a career in alternative cancer therapies.

It is in this waking up that there is a shaking up, and a passion is invoked that was before dormant.

And so it is with our economy, more small business startups are beginning each day, as people no longer wait for their fate to be at the mercy of someone or something else. The creativity that is erupting from individuals and entrepreneurs can be seen across the Internet, YouTube, blogs, Facebook, digital marketing accounts, and smart phone applications. Many more people have found their voice and are using it to expand on their passion.

NURTURING OURSELVES:

When things are going good it’s easier to be healthy and eat right. The challenge is to still make good food & life choices under stress.

Change is never easy and it’s hard to get up off of a couch that was really comfortable, the current stressors of today are upending that couch for many. It is affecting our health. The answer is not to look back to what was, the answer is to ask for the way to reveal itself, and develop healthy coping mechanisms in the interim.

Make your coping mechanisms a priority. Healthy coping mechanisms include anything that is supportive and nurturing to your mind, body, and spirit. (Some of you can rationalize that ice cream is nurturing. Frozen, fat, dairy, and sugar is in no way, shape or form nurturing.)

My last patient of the week, had been losing weight and really doing great on her food plan that she had been working on for about 2 months. She showed up completely frazzled, angry and hopeless at my office Friday afternoon regarding stress at work. When I took her blood pressure it was elevated, and she was giving herself hot flashes. She confided that she had not had any ice cream during the 2 months that we had been working together and that the incredible stress of the previous week sent her literally head first into the freezer. Although she knew that after eating ice cream she felt terrible, she couldn’t resist the urge to eat it right then and there. Negative coping mechanisms can be extremely deleterious to our health if we aren’t careful. Self-defeating choices include sweet treats, alcohol, smoking, soda, and impulsive behaviors.

This situation in particular is a classic case of emotional eating. Most of us do it to one extent or another, for some it’s mashed potatoes, chocolate, ice cream, or pastries, the list is endless. All sugar and carbohydrates boost our serotonin, which is a temporary antidepressant and makes us feel immediately better. Remember the nothing-good lasts, so then we crash, often feeling worse then before we ate it. She and I explored the situation, and discussed where she could work on directing her energy, we then discussed alternative coping mechanisms that included exercise, talking with friends or her spouse, walking on the beach, and others.

Stress, mental, physical, and emotional is all around us. Our stressors are actually becoming greater as the digital age continues to develop. This is because we now have within second’s access to events happening around the world, and to literally feel the impact of them. Now something happening in Asia can directly affect our bank account, and devastation in Haiti, can keep many of us awake at night for hours and be on our minds for days. Our nervous systems are busy integrating thousands of millibits of information per minute coming in from our computers, telephones, Internet, radio, and iPods. Now more than ever in order to be balanced and in good health, we must develop healthy coping mechanisms, see the opportunity in adversity, and stop to smell the flowers, watch a shooting star and embrace the beauty of each moment.

 

Tags:  anxiety  stress 

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Strategic Approach to Andropause

Posted By Administration, Thursday, December 16, 2010
Updated: Friday, April 18, 2014

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by Zina Kroner, DO

Menopause has been grabbing all the headlines lately, but half the world faces a comparable syndrome that is more insidious and less predictable. This disease entity is andropause.

Unlike menopause which usually occurs at a predictable time, men's testosterone levels decline at different ages and different rates, sometimes slowly, and sometimes precipitously. Testosterone production by the testes reaches adult levels by age 17 (300-1000 ng/dL). The testosterone level remains constant until the fifth decade at which point it declines at a rate of 1.2 percent per year. But in some men, testosterone can drop prematurely and precipitously.
 
In the Baltimore Longitudinal Study of Aging (2001), it was demonstrated that free testosterone decreased at a constant rate with age and this decline was not related to other causes. Another study demonstrated that poor health may accelerate the natural age-associated decline in testosterone concentrations. One interesting finding is that studies that measured testosterone in the morning were more likely to show a decline in testosterone when compared to studies that measured testosterone in the afternoon. The logic behind this is that older men have little variation in their levels of testosterone throughout the day, unlike young men, who have peaks in their testosterone levels in the morning and troughs in the evenings.
 
