Print Page  |  Contact Us  |  Sign In  |  Join ACAM
ACAM Integrative Medicine Blog
Blog Home All Blogs

A Closer Look at MRIs & Scans in Sports Medicine

Posted By Scott Greenberg, MD, Thursday, November 3, 2011
Updated: Thursday, January 30, 2014

In an article appearing in the NY Times, October 29, 2011. Specialists and medical researchers concluded that "(MRIs) are easily misinterpreted and can result in misdiagnoses leading to unnecessary or even harmful treatments.”

Dr. James Andrews, best known for his surgical work on professional athletes, did his own experiment. He scanned the shoulders of 31 perfectly healthy professional baseball pitchers. Quoting the article, "The pitchers were not injured and had no pain. But the MRIs found abnormal shoulder cartilage in 90 percent of them and abnormal rotator cuff tendons in 87 percent.”

"If you want an excuse to operate on a pitcher’s throwing shoulder, just get an M.R.I.,” Dr. Andrews says.”

At the Magaziner Center for Wellness, we rarely if ever rely on an MRI. In our opinion these tests are a waste of money. A patient can come in with a big file of films and scans that cost them a lot of money out-of-pocket, and typically, there will be no useful information that will help us get the athlete back on the field. A skilled physician can make a more accurate determination of an athlete’s injury and treatment plan with a careful physical examination and history.

Unfortunately, there is a certain appeal to the patient to get an MRI, especially the athlete who thinks it is part of the normal process of treatment. It is sometimes difficult to get the patient to understand that when they get an MRI there will be a recommendation for a surgery that many times is unnecessary.

Before you consider the surgical option based on an MRI, before you take your star athlete off the field for a year of surgical recovery, a consultation with a doctor trained in non-surgical treatment of ligament and tendon injuries, such as Prolotherapy and PRP (Platelet Rich Plasma) Therapy, may be an option to explore.

This article was originally published at: http://www.drmagaziner.com/prolotherapynewjersey/why-mris-and-scans-are-not-an-important-part-of-our-sports-medicine-practice/

This post has not been tagged.

Share |
PermalinkComments (0)
 

Breast Cancer and Nutrition

Posted By Andrea Purcell, ND, Wednesday, October 12, 2011
Updated: Thursday, January 30, 2014

October is breast cancer awareness month. There are walks for breast cancer sponsored by various groups; many working to find a cure for cancer. A walk I recently attended was with Support Connection, a non-profit organization providing free support services for women with breast and ovarian cancer.

From a Naturopathic perspective, preventing cancer is the first step, curing and or surviving cancer is the second step. It seems as if many people miss the first step, and by the time they get to the second step there is a lot of fear involved.

There is some basic information that will keep you informed about how to prevent breast cancer and why conventional medicine often provides a false sense of security around this topic.

Point #1: Nutrition is important. Sadly, more often than not I come face to face with women with cancer and close family members who do not realize that nutrition has an impact on survival rate and overall health. Sugar feeds cancer cells and it lowers the immune system. Gluten and dairy products are inflammatory and will cause more inflammation slowing down the cellular repair processes. Certain vegetables such as dark green leafy greens, kale, cauliflower, broccoli, Brussels sprouts, and parsley have chemical compounds proven to prevent and fight cancer. Artificial colorings, flavorings, dyes, hormones, and preservatives in food are often suspect carcinogens.

Point #2: Most conventional doctors do not discuss nutrition with their clients. Nutritional biochemistry is not taught in conventional medical schools. The reason your doctor most likely did not discuss nutrition with you is because the importance of it is not stressed in medical schools.


Conventional doctors do two things very well:
Diagnose and treat disease with drugs and surgery. The key word is disease. If you have a disease they will either recommend drugs or surgery. If you are trying to prevent a condition that you don’t officially have yet, it means your conventional doctor can’t help you. Conventional doctors diagnose and treat diseases only. If you want to know how to help yourself with nutrition, or pursue natural therapies to help your body, do not expect to get all the information that you need from your conventional doctor.

Point #3: Mammograms do not prevent cancer, mammograms screen for cancer. A mammogram will not tell you if you will develop cancer next year or evaluate the current health of breast tissue. Therefore, mammograms have limitations. If you are relying on your annual mammogram to give you the green light, for another year of bad nutrition, and lack of exercise, think again. Wouldn’t it be a good idea to make some healthy lifestyle changes now? As Benjamin Franklin said, "an ounce of prevention is worth a pound of cure.”

Mammograms are not recommended in younger women for two reasons:
Reason 1:Younger women can have denser breasts, which create less visibility and therefore less accuracy on a mammogram.
Reason 2: Mammograms are x-rays. Repeated radiation of breast tissue can accumulate in the body and cause cellular damage to breast cells. X-rays are known carcinogens. Receiving a note that your annual mammogram is negative provides a false sense of security to a woman who may have some pre-disease states manifesting that will ultimately impact the health of the breast tissue.

Note from Dr. P:
As usual, naturopathic medicine has the other side of the story.
Nutrition, nutrition, nutrition, I can’t stress this enough! How can you expect your body to perform optimally for 40+ years on Frappuccino’s, lunch at the local sandwich shop, and take out? It just won’t. Yet, I see some highly educated women out there who put everything before food, nutrition, and feeding themselves. This has got to stop! Food is our gasoline; it provides the fuel for every body system. Usually we can "cheat” up until age 40 but as usual, you can only make withdrawals from the body for so long before it becomes bankrupt. I call it nutritional bankruptcy. From this point, we go into accelerated aging, the development of chronic diseases, hormone imbalance, depletion, and we are left wide open for cancer and other undesirable conditions.

Whole food is food that grows. When you are reviewing ingredients and food choices, ask yourself, have I ever seen this growing on a farm or in the soil? Hint: Frappuccino’s don’t grow on any farm anywhere.


Mammograms are an important screening tool, yet they need to be properly understood in order to see the whole story. Breast health is an indication of whole body health; the breasts cannot be separated from the rest of the body. Naturopathic medicine has a lot to offer women with pre-existing hormonal imbalances, which will enhance the health of breast tissue over time, reduce fibrocystic densities, and prevent cancer.

- Be Healthy, Happy, and Holistic

Tags:  cancer  nutrition 

Share |
PermalinkComments (0)
 

To Play or Not to Play? That is NOT the Question

Posted By Scott R. Greenberg, MD, Thursday, October 6, 2011
Updated: Thursday, January 30, 2014
Yesterday, hockey fans – were rocked by the news that Sidney Crosby would be placed on injured reserve (IR) on Monday, October 10th. There had been much anticipation surrounding Crosby’s return to the ice being sidelined since January when he suffered a severe concussion – a concussion that has left him with recurring headaches and dizziness.

Frankly, I am relieved to hear that the Pittsburgh Penguins’ medical staff decided that he is not yet ready to make a comeback. It’s not that I don’t want Crosby back in the game – I do. He is a dynamic player who brings incredible energy every time he takes the ice.

But, post-concussion syndrome requires more than a quick fix or a lessening of symptoms, which is difficult because among sports-related injuries, post-concussion syndrome is one of the most elusive and challenging problems to treat. While many patients will recover from their concussion, just as many will not. To make matters worse, as an athlete sustains repeat concussions, the chance of recovery becomes less
likely.

Since I don’t treat Crosby, I cannot speak to what his doctors are seeing. I do know that most patients who suffer from post-concussion syndrome will have normal blood work, normal MRI examinations, and normal vital signs. Since we cannot "see” an apparent cause of their symptoms by these traditional tests, a conventional treatment for post-concussion syndrome does not exist. Those that suffer from this disorder are asked to rest and possibly undergo physical and occupational therapy until symptoms resolve. They say waiting is the hardest part – add chronic pain to that and you have a recipe for disaster, proven by the Dave Duerson, the former Chicago Bears safety who suffered from the physical and psychological symptoms of post-concussion syndrome for more than 10 years before taking his own life last February. Duerson shot himself – in the heart, not the head, in order to preserve his brain which he requested be donated to science – specifically the science of looking at the long-term impact of severe hits to the head, the same type of hits that have grounded Crosby.

There is a better way to address post-concussion syndrome than just waiting it out and dealing with pain. In fact , we at the Magaziner Center for Wellness have been using innovative regenerative joint procedures to get many professional and collegiate athletes back in their respective games. We have had great success with prolotherapy, a holistic procedure that involves a series of injections into damaged ligaments, tendons, and joints that produce a healing response within the damaged tissue, ultimately leading to repair of the damage. The mechanism for this non-surgical repair is mediated through immune system modulators which cause the concentration of cells known as macrophages and monocytes along with chemicals known as chemokines, to remove microscopic debris and fix damaged tissues.


Agents used for Prolotherapy restoration include lidocaine, dextrose, phenol, glycerin, and more recently growth factors derived from the patient’s own body known as platelet rich plasma (PRP). The exact mixture or substance used in prolotherapy is not nearly as important as the precise diagnosis and treatment into the area of damage that is causing the symptoms of post-concussion syndrome.

So, how do injections into the neck and head cure the problems of concussion and head injury? The answer has to do with a complete understanding of what happens during a head injury. I have studied films of the hits that have caused devastating concussions and observed that trauma to the skull does not just damage the brain; it also creates a significant whiplash injury to the neck and the base of the skull. Within these areas lies the brainstem, an area of the brain that controls our balance and coordination, and supplies nerves to the muscles that control the eyes, ears, face, and portions of our autonomic nervous system (ANS). Injury to the cervical and skull base changes the relationship between the brainstem, base of the skull, and cervical canal, causing increased pressure on the nerve control that I have described above. This leads to many of the symptoms of post-concussion syndrome. Fortunately, prolotherapy and
PRP injections (injections of a patient’s own platelet rich plasma) into these damaged areas can normalize the relationship between the skull base and cervical canal, and relieve excessive pressure on the nerve. Once this happens, symptoms of post-concussion syndrome resolve!