As one ages, there is an increase in fat cells, which in turn causes an elevation in an enzyme called aromatase. This enzyme transforms testosterone to estrogen in the body. Secondarily, estrogen can indirectly cause an increase in a protein called sex-hormone-binding-globulin (SHBG), which binds to free testosterone and prevents its action. This protein will ultimately cause a decrease in testosterone.
At this point you should be asking "Does this apply to me or to my spouse/partner?"
 
There are theories that demonstrate that a decline in testosterone can cause a decline in mental function. In a study published in the Journal Of Clinical Endocrinological Metabolism in 2002, 407 men were studied ages 50-91 and subsequently demonstrated that those classified as having a low testosterone had lower scores on memory and visuo-spacial performance. The results of several pilot studies have tied low testosterone levels to Alzheimer's disease, in which there is a build-up of a toxic peptide called beta-amyloid. These studies showed that the toxic effects of this peptide are reduced by testosterone. Interestingly, testosterone levels were lower in Alzheimer's patients as compared to controls. It is unknown if these low levels cause or are caused by Alzheimer's disease. According to Dr. Jonathan Wright (co-author of Maximize Your Vitality and Potency), low testosterone levels are associated with moodiness, feeling weak, passivity, and reduced interest in one's surroundings.

 

 

 


In addition to having an effect on cognitive function, studies have shown correlations between a declining testosterone level and a decline in sexual function as measured by frequency of orgasm or intercourse or by sexual satisfaction (Journal of Clinical Endoclinology 1983). Studies also show that muscle mass, muscle strength and bone mineral density decline with age.
 
The first step in diagnosing andropause starts with a thorough evaluation at your physician's office. First, your doctor will obtain a complete medical history from you and perform a series of blood tests to see if you have testosterone deficiency and what may be causing it. Before starting any treatment, however, it is imperative to rule out underlying prostate cancer, just as we would rule out breast cancer in a woman contemplating estrogen therapy. The following are some examples of causes of low testosterone and approaches to them.
 
First, as discussed, in obese patients, there is excess aromatase enzyme activity causing the testosterone to convert to estradiol causing estrogen overload and testosterone deficiency. Poor liver function is another entity that causes excess estrogen because the liver then cannot detoxify the small amounts of estrogen that even men have. In this case, total testosterone levels would be normal and estrogen levels would be high as much of the testosterone is being changed into estradiol, and the free or usable testosterone levels would be low. This often occurs with excess alcohol consumption.
 
If you fall into the above category, you should maintain an appropriately high level of aromatase inhibitors in your diet. The recommendation is zinc 80mg daily. A supplement call chrysin, a flavonoid, together with piperine for enhance absorption into the bloodstream, functions as a mild aromatase inhibitor as well. There is a more potent aromatase- inhibiting drug called Arimidex (anastrozole), which can only be prescribed by your doctor. Arimidex is prescribed to estrogen receptor positive breast cancer patients to prevent hormones in the body from aromatizing into estrogen. It has not yet been FDA approved for other indications.
 
A diet that does not adversely affect liver function should be adhered to. This will of course include an alcohol-free diet, since even small amounts of alcohol are shown to augment estrogen in both men and women. Special attention should be paid to medications affecting the liver and should be reviewed with your doctor in detail. As estrogen excess may be a problem in the setting of liver dysfunction, a substance called indole-3-carbinol (or diindole methane or DIM)) found in special supplements or cruciferous vegetables can help to neutralize the excess estrogen. Most importantly, it is essential that you lose weight as it is the excess aromatase enzyme that is produced by the fat cells that convert the testosterone into the estrogen.
 
Second, an excess of sex-hormone-binding-globulin can bind much of the free- testosterone and therefore inactivates it. In this case, one will have low free testosterone, normal or even high total testosterone and normal estradiol levels. In addition to following the protocol that inhibits aromatase activity, take saw palmetto which can block the estrogen receptor sites in the prostate cells and therefore reduce the effects of excess estrogen. Saw palmetto also blocks the conversion of testosterone into a hormone, DHT, which has been directly linked to the development of prostate disease.
 
Methanolic extract of nettle can also inhibit SHBG. It binds to SHBG and therefore blocks its testosterone binding effects, thus allowing more testosterone to be in its natural free state. This root has also been used for benign prostatic hyperplasia. It inhibits the binding of dihydrotestosterone ( DHT), a prostate growth stimulator, to the prostate.
 