Prolotherapy and PRP injections are certainly the silver lining around a dark cloud, but must be used with caution. Having performed well over 50,000 procedures in my career, I know it takes an extreme amount of skill and dexterity to treat damage from concussion. However, successful treatment leads to regaining the patient’s life, allowing them to function again without pain, headache, blurred vision, and all of the other
lingering symptoms of concussion. While there has never been a controlled clinical trial on prolotherapy for treatment of post-concussion syndrome, the results speak for themselves … on and off the ice.

Tags:  concussion  sports medicine 

Share |
PermalinkComments (0)
 

CoQ10 for Migraines

Posted By Rosemarie Salo, Pharm.D., Wednesday, October 5, 2011
Updated: Thursday, January 30, 2014
Peer Reviewed by: Brian Solow, M.D., FAAFP

Migraine headaches are a common, chronic, debilitating neurovascular disorder. Migraine attacks may start at any age, but the incidence peaks in early to mid-adolescence. Overall, the one year prevalence of migraines is 11 percent: 6 percent for men and 15-18 percent for women in the United States and Western Europe. The frequency of attacks is 1.5 per month and each attack lasts about 24 hours. About 10 percent of patients have weekly attacks, and 20 percent have attacks lasting for 2-3 days.

Five percent of the general population has at least 18 days of migraine per year, and about 1 percent has at least 1 migraine attack per week. Most patients in the United States have not seen a physician for migraines during the previous year, nor have they been given a medical diagnosis for migraines. Most of these patients use over-the-counter medications versus prescription drugs due to side effects associated with conventional therapies.1 The side effects include, but are not limited to, dizziness, somnolence, impotence, fatigue, dry mouth, and weight gain.

Treatments can be divided into nonpharmacologic and pharmacologic therapies. Non-pharmacologic therapies include lifestyle changes such as eliminating food triggers, obtaining regular sleep and exercise, avoiding high stress situations, increasing relaxation methods, becoming educated of the disorder, and knowing of treatment options.



Pharmacological therapies that are usually prescribed for acute attacks include NSAIDS, ergot derivatives, and triptans. Patients who suffer from frequent, long endured, severe attacks should be candidates for preventative therapy. Preventative therapy is recommended when the frequency of attacks increase, or when the attacks become unresponsive to acute therapy.

Types of medications used for preventive therapy include beta-blockers, valproate, and tricyclic antidepressants. Other promising drugs include gabapentin and topiramate. On average, two thirds of patients who have been administered these types of medications have had a 50 percent reduction in the frequency of migraines.1

A mitochondrial defect is thought to play a role in the pathophysiological mechanism of migraines based on MRS4 and DNA5 analysis taken from a subset of individuals. Coenzyme Q10, also known as ubiquinone, is a naturally occurring substance and an essential element of the mitochondrial electron transport. Coenzyme Q10 may have clinical benefits for hypertension, angina, heart failure, and diabetes. Doses up to 600 mg per day have been well tolerated. If a mitochondrial impairment does in fact play a role in the pathophysiology of migraine headaches, coenzyme Q10 may be used as a medication for preventative treatment. An open label trial was conducted by Rozen et al. (2002) to assess the efficacy of coenzyme Q10 as a preventative therapy for migraine headaches. The study encompassed a total of thirty-two patients (26 women, 6 men) with a history of migraines with or without aura. Subjects included in the study experienced between two and eight attacks per month, had a 1-year history of migraines, and had not
received medications 2 months prior to the trial. During the study each subject was given a dose of 150 mg every morning of coenzyme Q10. Each subject was also given a diary to assess their attacks addressing symptoms, duration, and severity. Standard laboratory studies were conducted baseline and after 3 months of coenzyme Q10 administration. The percentage of patients who achieved at least a 50% reduction in the frequency of headache days after coenzyme Q10 administrations was the primary outcome measure.

Thirty-one out of thirty-two patients completed the study. One patient was lost to follow up. A minimum 50% reduction in the number of days with migraine headaches was seen in 61.3% of the subjects, and a minimum 25% reduction in the number of days with migraines was seen in 93.5% of the subjects. No improvement with therapy was seen in only two subjects. The average duration time for each migraine declined from 7.34 to 2.95 days after 3 months of therapy (P<0.0001). The mean frequency of attacks (mean number of migraine attacks in the last 60 days of treatment) declined from 4.85 baseline to 2.81 by the end of the study (P<0.0001). After 1 month of treatment the mean reduction of migraine frequency was 13.1% and increased to 55.3% by the end of the study. Coenzyme Q10 was equally effective in patients with or without aura. In addition, no significant adverse effects were associated with the administration of coenzyme Q10, and coenzyme Q10 was well tolerated.

Based on this study, coenzyme Q10 appears to be a promising choice for migraine prevention. Placebo-controlled trials are now warranted to determine its true efficacy in migraine prevention. Patients may choose not to use conventional types of medications due to side effects such as impotence and fatigue. Until further studies are conducted, coenzyme Q10 should be considered for patients who have failed conventional therapy without concern of significant risks.

Coenzyme Q10 is available as 300mg softgels from the McGuff Company.

References:
1. Goadsby P, Lipton R, Ferrari M. Migraine current understanding and Treatment. N Engl J Med 2002; 346(4):257-70.
2. Rozen TD, Oshinsky ML, Gebeline Ca, et al. Open label trial of Coenzyme Q10 as a migraine preventive. Cephalalgia
2002;22:137-141.
3. Welch K, Ramadan N. Mitochondria ,magnesium, and migraine .J Neurological Sci 1995; 134:9-14.
4. Montagna P, Cortelli P, Barbiroli B.Magnetic resonance spectroscopy studiesin migraine. Cephalalgia 1994;14:184-93.
5. Bresolin N, Martinelli P, Barbiroli B et al. Muscle mitochondria deletion and P NMR spectroscopy alterations in migraine
patients.J Neuro Sci 1991;104:182-9.
6. Collins C, Kemper K. Co-Enzyme Q10(CoQ10 or Ubiquione). The Longwood Herbal Task Force and The Center for
Holistic Pediatric Education and Research. Peer Review performed by Brian Solow, M.D.,FAAFP, Clinical Professor of
Family Medicine, University of California, Irvine, College of Medicine

Tags:  migraines  nutrition 

Share |
PermalinkComments (0)
 

Interview with Exchange Speaker & Environmental Health Hero Ted Schettler, MD

Posted By Administration, Tuesday, October 4, 2011
Updated: Thursday, January 30, 2014
Dr. Ted Schettler will be speaking during the General Session at Exchange 2011 on the topic of Environmental Diabetogens on Friday, November 18, 2011, from 11:00 am - 12:00 pm. Learn more about Dr. Schettler in our interview with the Environmental Health Hero.

Interview conducted by Michelle Schiavo - Social Impact Coordinator for ACAM.

ACAM: How did you become interested and involved in environmental health issues?

Dr. Schettler: I practiced clinical medicine for many years with a parallel interest in the environment and environmental health. It always seemed rather intuitive to me that there is a strong link between environmental variables and human health. It was also striking to me that that connection was not typically realized in the world of clinical medicine. Of course there were a few exceptions; individuals that more readily saw that connection than others, and things like lead poisoning of children has a long history of attention in medicine, but it was a rather limited number of topics in environmental health that had made their way into clinical medicine. And I just felt that a lot of the diseases and disorders that we see in clinical medicine have an environmental link, to some extent at least, and it was increasingly interesting to me which helped to shape the more recent part of my career.

ACAM: How important do you think environmental exposures to toxins like endocrine disruptors are in the etiology of type 2 diabetes?

Dr. Schettler: This is a topic of intense research and a very good question that I don’t know and I don’t think that anyone really knows the answer to. We know that type 2 diabetes is what we may call a multi-factorial disease, where there are a number of things that contribute to it. Historically we’ve been aware that as populations of people tend to become obese and change their diets in certain ways they’re at increased risk for developing type 2 diabetes. Only in the past 10 or 15 years has the idea that environmental chemicals may be contributing to type 2 diabetes has had any real traction at all. Even today I think that the extent to which environmental chemicals explain the population variants of type 2 diabetes, I don’t think any of us really knows the answer to that yet.

I was recently at a conference where the main topics were both obesity and diabetes and their links to environmental chemicals. Most of the world’s experts were there, both epidemiologists and basic bench researchers, looking at the evidence and trying to come to some conclusions about how strong the links are, what we know and what don’t we know, and what should the research agenda look like. I think that even after that conference the jury is still out as to the extent to which environmental chemicals explain what we are seeing in the general public. But, it’s certainly now very plausible that the environmental chemicals are important contributors and it’s getting a lot of research attention.



ACAM: Would you say that the medical community is then understanding the importance of environmental exposures in the worldwide epidemic of diabetes?

Dr. Schettler: No, because the research interest is coming both from the field of toxicology and epidemiology and I think it’s fair to say that those findings (with certain exceptions obviously) have simply not made their way into mainstream clinical medicine. I would venture to say that many typical clinicians have not even heard of the issue, although it is possible that more have heard of it now because it is making its way into the newspapers a bit. But, the medical journals that clinicians tend to read don’t cover this topic and many other environmental health topics very regularly, so it would be very easy for clinicians to completely miss this unless they happen to be reading a little bit more widely than many clinicians do.

ACAM: You do environmental health work and research on behalf of several organizations. What are you currently working on to spread this important message?

Dr. Schettler: One of the projects that I have been working on for about the last 5 years or so is a report that I co-authored with several colleagues called, Environmental Threats to Healthy Aging. We had looked previously at environmental contaminants and environmental chemicals and how they influence both reproductive health and child development, specifically things like neurological developments in children which prompted our interest in what’s going on in the other end of the lifespan. What do we know or what don’t we know about the effects of environmental variables on older people. And as we got into that literature several things became clear. First was that we needed to have a very expansive view of what the environment is. So, it’s not just environmental chemicals but it’s things like social circumstances, diet, nutrition and so on. If you look at the built environment and whether or not people are living in a place where they can safely walk the streets and get regular exercise will influence whether or not they do get exercise. Secondly, even if we’re interested in the effects of environmental variables on health later in life it turns out that we have to look at the whole lifespan because a lot of what happens early in life, both during fetal development, childhood and early adulthood, influence health status later in life. So, it really ends up requiring a lifespan approach.

We published Environmental Threats to Healthy Aging, which covers a number of chronic diseases and conditions that are prevalent in our time, things like diabetes, cardiovascular disease and cognitive decline - dementia, Alzheimer’s disease and so on. Now we’re working to get this information out into the mainstream through multiple channels; grand rounds presentations to clinicians, getting shorter articles into medical journals, and getting other organizations that are particularly interested and concerned with the health of elders informed and interested in this topic. It’s really a multi-pronged approach to try to get this information out.

ACAM: How did it feel to earn the title of Environmental Health Hero for 2011 from Health Care Without Harm?

Dr. Schettler: It was a great honor and I’m especially grateful because I was chosen by my colleagues. I truly feel that I received the award on behalf of a whole community of people. This work in environmental health is truly community activity without question. We are picking up where people who came before us did, and this work is a collaboration, I think most of us couldn’t accomplish much doing it alone.

It was also an opportunity to reflect on the work that we’ve been doing at Health Care Without Harm to try and improve the environmental performance of the medical industry. Plus a chance to point out that the real gains to be made in terms of reducing the environmental footprint of the medical industry would be keeping people from getting so sick in the first place. We have so many high-tech interventions that we bring to people that are sick with preventable diseases. All the cardiovascular disease, diabetes, many different kinds of cancer, and so on are diseases and disorders that we know an awful lot about how to prevent and by preventing these diseases and conditions we will reduce the need for these high-tech interventions. As we know from the debate that’s going on right now in this country about the need to reform Medicare, it’s because these high-tech interventions are going to break the bank. In addition to the economic impacts are also environmental impacts. All of the surgeries, all of the medical equipment, all of the resources that are used to create that equipment and to use it, to transport it, dispose of it and so forth have a real environmental consequences. So I used this award as an opportunity to talk a little bit about the opportunities for disease prevention. You know, the greenest surgery is the one that’s never done. Just like, the greenest building is the one that’s never built. And we know a lot about how to reduce this demand on expensive healthcare interventions. So I do think that that is a frontier that we need to explore more seriously and more regularly.

This post has not been tagged.

Share |
PermalinkComments (0)
 

The Real Issue with FAT

Posted By Matt Angove, ND, NMD, Monday, October 3, 2011
Updated: Thursday, January 30, 2014

Are your eating habits making you FAT?

For the average "weight loss” specialist, calorie reduction and exercise are the mainstay of their weight loss programs. I think the best word to describe the plight of most people trying to lose weight is FRUSTRATION!

This frustration is due to the fact that the weight loss program being practiced is not going to lead to lasting weight loss. Lasting weight loss or much more importantly FAT loss requires a complete transformation of daily habits. It also necessitates finding the real issue (aka cause) for fat gain.

When it comes to weight loss, you can be so right and yet be completely wrong.

As I have seen it, the focus of people trying to lose weight is set on "low-fat” and "sugar-free” foods. On the label, it looks like a dieters dream but in the body, it is an inflammatory mess. And if the pro-inflammatory effect wasn’t enough, these foods aren’t satiating, and many of them even trigger hunger signals.

Fat cells generate inflammatory chemical messengers (called cytokines), and those chemicals eventually trigger a reaction for cells to stop listening to two important hormones: insulin and leptin.

So, if you are going to bump the FAT forever, you have to get the inflammation under control. Inflammation decreases the cells sensitivity to insulin and leptin.

When cells become resistant to insulin, glucose gets converted into fatty acids and stored as fat instead of being used as energy. NOT WHAT WE ARE LOOKING FOR!

When the hypothalamus becomes resistant to leptin, the hormone that indicates satiety, people will consume more calories than necessary. Also, NOT WHAT WE WANT!

As a dietary starter, this requires eliminating foods that are inflammatory, such as processed sugars, synthetic sweeteners, hydrogenated oils, over-cooked foods, and foods a person is allergic to. You can make it really easy on yourself by simply just eliminating food items that come in a box.

In addition to switching to a whole foods based diet, specific anti-inflammatory nutrients should be added. Omega-3 fatty acids and probiotics should be at the top of the list, as well as magnesium, curcumin, and ginger to name a few.

This is what we call a long-term, sustainable solution!

Tags:  nutrition  weight 

Share |
PermalinkComments (0)
 

Digestive Health = Total Body Health

Posted By Administration, Wednesday, September 28, 2011
Updated: Thursday, January 30, 2014
Most of us don’t pay attention to body processes unless we have annoying or painful symptoms. Let’s take digestion for example: gas and bloating are annoying and abdominal cramping is painful.

According to the American college of Gastroenterology, over 95 million people in the US suffer from some type of digestive problem. Americans spend more than $100 billion annually on over the counter digestive care products. Wait periods for seeing GI specialists are sometimes upwards of 3 months. Frankly speaking, there is a lot of ground to cover when it comes to digestive health. There is the upper GI (stomach & esophagus), lower GI (colon) as well as the Liver and Gallbladder!

The digestive system is responsible for breaking down everything we eat and drink, extracting the vitamins & minerals from it and turning it into energy for the body. This is an amazing and difficult job considering what some of us eat. Nevertheless even with a good diet, over time, the digestive system becomes weak and symptoms can develop. This simply means the digestive system needs a tune up so it can function optimally once again.

A busy life on the run is a strain on digestive function. The digestive system works best when we are relaxed and can peacefully eat and chew our food. This is the parasympathetic nervous system at work which is fondly referred to as "the rest & digest nervous system”. Incidentally this is also the nervous system, which allows us to have a restful sleep. Disturbed digestion often goes in conjunction with disturbed sleep.

Conventional medicine focuses on symptom suppression to treat digestive disorders. We have antacids, anti-diarrheas, bowel relaxers, inflammation blockers, all aimed at quieting the symptoms down. Remember that symptoms are our body’s way of telling us that something is wrong and needs to be fixed. Suppression is not the same as fixing a problem.

Many people have food sensitivities and allergies that put a strain on the digestive system. Two of the most common allergens are gluten and dairy products. Gluten is a protein found in wheat, rye, and barley. It is a sticky substance that helps keep breads moist. Often patients feel better when they avoid gluten and diary products over a period of time. The minimum elimination time is three weeks. This helps de-stress the digestive system and allow it to heal.

For assistance with following a gluten free diet, click here!

Note from Dr. P:
Good digestive health is critical for our overall health.
Based on the above statistics, the American population is suffering from poor digestive health. As digestive health continues to decline, more people will be looking towards natural medicine to support digestive function. Integrative Medicine offers many remedies that have been successfully used for over 100 years focused on restoring and repairing this system. Remember that Integrative natural medicine focuses on treating the cause not suppressing the symptoms, in this way health is restored. Often patients ask me if they will need to take supplements forever. Nothing is forever, because natural medicine treats the cause. Often the digestive system can bounce back without the need to rely on supplements long term.

-Be Happy, Healthy & Holistic

Tags:  Andrea Purcell ND 

Share |
PermalinkComments (0)
 

New ACAM Module: Lab Assessment - Stool Testing

Posted By Administration, Thursday, September 22, 2011
Updated: Thursday, January 30, 2014

Irvine, Calif -- The American College for Advancement in Medicine (ACAM) is pleased to add the Lab Assessment of Stool Analysis for gastrointestinal issues to their curriculum of integrative medicine education.

For the first time ACAM will offer Lab Assessment: Stool Testing at the ACAM Learning Center in Orange County, California, October 21-22, 2011.

"This workshop is a great opportunity for ACAM to assist in the professional development of physicians with the goal of improving patient health,” said Rachel Weaver, Director of Education and Operations for ACAM.

Faculty for this course is made up of physicians and researchers that will work closely with learners to impart skills and strategies for the assessment and treatment of GI health. To register for the course and obtain more information please visit: www.acam.org.

About ACAM: The American College for Advancement in Medicine (ACAM) is a not-for-profit Organization dedicated to educating physicians and other health care professionals on the safe and effective application of integrative medicine. ACAM's healthcare model focuses on prevention of illness and a strive for total wellness. ACAM is the voice of integrative medicine; our goals are to improve physician skills, knowledge and diagnostic procedures as they relate to integrative medicine; to support integrative medicine research; and to provide education on current standard of care as well as additional approaches to patient care.

The ACAM Learning Center is located at:

65 Enterprise, Aliso Viejo, CA 92656

Tags:  gut health 

Share |
PermalinkComments (0)
 

INOSITOL 500 MG 100 Capsule from McGuff

Posted By Administration, Tuesday, September 20, 2011
Updated: Thursday, January 30, 2014

INOSITOL 500 MG 100 CAPSULE

Inositol is prevalent in the heart and brain. It is found in every cell membrane, assists the liver in processing fats, and contributes to the function of muscles and nerves. It is unofficially referred to as "vitamin B 8”. The natural source is usually derived from soy. Ours contain no detectable GMO’s, important for those who wish to avoid genetically modified soy.

  • Mild lipotropic that lowers cholesterol and removes fat from the liver
  • May help treat nerve disorders and improve diabetic neuropathy
  • Has a calming effect, may help those diagnosed with depression, anxiety, and Obsessive Compulsive Disorder (OCD).
  • Can reduce some side effects of lithium without reducing benefits
  • Helps reduce lithium induced psoriasis

Contains no artificial flavors, colors or preservatives; no wheat, gluten, milk, eggs, peanuts, tree nuts, crustacean shellfish or fish.

To view or download a product information sheet: visit:

http://www.mcguffmedical.com/products.aspx?product=5362

Item #: 4626

100 Capsules

Serving Size: 1 Capsule
Servings Per Container: 100


Amount Per Serving

% Daily Value*

Inositol 500 mg*

*Percent Daily Values are based on 2,000 calorie diet.

† Daily Value not established.

Other Ingredients: Rice Flour, Gelatin (capsule) and Magnesium Stearate (vegetable source.)

This post has not been tagged.