A third cause of low testosterone is failure of the pituitary gland to produce a hormone called leutenizing hormone (LH). One of the functions of LH is to stimulate testosterone production by the testes. In this case, the levels of total testosterone would be low as there is a problem with production.
Fourth, if the testes themselves lose their ability to produce testosetrone, there would be an elevated LH, which would act as a stimulant to produce testosterone. Total testosterone would be low. Patients like these are candidates for testosterone replacement.
 
Lastly, DHEA, a precursor hormone to testosterone and estrogen, may be low and worsen the consequences of borderline testosterone. The solution here is to supplement DHEA under a doctor's supervision.
 
Physicians have prescribed testosterone administered via creams, tablets, patches, lozenges and injections. Such preparations can lead to normalization of testosterone and improvements in muscle strength, libido, mood and bone density. They may also be associated with side effects, so care must be taken to use the right form of replacement and dosage. There is no "one size fits all" approach.
After initiating testosterone, during the first few months, some men may note effects seen in normal puberty, such as acne and gynecomastia. In men over the age of 50, worsening of prostate symptoms may occur, although sometimes they improve. If, however, the testosterone is not taken in excess and used to maintain a normal serum testosterone, there is no reason to believe that these men are more likely to develop these conditions than men who produce their own natural testosterone. Nevertheless, a PSA and a digital rectal exam and close monitoring of hormone levels must be adhered to.

Tags:  andropause  prevention 

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Telomeres and Aging

Posted By Administration, Tuesday, December 14, 2010
Updated: Friday, April 18, 2014

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by Joel Lopez, MD, CNS

Besides looking at the mirror, another objective way of telling how fast a person is aging is through telomere testing. Before anything else, what are telomeres? Telomeres are sections of DNA at the end of each chromosome that serves as a cap to your genetic material. Every time a cell replicates, its telomere will become shorter. Shorter telomeres imply a shorter life span for the cell.

What effect does telomere length have on my health and wellness? Age adjusted telomere length is the best method to date to assess biological age using structural analysis of chromosomal change in the telomere. Serial evaluation of telomere length is an indicator of how rapidly one ages relative to a normal population. Therapies directed at slowing the loss of telomere length may slow aging and age-related diseases.

Does diet have any effect on telomere length and repair? An inflammatory diet, or one that increases oxidative stress will shorten telomeres faster. This would include refined carbohydrates, fast foods, processed foods, sodas, artificial sweeteners, trans fats and saturated fats. A diet with a large amount and variety of antioxidants that improve oxidative defense and reduces oxidative stress will slow telomere shortening. Consumption of 10 servings of fresh and relatively uncooked fruits and vegetables, mixed fiber, monounsaturated fats, omega-3 fatty acids, cold water fish and high quality vegetable proteins can prevent premature shortening. In addition, caloric restriction is advised combined with an exercise program. Fasting for 12 hours each night at least 4 days per week may also be protective.

What lifestyle modifications are likely to be helpful? One should achieve ideal body weight and body composition with low body fat (less than 22% for women and less than 16% for men). Decreasing visceral fat is very important. Regular aerobic and resistance exercise for at least one hour per day, sleeping for at least 8 hours per night, stress reduction, discontinuation of all tobacco products and bioidentical hormone therapy may decrease the rate of telomere loss.

How do you measure telomere length? The Patient Telomere Score is calculated based on white blood cells (T-lymphocytes). This is the average compared to telomere length on lymphocytes from a sample of the American population in the same age range. The higher the telomere score, the “younger” the cells. A Telomere Score that is above the average line is desirable.

What can I do to reduce my rate of telomere loss? Shorter telomeres have been associated with metabolic abnormalities, obesity, and several degenerative diseases including cancer, dementia, and cardiovascular disease. In vitro studies have shown that telomeres are highly susceptible to oxidative stress, which will shorten telomere length and enhance cellular aging. Minimizing associated risk factors that are linked to shortened telomere activity is recommended and include:

Reduce oxidative stress

Correct micronutrient deficiencies, especially vitamin D

Change sedentary lifestyle, increase physical activity

Avoid weight gain or obesity

Correct insulin resistance

 

Tags:  anti-aging  telomeres 

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