Share |
PermalinkComments (0)
 

Mitochondrial Dysfunction

Posted By John Gannage, MD, MCFP, DH, Monday, September 12, 2011
Updated: Thursday, January 30, 2014

I had a patient ask me an interesting question some 6 years ago: "What do you think is the most important medical development that you’ve learned about in the past year?” At the time, because I had just returned from an ACAM conference and heard a presentation by Dr. Michael Holick, MD, I responded: "The importance of Vitamin D deficiency in disease, how human levels are lowered by sunscreen use and sedentary living indoors, and why it is important to keep Vitamin D in a healthy range.” I meant it, so much so it was the cover story of my newsletter back then with the headline "Here Comes the Sun - And I Say It’s Alright!”, but he seemed caught off guard, expecting an innovative surgery or new genetic discovery I suppose. Of course, now the Vitamin D story has been told, the bandwagon has been weighed down with all the converted, and more frequently we are hearing about disease connections related to D deficiency (although I remain cautious about massive oral doses, the subject of another blog perhaps).

What’s my point? Well, I like his question, and ask myself the same one in my head periodically: "What’s an important medical discovery that you’ve learned for yourself recently, John?” I like to answer with a theory or discovery that applies to my daily practice, something measurable and that is changeable - something that affects a cross-section of illness that, when treated, can have a profound impact on human suffering. My answer is the subject of today’s blog: mitochondrial dysfunction, its impact on disease, and what I’ve discovered can be done about it in my patient population. I present some concepts in simplistic form.

I sketched the mitochondrion in Cell Biology on a large bristol board in 2nd Year University. I loved studying the cell back then, adored biology, and spent countless hours perfecting my drawing of a human cell. It’s ironic that 25 years later I’m writing about this cell organelle as a medical doctor (and looking at cells every day under a microscope!)

The mitochondria are the little power plants suspended in each cell alongside other cell parts like the nucleus. There may be 2500 of them in a single cell (except RBC’S). An important mitochondria task is to make the energy used to power cell functions, and in turn required by tissues and organs for proper functioning. They are important for brain, muscle and heart function in particular, as these organs utilize the most energy. On the folded membranes and in the matrix of a mitochondrion, units of energy are made after conversion from foods we eat, in a cascading of biochemistry known as Krebs Cycle and the electron transport chain. Nutrients are needed as cofactors in the cycle, oxygen is required, and contaminants like mercury, lead or pesticides can damage the membranes such that the processes slow down, energy is depleted and/or cells die. This in turn leads to poorly functioning organs. For the brain, this means impaired learning, decreased executive functioning, poor attention, speech and language dysfunction, and so on. This occurs because the brain disproportionately requires more energy and oxygen than the other organs do.

What’s interesting about mitochondria, as Figure 1 shows, is the presence of its own DNA, separate from the DNA housed in the nucleus of the cell. Mitochondrial DNA can mutate and be damaged, in a fashion that impacts energy production, by toxins, viruses or radiation. An important process in DNA damage and membrane leakage, leading to cell damage and death, is oxidative stress - accelerated by pollution of all kinds, and exacerbated by antioxidant deficiencies.

In my medical clinic, the practical application of these concepts translates first into a requirement to test for mitochondrial dysfunction, as I seek to manage developmental issues in children, particularly autism and global developmental delay. And just like my testing of Vitamin D, when I too often found easily correctable deficiency, I often discover evidence for mitochondrial dysfunction in children with neurodevelopmental issues. The next step is to provide the nutrient co-factors that improve energy production in the brain and muscle, while simultaneously addressing pro-oxidant exposure in a child’s diet, intestinal and other tissues, home, and immediate environment. The mitochondria can be sped up, protected from damage, or increased in numbers to meet energy demands in vital organs like the brain. The results I’ve observed to date include: improved cognitive functioning, increased endurance, better muscle tone, and more easily attainable developmental milestones.

Just like the Vitamin D story, starting out as an alternative view prior to becoming conventional practice, mainstream medicine will look to the mitochondria in the future to explain autism and other neurologic diseases, like Parkinson’s Disease, syndromes like Chronic Fatigue and Fibromyalgia, and I suspect cardiac cases as well. It is a fruitful place to look, since it explains what I have always felt to be true: that much human illness, organ dysfunction and premature aging occur at the interface between nutrient deficiency and toxic overload, with this organelle’s dysfunction acting as a major player.

This post has not been tagged.

Share |
PermalinkComments (0)
 

B Vitamin May be of Value in Ovarian Cancer and Breast Cancer

Posted By Nalini Chilkov, LAC, OMD, Thursday, September 8, 2011
Updated: Thursday, January 30, 2014

Niacinamide, a B Vitamin, may be of value to women with genetic risk of Breast Cancer and Ovarian Cancer.

Why are some women more prone to developing breast cancer and ovarian cancer? This is a complex question. Every person and every cancer constitute a unique and complex set of contributing factors.

One factor, related to genetics, is the inability to repair damaged DNA(damaged genetic material inside the cell) effectively. Damaged DNA, like damaged software, will send out incorrect operating instructions to the cells in our body. This can lead to uncontrolled growth and the development of cancerous tumor cells.

For those patients with genetics that lead to inefficient and poor DNA repair who are therefore at high risk for aggressive cancers there is a new class of drugs called "PARP inhibitors” undergoing research and approval. While waiting for PARP inhibitor drugs to finally be approved and available studies have demonstrated that the B vitamin Niacinamidealso acts as a PARP inhibitor in doses that yield a pharmacologic effect. Studies used 1.5 grams (1500 mg) three times daily. PARP inhibition allows damaged DNA in the cell to be repaired. Cells with damaged DNA are prone to develop into malignant cancerous cells.*

Women who are positive for the BRCA1 gene are known to have poor DNA repair. These women may benefit from PARP inhibitors. BRCA1 is associated with aggressive and often lethal breast cancer as well as colon cancer.

Recently another gene associated with poor DNA repair has been identified.This gene, RAD51D,is associated with increased risk for ovarian cancer. PARP Inhibitor drugs as well as Niacinamide may also be of value to these women.

Here is an excerpt from article that appeared in Reuters Mon, Aug 8 2011By Kate Kelland LONDON (Reuters) – Women who carry a faulty copy of a gene called RAS51D have an almost one in 11 chance of developing ovarian cancer,scientists said on Sunday in a finding they called the most significant ovarian cancer gene discovery for more than 10 years.

Tests to identify those at highest risk are expected to be available within a few years, according to Cancer Research UK, and may lead some women to decide to have their ovaries removed in order to beat the disease.

The finding should also speed the search for new drugs.

Laboratory experiments already suggest that cells with faulty RAD51D are sensitive to PARP inhibitors – a new class of drugs designed to target cancers caused by faults in two known breast and ovarian cancer genes, BRCA1and BRCA2.

For the latest study, researchers from Britain’s Institute of Cancer Research compared the DNA of women from 911 families with ovarian and breast cancer to DNA from a control group of more than 10,000 people from the general population.

"Women with a fault in the RAD51D gene have a one in 11 chance of developing ovarian cancer,” said Nazneen Rahman of the Institute of Cancer Research and The Royal Marsden in London, who led the study and published its findings in the journal Nature Genetics.

Ovarian cancer can remain hidden for a long time and thus is often not discovered until it is advanced.

An estimated 230,000 women worldwide are diagnosed with ovarian cancer each year. Most are not diagnosed before the cancer has spread, and up to 70 percent of them die within five years.

Speaking to Reuters in a telephone interview she said the identification of RAD51D pointed to PARP inhibitors as a new class of drugs that might offer fresh hope. Initial tests in the laboratory found that cells with faulty RAD51D were highly sensitive to this class of drugs.

"PARP inhibitors work because they were designed to target DNA repair pathways,” she said. "They haven’t been used in patients in that context yet but we would predict they would behave in the same way.”

SOURCE: bit.ly/rdeooV Nature Genetics, online August 7, 2011.© Thomson Reuters 2011. All rights reserved.

*Niacinamide Monograph Alternative Medicine Review December 2002

Always consult your physician regarding any nutritional program. These statements have not been approved by the FDA and do not constitute medical advice or treatment which is between you and your physician.

Tags:  cancer  nutrition 

Share |
PermalinkComments (0)
 

Rachel Weaver named Director of Education and Operations

Posted By Administration, Tuesday, September 6, 2011
Updated: Thursday, January 30, 2014

IRVINE, California—September 6, 2011—ACAM's Executive Committee today announced that Drew McGray has resigned as Director of Marketing and Operations, and the Board has named Rachel Weaver, previously ACAM's Education and Compliance Manager, as his successor.

Drew will continue to serve the Organization in a marketing - consulting capacity and will advise ACAM's marketing team as needed.

"We are deeply grateful for his contributions to ACAM’s mission of advancing education in the practice of medicine. He will be sorely missed. He has however assembled a very competent team and we look forward to working to bring ACAM to its next level of greatness,” said Neal Speight, ACAM's President-Elect on behalf of the Executive Committee.

"We have complete confidence that Rachel is the right person to continue ACAM's forward momentum. She is an accomplished businesswoman with demonstrated leadership ability andexercisessound judgment." Said Jeffrey Morrison, CFO of ACAM. "We are excited for ACAM's forward-looking outlook," he added.

As part of ACAM's succession plan, Megan Marburger, previously ACAM's Events Manager, will oversee sales and marketing. Megan's diverse industry experience places her as the ideal candidate for this position.

As ACAM's Education Program Manager, Rachel is responsible for the Organization's global education and curriculum development. She has a five-year history with ACAM and has produced 12 educational events, many of which were planned in accordance with ACCME Policies and Procedures and were eligible forAMA PRA Category 1 Credit (TM).Rachel is well-versed in regulatory compliance, educational design, and department management.

About ACAM:

The American College for Advancement in Medicine (ACAM) is a not-for-profitOrganizationdedicated to educating physicians and other health care professionals on thesafe and effective application of integrativemedicine. ACAM's healthcare model focuses on prevention of illness and a strive for total wellness. ACAM is the voice of integrative medicine; our goals are to improve physician skills, knowledge and diagnostic procedures as they relate to integrative medicine; to support integrative medicine research; and to provide education on current standard of care as well as additional approaches to patient care.

ACAM enables members of the public toconnect with physicianswho take an integrative approach to patient care and empowers individuals with informationabout integrative medicine treatment options.

Celebrating more than a quarter century of service, ACAM represents more than 1,500 physicians in 30 countries. ACAM is the premier organization of its kind in the world dedicated exclusively to serving the needs of the integrative medicine industry.

Contact:

Corporate Communications - Michelle Schiavo
michelle.schiavo@acam.org
949.309.3520

Tags:  welcome 

Share |
PermalinkComments (0)
 

The ACAM Store is Now Open

Posted By Administration, Thursday, September 1, 2011
Updated: Thursday, January 30, 2014

Irvine, Calif -- The American College for Advancement in Medicine (ACAM) is excited to announce the grand opening of the ACAM Store on the ACAM website (www.acam.org).

Guests may browse the ACAM Store for Protocols, Syllabi and ACAM Logowear. The store's current Featured Product is The Definitive Guide for Intravenous Therapy with Nutrients, written by W.A. Shrader, Jr., MD. The book includes an overview ofIV therapies, calculation of osmolarity, specific protocols, and waiver forms.

"We're thrilled to expand our options for allowing physicians to acquire the resources they need for professional development," said Drew McGray, Director of Marketing and Operations for ACAM.

Look for the ACAM Store at www.acam.org under Health Resources.

About ACAM:The American College for Advancement in Medicine (ACAM) is a not-for-profit Organization dedicated to educating physicians and other health care professionals on the safe and effective application of integrative medicine. ACAM's healthcare model focuses on prevention of illness and a strive for total wellness. ACAM is the voice of integrative medicine; our goals are to improve physician skills, knowledge and diagnostic procedures as they relate to integrative medicine; to support integrative medicine research; and to provide education on current standard of care as well as additional approaches to patient care.

Tags:  education 

Share |
PermalinkComments (0)
 

The Most Important Intracellular Antioxidant

Posted By Matt Angove, ND, NMD, Wednesday, August 24, 2011
Updated: Thursday, January 30, 2014

It is the most important antioxidant inside the human cell!

It is the measure used by scientists to indicate cellular health. According to Dr. David Perlmutter, MD who is an innovate expert in neurological disorders, glutathione leads the charge in brain research around the world.

Glutathione regenerates a popular antioxidant most people have heard of, Vitamin C. Vitamin C then works to recycle a fat-soluble brain friendly antioxidant Vitamin E and the cycle continues. Vitamin C is no doubt an extraordinary nutrient that every human would do well to take regularly. However,vitamin C works its magic outside of the cell whereas glutathione exerts its life sustaining effects inside the cell.

Fibromyalgiais a condition of severe mitochondrial dysfunction. Your mitochondria are the energy hub of every cell. They literally provide the currency by which you go about living, laughing and eating broccoli. In this condition, it is as if maple syrup has been poured over the mitochondria, making them slow and sluggish (think: a broken ATM or one with a line around the corner and you have a "hot” date waiting). This leads to massive fatigue and chronic unremitting muscle pain as toxins are not able to be cleared from cells. Glutathione just happens to be a potent enabler of mitochondrial function! Consider glutathione as the gold backing your mitochondrial money factory.

This tripeptide likes to have its hands in everything!

It functions in the synthesis, protection and repair of DNA (keeps you from getting cancer). It is also present for the synthesis of proteins, the transport of amino acids (so you can build and repair damaged tissue), the elimination of heavy metals, the removal of toxins and carcinogens and on the side, it enhances natural killer cell activity (helps find and fight cancer if you have it). Glutathione is structurally unusual, which allows it to react with would be "bad guys” keeping them from harming your cells.

Glutathione also resides over the activation of enzymes, which are considered the fire of cellular life. Free radical damage is the foundation of all degenerative disease and LOW glutathione is the enabler of free radical damage. Hence the aging process..

That said, it is no wonder whyglutathione is paramount for optimal mitochondrial functioning.

Tags:  glutathione  neurology 

Share |
PermalinkComments (0)
 

Tips for Healthy Eating

Posted By Andrea Purcell, ND, Tuesday, August 16, 2011
Updated: Thursday, January 30, 2014
Many of the patients who come to me initially do not have good diets. They may be too busy to shop and prepare meals, or not know how to prepare healthy food on the go. By the time someone ends up in my office they have a medical necessity and are in desperate need of a dietary turnaround for their health.

If someone has been eating poorly, I try to make food adjustments that are better but not perfect so as not to overwhelm him or her. In light of that attempt on my part, occasionally when I present a person with an individualized food plan they may become overwhelmed. This depends on the individual. For some, dietary changes are exciting and for others they can be down right daunting.

In this blog I am enclosing my 8 food tips to help someone shift towards a new dietary practice. Read on…

1) Start slowly: Read over the entire food plan and go on a shopping field trip to the local health food store, farmers market, or Trader Joes. Browse through the aisles; compare what the plan says to what you see on the shelves. Check out the vegetables, which ones would you normally bring home, try something different.
2) Focus on breakfast: Read the food plan and incorporate changes to your typical breakfast routine each morning during week one. Do not change lunch or dinner until the following week. Really work at becoming familiar with your new breakfast routine.
3) Simple and delicious: Keep meals simple but hearty. For example plain quinoa flakes can be dressed up with chopped apple, walnuts, flax seeds, stevia and cinnamon.
4) Invest in a good cookbook: Check out my cookbook,Feed your Cells!What can I say I’m biased, for years my patients asked me to recommend a good cookbook and I couldn’t so I wrote my own.
5) Get Inspired! Ever go to a restaurant, have a fantastic meal and try to re-create it at home? Well do it!
6) Think Positive: Instead of feeling deprived, think about how all of the new adventures in vegetables that you are having is helping your body to detoxify and ward off cancer.
7) Make one meal go a long way. You will read about this in my cookbook but there should always be leftovers for lunch. I will cook a pot of lentils on a Sunday and have them over quinoa and spinach for breakfast and lunch for two days in a row. That saves a LOT of time.
8) Transition from fake to real. Ask yourself does this food grow out in nature? Have I seen this food on a farm? If the answer is yes, then it is probably real. Real food gives us life.

Note from Dr. P:
Remember when you were a kid and learning to ride a bicycle? You didn’t ride that bicycle perfect the first time you tried. For some reason when we become adults we do not give ourselves the compassion of trial and error. We become impatient with ourselves when something is difficult. Healthy eating is a necessity, you pay now or you pay later. When you are ready to embrace good health, the path reveals itself. Adapting to a new way of eating and adopting new food behaviors take time. Try to break it down into bite size pieces and before you know it you will be shopping, cooking, and eating healthy, nutritious food. Looking for healthy recipes?Buy my book!

-Be Healthy, Happy & Holistic

Tags:  health  nutrition  weight 

Share |
PermalinkComments (0)
 

A Comprehensive Review of the Safety and Efficacy of Bioidentical Hormones

Posted By Deborah Moskowit, ND, Thursday, August 11, 2011
Updated: Thursday, January 30, 2014

Abstract

Numerous forms of estrogens and progestins are utilized for the treatment of menopausal complaints and associated conditions that occur temporally. Although known to be different with respect to molecular structure, receptor affinity, metabolism, and other physiological traits, most have been treated as if they were clinically identical. The majority of these hormone preparations, commonly referred to as hormone replacement therapy (HRT), should perhaps be more aptly referred to as hormone substitution therapy, as most of the therapies utilized do not exactly match those produced in the body.Research indicates these synthetic hormones vary clinically in safety and efficacy. As such,women and their physicians have, in increasing numbers, been opting for the use of bioidentical hormones; i.e., those that match the structure and function of hormones produced in the body.With greater utilization and research surrounding bioidentical hormones, the differences can now begin to be fully assessed and appreciated. This article reviews the disparities between synthetic and bioidentical estrogens and progestins/progesterone with respect to safety and efficacy;special attention is devoted to clinical outcomes in the breast, endometrium, bone, cardiovascular system, and brain. The studies reviewed suggest bioidentical progesterone does not have a negative effect on blood lipids or vasculature as do many synthetic progestins, and may carry less risk with respect to breast cancer incidence. Studies of both bioidentical estrogens and progesterone suggest a reduced risk of blood clots compared to nonbioidentical preparations. Bioidentical hormone preparations have demonstrated effectiveness in addressing menopausal symptoms. The author advocates for continued research on bioidentical hormones and concludes there is  currently sufficient evidence to support their preferred use over that of their synthetic cousins.(Altern Med Rev 2006;11(3):208-223)

Introduction

Over the last decade, women and their physicians have in increasing numbers been opting for the use of natural, bioidentical hormones for treatment of symptoms of menopause and to support bone and heart health. (1) The trend away from the use of conventional synthetic hormones, toward those specifically matching the hormones produced in humans (bioidentical)has been driven by several factors, including a global trend toward everything "natural” as seen in the increased interest in organic foods and complementary and alternative medicine (CAM). Perhaps the most significant factor driving the increased interest in bioidentical hormones is the rising fear or suspicion of the "synthetic” hormones used in conventional hormone replacement therapy (HRT). Over the last decade, research-based media reports of risks associated with conventional HRT have prompted women’s concerns and altered the approach to hormone use. (2,3) This has been most evident following the results of the U.S. government-sponsored Women’s Health Initiative (WHI) study in 2002. The WHI study results led to the conclusion of experts in the field that the risk of using conventional HRT (non-bioidentical hormones), specifically Premarin®and Provera®, outweighed the benefits provided. (4) This report was followed by a significant decline in the use of synthetic hormones at menopause, and a growing number of women and their physicians utilizing and advocating the use of bioidentical hormones. The question, without the value of a similar long-term study looking at bioidentical hormones, is whether or not the evidence exists to support their preferred use over their synthetic cousins.

Hormone Changes Surrounding Natural (Non-induced) Menopause

Menopause is defined as the cessation of menstruation occurring as a result of the loss of ovarian follicular activity. At birth, a woman has a million eggs, by puberty a mere 300,000. This loss of eggs is referred to as atresia, a natural, albeit incompletely understood, process whereby the follicles enter an incomplete growth phase. This process continues throughout a woman’s life. Thousands of follicles are lost to atresia compared to one or a few lost each month to ovulation. As a woman ages and as a result of the decreasing follicles, follicle-stimulating hormone (FSH) levels gradually increase and the cycle begins to shift, with a shortening of the follicular phase that can begin as early as a woman’s 20s. (5,6) In the 10-15 years prior to menopause, this rate of follicular atresia begins to accelerate. (7,8) Perimenopause is the term used to describe the time of transition between a woman’s reproductive years and cessation of menstruation. Typically perimenopause occurs between the ages of 40 and 51 and can last anywhere from six months to 10 years. During this time, hormone levels fluctuate and decline naturally, although not necessarily in an orderly manner.

Perimenopause often begins with an alteration in cycle and bleeding regularity due to fluctuatin ghormones, anovulatory cycles, and changes in timing of ovulation. Cycles may be long or short, ovulatory or anovulatory. (8) Even women who cycle regularly during perimenopause can have significant variability in hormone levels. (7) Progesterone levels drop with anovulatory cycles and a decline in luteal function.Estrogen levels fluctuate in response to rising FSHlevels and provide feedback inhibition to FSH. (6) Significant variability may occur in estradiol and inhibin (a hormone that inhibits FSH), and gonadotropins may rise abruptly. (5,6,9) Testosterone levels decline with age and do not appear to change significantly with natural menopause. By menopause, few follicles remain, yet intermittent estradiol production from the ovaries may still occur. (8,9) Adrenal androstenedione is the primary source of estrogen after menopause; sex hormone-binding globulin falls slightly. (10) FSH levels remain high for several years after menopause, after which levels decline considerably. (10,11)

Although FSH is commonly used, there are no consistently reliable endocrine markers to establish a woman’s menopausal status. (9) Shifts in hormones contribute significantly to a sense of physical,mental, and emotional imbalance that may characterize a woman’s experience of menopause. As a clinician, it is important to note the changes that occur,link them to the physiology of the various hormones,and address imbalances individually. Addressing other aspects of endocrine health is also necessary and may involve assessing adrenal and liver function, as well as diet, exercise, and other lifestyle factors.

Problems with Conventional HRT

In July 2002, after determining that estrogen in combination with progestin increased a woman’s risk of breast cancer, coronary events, stroke, and blood clots, the National Institutes of Health (NIH)prematurely halted the first part of the WHI, a study designed to identify the risks and benefits associated with long-term hormone use. In this study, 16,608healthy postmenopausal women with a uterus, ages50-79, were randomized to either test or placebo group. (4) The test group received a combination of equine estrogen and synthetic progestin (PremPro®);no bioidentical hormones were used. At the time the study was halted, PremPro compared to placebo resulted in:

  • t26-percent increased risk of invasive breast cancer (eight additional cases per 10,000 women per year);
  • t29-percent increased risk of myocardial infarction (MI) or death from coronary heart disease (CHD) (seven additional cases per 10,000 women per year);
  • t41-percent increased risk of stroke (eight additional cases per 10,000 women per year);and
  • t200-percent increased risk of blood clots (18 additional cases per 10,000 women per year).
  • The WHI study also confirmed benefits seen in previous studies, most notably:
  • t33-percent decreased risk of hip fracture (five fewer fractures per 10,000 women per year);
  • t37-percent decreased risk of colorectal cancer (six fewer cases per 10,000 women per year); and
  • tRelief of menopausal symptoms like hot flashes and vaginal atrophy.

An ancillary study the following year, the Women’s Health Initiative Memory Study (WHIMS),demonstrated additional risks for women on combination equine estrogens and synthetic progestins. The study found combination therapy doubled the risk of developing dementia in women age 65 and older. (12)

Even prior to the WHI and WHIMS studies,relatively few women who might benefit from HRT chose to use it, despite the previous findings that HRT has established benefits for the treatment of menopausal complaints, reduction in bone loss, and some beneficial effects on the cardiovascular system. (13-15) In addition, women prescribed HRT often discontinue it before long-term benefits are realized. The most common reasons for discontinuation of HRT are unwanted side effects and weight gain, with one-third to two-thirds of women discontinuing it within the first two years. (13,14,16-18) Most side effects are attributed to the synthetic progestin portion of HRT, with the most common complaints being bloating, breast tenderness, and irregular bleeding. (13,14,19) Secondary reasons for discontinuation include fear of cancer and recommendation by a physician.

For women not initiating HRT, reasons cited include: HRT perceived as unnecessary, a preference to not take medications, a fear of the effects of long-term HRT, confusion over the scientific information as presented in the media, and the view that menopause is a natural event. (2,3,14,20) Use of HRT was correlated with older women’s wishes to reduce osteoporosis risk, while younger women sought relief from menopausal symptoms, predominantly vasomotor flushing. (2,19) Given this information, it should follow that utilizing hormones that have fewer side effects andrisks, correlate with a woman’s perception of "natural,” and address long-term health benefits could increase hormone use and therefore improve a woman’shealth and well-being. Bioidentical hormones mayprovide these benefits.

What is Bioidentical HormoneTherapy?

Bioidentical hormones are identical to hormones produced endogenously. In the case of HRT,these include estrone (E1), estradiol (E2), estriol(E3), and progesterone (P4). Although bioidenticalhormones have long been utilized in other countries,the United States has predominantly used non-bioidentical hormones for the past 40-45 years, beginning with the introduction of oral contraceptives inthe early 1960s.

The differences in the actions, risks, and benefits of various hormones depend on numerous factors, including method of administration, absorption,bioavailability, metabolism, receptor affinity, receptor specificity, and molecular structure. (21,22)

Bioidentical versus SyntheticEstrogens

The body naturally produces three mainforms of estrogen: estrone, estradiol, and estriol. Bioidentical estrogens are molecularly identical to these naturally produced estrogens. Synthesized in the ovaries and metabolized in the liver, estradiol is the mostphysiologically active form of estrogen. Increased serum estradiol levels are linked to an increased risk ofbreast and endometrial cancer. (23) Estrone is converted reversibly from estradiol in the liver and small intestine and increases after menopause when the adrenalglands play a more prominent role than the ovaries inhormone synthesis. Like estradiol, increased estronelevels are linked to an increased risk of estrogen-receptor positive (ER+) breast cancer and an increase in breast density, an independent risk factor for breast

Table 1. Synthetic and Bioidentical Estrogen Preparations Available in the United States

Table1
Table 2. Synthetic Progestin and Bioidentical Progesterone Preparations Available in the United States

Table2
cancer. (24,25) Both estradiol and estrone can be metabolized to estriol, which is the primary urinary metabolite. Estriol is considered the "weakest” estrogen, as it has a shorter-acting effect than estradiol or estrone. (26) However, depending on sufficient dosing and route of application, estriol can attain a full estrogenic effecton target tissue, such as the vaginal mucosa. (26) Estriolremains intact when supplemented orally (i.e., unlike estradiol, estriol is not converted to estrone, nor is it converted to estradiol). (27) In Europe and China, estriolis commonly used for HRT. A comprehensive review of the safety and efficacy of estriol suggests it maybe safer than estrone or estradiol, but can still have a stimulatory action on the endometrium and breastwhen given in high doses. (28)

In a comparison of bioidentical (estropipate,estradiol) versus non-bioidentical estrogens (ethinylestradiol, conjugated equine estrogens, diethylstilbestrol), non-bioidentical estrogens had significantly exaggerated responses across multiple hepatic and non-hepatic measures of estrogenic effects. (29)

The predominant estrogen currently prescribed in the United States is Premarin, a brand name for conjugated equine estrogens (CEE). Premarincontains approximately 100 distinctly different estrogens, mainly estrone sulfate, equilins, equilenins, and alpha-estradiol, all of which are estrogens occurring naturally in horses; with few natural to the human body. Over 30-percent drop in sales revenues from both Premarin and PremPro occurred following reports of the WHI study. (30)

Many estrogen formulations presently available in the United States contain bioidentical estrogens (Table 1). A growing number of conventional and CAM physicians are now prescribing "Tri-Est,”or "Bi-Est,” nicknames given to individually-compounded formulations of estriol, estrone and estradiol, or estriol and estradiol, respectively. Licensed pharmacists can fill a doctor’s prescription for these combinations of natural estrogens in a variety of doses and delivery systems to specifically address patient needs.

Natural Progesterone versus Synthetic Progestins

Inconsistency in use of the terms "progesterone,” "progestin,” and "progestogen” has led to confusion over these substances. Progesterone refers to a single (note the "one” at the end of the term)molecular structure that is identical to the progesterone molecule that the body makes, also referred to biochemically as "P4.” Progestogen is the category of hormone molecules (natural and synthetic) that act like progesterone in the uterus. Progestin generally refers to synthetic progestogens. See Table 2 for a list of commonly prescribed progestogens.

Progesterone was originally procured by extraction methods from animal placenta. Natural progesterone products today are produced in a laboratory setting via a process designated as the "Marker Degradation” from saponins found in soy and Dioscoreavillosa (wild yam). Hudson presents a detailed historic perspective of the series of events surrounding the discovery of this process. (31)

Progesterone was first used as HRT in 1934for the treatment of ovariectomized women. (32) Due to significant first-pass effect of progesterone, synthetic progestins were developed in the 1940s, either fromprogesterone (e.g., medroxyprogesterone acetate) or from testosterone (e.g., 19-nortestosterone). (33) Progestins mimic the body’s progesterone closely enough to bind to progesterone receptor sites, but do not deliver the full range of "messages” a natural progesterone molecule does. A synthetic progestin, for example,may have similar effects on the endometrium, yet can initiate widely different actions elsewhere in the body (e.g., brain, mineralocorticoid receptors, etc.)depending on the classification of the particular progestin (nortestosterone derivatives, ethyl-13 derivatives, progesterone derivatives, or norprogesterone derivatives.) (34,35) These different progestins have been mapped as to affinity to androgen, progesterone,glucocorticoid, and estrogen receptors. (36) In contrast to progesterone, 19-nortestosterone derivatives are known to have estrogenic properties, which could be attributed to their estrane structure (an 18-carbon tetracyclic hydrocarbon nucleus that is the parent structure to all estrogens) or to the production of estrogenas a metabolite. (37) Derivatives of 19-nortestosteronehave been shown to increase the growth of ER+breast cancer cells in vitro. (38) A paper published in 2000 discussed the development of newer synthetic progestins that more closely fit the profile of bioidentical progesterone. (39)

Estrogen, Progesterone, or Both?

Current recommendations from the American College of Obstetricians and Gynecologists suggest that estrogens be prescribed in conjunction with progestins (to prevent endometrial hyperplasia) when a woman has an intact uterus; (40) conversely, unopposed estrogens are the norm post-hysterectomy. Although progesterone and estrogen receptors both exist in tissue outside the uterus, it has not been thought necessary to provide progestins after the uterus is removed.

In contrast, when using natural hormones,many physicians consider the concomitant use of progesterone with estrogen to be an important aspect of bioidentical hormone therapy and hormonal balancing. The growing research on the synergism of thesetwo hormones, as well as an expanded understanding of progesterone’s effect in the body, are prompting some to recommend these hormones be prescribed together, regardless of the presence or absence of auterus. (41,42)

When considering estrogen replacement during perimenopause and early menopause, thelevel of endogenous estrogen production must also be considered, since elevated FSH levels can be associated with either increased or decreased levels of estrogen. (9,11) Since progesterone levels can fall first with the advent of an ovulatory cycles, some women may do well with progesterone-only supplementation during perimenopause, which may help balance the effects of unopposed endogenous estrogen production. FSH, although commonly used as a diagnostic indicator of menopause, may not be the most reliable tool for determining estrogen needs perimenopausally. (9) One should also note that women with a greater amount of body fat can produce a significant amount of endogenous estrogen postmenopausally. This can occur exclusively through aromatization of estrogen sfrom adrenal and rostenedione by the fat cells. (10) In one study, 10-15 percent of postmenopausal women produced enough estrogen to build the endometrial lining, further emphasizing the need to determine individually the potential hormonal needs of each woman during the climacteric.

Hormone Synergy

Hormone function can be affected by the presence of other hormones, as is seen in the synergistic effects of E2 and P4. (41,43) Even the receptors can exhibit synergism, although the exact mechanisms have not been fully elucidated. (44,45) An example of this phenomenon in clinical practice is the synergistic antiovulatory effects of estrogen and progestogens resulting in efficacy of lower-dose oral contraceptives equal to that of higher-dose regimens. More recently,a study found estradiol in combination with progesterone inhibited bone resorption to a greater degree than either hormone alone. (46)

Differences in Hormone Delivery

Continuous versus Pulsed Delivery

There is sufficient evidence to suggest the pulsatile delivery of estrogen and progesterone that occurs naturally serves to enhance the functioning of these hormones in the body. (47-49) In theory, continuous application of hormones may serve to down-regulate receptors, contributing to a general decrease in the activity of those particular hormones. Research has demonstrated that sequential pulsed estrogen and progestin therapy allows for smaller amounts of hormones to be used. (47) Reduced dosage would translate to reduced likelihood of unwanted side effects as well as a reduced impact on the liver via metabolism of supplemented hormones. This also supports the most recent U.S. Food and Drug Administration recommendation surrounding hormone therapy for women that advocates using the lowest effective dose for the least amount of time necessary. (50)

Routes of Administration

Many different routes of delivery are available for natural hormones, including oral, transdermal (patch), percutaneous (cream, gel), intramuscular(IM), subcutaneous, sublingual, vaginal (gels, cream,tablet, ring, and pessary), and nasal. The route of administration can confer differences in absorption,metabolic pathway, and bioavailability. In general,the oral route leads to more rapid metabolism and a greater impact on hepatic processes, requiring larger doses than those bypassing the entero-hepatic circulation. The same sized doses of progesterone and estradiol resulted in greater circulating blood levels when delivered vaginally compared to oral administration, due to entero-hepatic metabolism. (51) In comparing different E2 delivery systems, percutaneous, transdermal, and vaginal delivery resulted in a reduction in metabolism to E1 via the entero-hepatic circulation. (51-53) Side effects common with oral E2 were not seen when administration was via the percutaneous or transdermal routes. (54,55)

Approximately 90 percent of oral progesterone is metabolized by the "first pass effect” (caused by shunting through the entero-hepatic circulation),leading to difficulties in dosing as well as an abrupt increase in 5-alpha-progesterone metabolites. (56) Oralprogesterone administration resulted in higher levels of progesterone metabolites (deoxycorticosterone, deoxycorticosterone sulfate, and 5-alpha and betapregnenolone) when compared to vaginal administration. (51-57) A study by Hermann et al compared 80 mg progesterone daily via a topical cream (Pro-Gest®)to 200 mg oral micronized progesterone (OMP) as Prometrium®daily and found no difference between the two products with respect to steady-state blood levels of progesterone as measured by area under thecurve (AUC). (58) In another comparison study, similar endpoints were achieved with 300 mg oral micronized progesterone and 90 mg vaginal progesterone,with fewer side effects of drowsiness noted with the vaginal application (an effect attributed to 5-alphaand beta metabolites of progesterone). (59)

It is important to note that progesterone and its metabolites have differing effects in the brain,uterus, smooth muscle, and oocyte. (60) For example,depressive effects of progesterone are predominantly attributed to pregnane metabolites, such as allopregnanolone, as opposed to progesterone itself. Given the increase in metabolites seen with OMP, vaginalor topical delivery systems may reduce expression of side effects attributed to these metabolites.

Because numerous factors can influence intestinal absorption and metabolism, some preparations may have more variable effects. In a study of the pharmacokinetics of oral versus IM administration ofE2, 4 mg IM demonstrated a rate of release into the bloodstream that achieved therapeutic levels over 2-4weeks (depot effect). To achieve the same therapeutic equivalency with an oral dose, some individuals required as much as 2 mg daily for three weeks. (61)

Oral micronized progesterone also exhibits substantial variability in absorption among individuals. In one study, maximum serum concentration ranged from 15.72-625.98 ng/mL, following a single300 mg dose; the authors also noted that absorption increased with age. (62) In a separate study of percutaneous absorption of a progesterone cream, the authors reported moderate variability among individuals. (63)

Forms of Administration

The base of a cream, gel, or suppository can also affect absorption. In a study of topical applications comparing progesterone in a hydrophilic gel, lipophilic base, and emulsion-type base, (64) the emulsion-type base led to a two-fold greater AUC and peak plasma concentration than either the hydrophilicgel or lipophilic base. (64) Another study by the same authors comparing two suppository bases found anemulsion-type base resulted in improved pharmaceutical availability when compared to a lipophilic baseof cocoa butter. (65) A comparison between the percutaneous and vaginal delivery systems found the elimination half-life for the three transdermal forms ofprogesterone was in the range of 30-40 hours, (64) compared to the cocoa butter vaginal suppository with anelimination half-life of 9-10 hours and the emulsionbased suppository with an average elimination halflife of 14 hours. (65)

Physiological levels of serum progesteronewere reached via a novel nasal spray application. (66) Also unique is an effervescent progesterone vaginaltablet that results in adequate serum progesterone levels. In this study there was significant age-related difference in time of maximum concentration (Tmax),with women over 40 years attaining a lower Tmaxthan younger women. (67)

Given the differences that abound in both thetype and route for administration of hormones, physicians should assess an individual woman’s need forhormone therapy and tailor the regimen to her needs.

Effect of Hormones on theCardiovascular and EndocrineSystems

Hormones have multiple effects on the cardiovascular and endocrine systems, including eliciting actions on blood pressure, vascular tone, hemostasis, lipid metabolism, cardiac vasospasm, andglucose metabolism.

Blood Pressure Effects

Progesterone antagonizes mineralocorticoidssuch as aldosterone. Since aldosterone enhances sodium retention and potassium loss via the urine, antagonism of this effect results in increased sodiumexcretion in the urine. This effect on sodium loss hasbeen shown to reduce blood pressure in hypertensivepatients in some studies, as well as ease symptoms ofwater retention. (68,69) This anti-mineralocorticoid effectis not seen with the majority of available syntheticprogestins. Moreover, some progestins enhance estrogen activity, contributing to the potential for increased blood pressure. (70,71)

In normotensive patients, progesterone candecrease sympathetic vascular tone, without concomitant drop in blood pressure. (72) Progesterone acts viathe nitric oxide pathway to enhance vasodilation andimprove microcirculation. (73,74) In animal studies, endogenous and low-dose parenteral E2 have also beenshown to increase vasodilation. (70)

Blood Clots

Estrogen replacement therapy is known toincrease the risk of blood clots. High-dose estrogens,especially synthetic and oral estrogens, increase liverprotein synthesis, including coagulation factors. Oralestrogens also increase angiotensin, and may raiseblood pressure and stroke risk in susceptible women. (70) In a randomized crossover study, estriol did notaffect hemostatic function, whereas ethinyl estradioldecreased prothrombin time while increasing plasminogen and factor VII. (75) In the WHI study, CEEwith medroxyprogesterone acetate (MPA) was shownto increase blood-clotting events. (76)

In contrast to synthetic hormone use, a recentstudy evaluating progesterone cream for safety andefficacy found no markers for inflammation or clotting. (77) The study also found that in women with higher than normal cortisol levels, there was a marked decline in the level of cortisol to the normal range whileusing progesterone cream compared to placebo. (77)

Hormone Effects on Lipids,Atherosclerosis, Vasospasm, and InsulinResistance

Activated by stress, increased cortisol hasbeen associated with an increased risk of atherosclerosis, obesity, and other manifestations of heart disease. Cortisol can contribute to atherosclerosis by increasing cholesterol ester formation. While estrogenwas seen to have no effect on cholesterol esters, progesterone blocked cholesterol ester formation, signifying an anti-atherogenic effect of progesterone. (78)

Whereas some synthetic progestins areknown to exert a negative effect on blood lipids, bioidentical progesterone does not appear to do so. (79,80) Inthe Postmenopausal Estrogen and Progestin Interventions (PEPI) Trial, oral micronized progesterone faredsignificantly better than MPA, as OMP did not bluntthe beneficial effects of estrogen on HDL elevation. (81) This was also found in an earlier study comparingprogesterone with both nortestosterone and MPA. (82)

Third generation progestins, such as norgestimate and desogestrel, have not demonstrated thissame adverse effect on serum lipids. (83)

MPA increases the extent of atherosclerosisin coronary arteries, suppresses the protective effect of estrogen on arterial injury, increases insulinresistance, and attenuates the beneficial effects ofestrogen on vasodilation. (84-86) This is consistent withfindings that synthetic estrogen as well as 19-nortestosterone can result in a decrease in glucose tolerance, whereas glucose metabolism is unaffected byP4. (87) Progesterone has furthermore been shown tohave an antiproliferative effect on vascular smoothmuscle in normal human and animal tissues as wellas in models simulating hyperinsulinemia and hyperglycemia. (88,89)

In two studies comparing E2 and P4 with E2and MPA, E2 and P4 protected against coronary hyper-reactivity and subsequent coronary vasospasm,whereas coronary vasospasm was increased in monkeys receiving MPA. (90,91) In a separate study, the sameauthors demonstrated an inhibition of coronary vasospasm with topical progesterone cream in pre-atherosclerotic primates. (92)

One study comparing MPA to progesteronedemonstrated progesterone reduced the risk for arteriosclerosis by inhibiting vascular cell adhesionmolecule-1 (VCAM-1), whereas MPA did not. (93) Thediffering effects of progesterone and MPA supportprogesterone as a better option.

Progesterone and 17beta-estradiol both inhibited cardiac fibroblast growth, with the effectsof 17beta-estradiol enhanced by P4, suggesting thecombination may help protect postmenopausal women against cardiovascular disease. (94)

Normal liver function is essential for lipidmetabolism. Synthetic progestins retain undesirableeffects on liver metabolism, even when administeredthrough the skin. (83) In regard to estrogen, a comparison between orally administered ethinyl estradiol(EE) and E2 demonstrated beneficial effects on serumlipids (EE>E2); however, EE demonstrated a markedincrease in liver protein synthesis, including sex-hormone binding globulin (SHBG) and pregnancy zoneprotein (PZP), markers of increased estrogenic effect. (95) SHBG elevation can result in lower testosterone activity due to its greater affinity to testosteroneand dihydrotestosterone than estrogen.

Natural progesterone, in either oral, vaginal,or topical administrations, has demonstrated safety inits effects on lipid metabolism and blood clotting. (77,80,96) The research to date looking at cardiovascular riskpoints to bioidentical hormones, particularly progesterone, as the hormone therapy of choice to supporthealthy vascular function.

The Effect of Hormones on the Breast

In the past, the effect of synthetic progestinson the breast was unclear. Whereas progestins havebeen used historically to treat some forms of advancedbreast cancer, a re-evaluation of results of a cohortstudy suggest an increased risk in the occurrence ofbreast cancer in women using combined HRT (predominantly CEE plus MPA) beyond that seen withunopposed estrogen; the risk increase, however, wasnot statistically significant. (97) Recently, the effect ofHRT on breast tissue was demonstrated in the WHIstudy. A 26-percent increased risk of invasive breastcancer was seen in women using a combination ofCEE and MPA compared to placebo. (4)

Several reviews suggest a protective effectof progesterone and some progestins on normal andpathological breast tissue, including a strong anti-proliferative effect both in the presence and absence ofestrogens. (98-102) Low endogenous progesterone levelswere also correlated with a five-fold increase in premenopausal breast cancer risk in women experiencing infertility when compared with infertile womenwith normal hormone levels. (103) In women undergoing breast surgery for benign breast conditions, pretreatment with topical estrogen resulted in increasedepithelial proliferation compared to a reduction inproliferation seen with percutaneous progesteronetreatment; furthermore, progesterone reduced estrogen-induced proliferation when both treatments wereused. (104) An in vitro study evaluating the effect ofprogesterone on the growth of T47-D breast cancercells demonstrated increased apoptosis as mediatedby the regulation of genes controlling apoptosis. (105) Ina review by Desreux et al, the authors emphasizedprogesterone’s role in supporting healthy breast homeostasis. (106) Progesterone opposes the proliferativeeffects of estradiol in the breast, (106,107) a role not seenwith synthetic progestins. (106)

A large cohort study involving 1,150 Frenchwomen with benign breast disease showed no increase in breast cancer risk with women using topical progesterone cream (RR=0.8), a common European treatment for breast mastalgia. Furthermore,the researchers noted a decrease in breast cancer riskamong women using progesterone cream plus an oralprogestogen (RR=0.5), compared with women usingoral progestogens alone. (108)

Two recent studies point to a difference inbreast cancer risk when comparing synthetic progestins to bioidentical progesterone as a part of theHRT regimen. A French cohort study involving 3,175postmenopausal women predominantly using naturalHRT (83 percent using transdermal estradiol and anon-MPA progestogen – progesterone and others)found no increased risk in users of these forms ofHRT.109The French E3N-EPIC cohort study is probably the most significant examination of the differences between progestogens and breast cancer risk.It assessed the risk of breast cancer associated withHRT use in 54,548 postmenopausal women and foundthe risk was significantly greater (p<0.001) with HRTcontaining synthetic progestins (RR=1.4 [1.2-1.7])than with HRT containing micronized progesterone(RR=0.9 [0.7-1.2]). (110) Although there are no prospective trials looking at the safety of bioidenticalprogesterone with respect to the breast, these largecohort studies, in combination with studies examining the effects of progesterone on normal and cancerous breast cells, do provide enticing evidence for thesafety of bioidentical progesterone.

It is well understood that, due to proliferativeeffect on normal breast cells as well as on numerousbreast cancer cell lines, estrogens are contraindicatedfor women at risk for breast cancer, because, as referenced above, increased estrone and estradiol levelsare associated with an increased risk of breast cancer.The supplementation of either of these forms of estrogen increases serum estradiol and estrone due tothe pathways by which they are metabolized. In contrast, several studies have demonstrated an inverserelationship between estriol levels and breast canceras well as antitumor effects of estriol. (27, 111-113) However, while there is reason to believe that estriol inlow doses could be protective for the breast in someindividuals, when supplementing estrogens, one mustalso consider the differences among individuals withrespect to metabolism. A recent study looking at theeffects of 14 different endogenous estrogen metabolites demonstrated proliferative, antiproliferative, andbi-phasic effects on a specific human breast cancerline (MCF-7), further emphasizing the importance ofindividualized consideration. (114)

The Effect of Hormones on theEndometrium

Both OMP and vaginal delivery of progesterone result in sufficient end-organ effect on the uteruswith doses beginning at 100 mg daily x 25 days/month or 45 mg every other day for six doses/month,respectively. (83,115,116) Similar end-organ results havebeen seen using percutaneous progesterone cream. (117)

Hormones and Menopausal Symptoms

Although most physicians attribute vasomotor flushing to a lack of estrogen, progestogens canhave a beneficial effect. (118) A study using a progesterone cream applied to the skin resulted in a significantreduction in the number and intensity of hot flashes in83 percent of the study participants, as well as benefits in other quality-of-life measurements.(119) In a separate study, subjects receiving 20 mg of topical progesterone cream daily for four weeks demonstratedsignificant improvement of menopausal symptoms,measured by Greene Climacteric Scale scores. (77)

In a study comparing the effects of CEE plusMPA to CEE plus OMP in postmenopausal women,the latter group had significantly improved sleep efficiency over the synthetic progestin group. (120) Anotherstudy comparing MPA to OMP found micronizedprogesterone to be better tolerated than MPA, as wellas conferring additional benefits in cognition and improvement of menstrual problems. (121)

Oral and transdermal estradiol preparations have been found to confer benefit for menopausal symptoms and vaginal cytology, as well asreduce bone loss in postmenopausal women. (53,55) Estriol has also been demonstrated to reverse vaginalatrophy. (122,123) Estriol doses must be increased up tothree times the dose of estradiol to achieve similareffects (e.g., reducing hot flashes and vaginal drynessin menopausal women) and is typically dosed twicedaily to achieve steady blood levels. (27)

Hormones and Bone Health

Bone turnover increases at menopause andmay remain high for 25 or more years following thelast menstrual cycle. (124) Hormonal control of boneturnover is not limited to a single hormone, but ratherthe complex interrelationship of a number of steroidand other hormones, including estrogen, progesterone, testosterone, corticosteroids, vitamin D, thyroidhormones, and retinoids. (125) When given alone, estrogens have a known beneficial effect on limiting boneloss as well as reducing the number of fractures. Studies with progesterone alone are mixed. Progesteronesupports bone health through its effects on the proliferation and differentiation of human osteoblasts. (126) Several animal and human studies have demonstratedprogesterone’s positive effect on bone formation aswell as inhibition of bone resorption.(127-130) However,double-blind placebo-controlled studies in humanshave yet to demonstrate a significant increase in bonemineral density (BMD) or a reduction in fracturerate with progesterone alone. One short-term humanstudy of OMP showed no difference in markers ofbone resorption compared to placebo.(131) Longer-termstudies evaluating BMD and fracture rate are neededto determine the value of progesterone supplementation alone for preventing or treating osteoporosis.Several studies looking at estrogen and progesteronesupplementation suggest estrogen and progesteronehave distinct and complementary roles in the maintenance of bone.(46,130,132) Testosterone can also decreaseurinary calcium loss and bone resorption.(76,133)

Hormones and the Brain

Progesterone has numerous beneficial effectson the brain and nervous system, including supporting myelin formation and activating GABA receptors.(134) Progesterone also plays a role in the reductionof ischemia in the brain and decreasing the inflammatory response after traumatic brain injury.(135,136) Areview of progesterone’s effect on the brain suggestsviable therapeutic possibilities for the prevention andtreatment of neurodegenerative diseases, as well asfor repair processes and preservation of cognitivefunction with age. (137) Synthetic progestins do not sharethese physiological effects. In fact, the WHIMS foundequine estrogen plus synthetic progestins (PremPro)doubled the risk of developing dementia in womenage 65 and older. (12)

Estrogens have known physiological effectson the brain, including improved blood flow via vasodilation and stimulation of serotonin and norepinephrine, which can impact nerve cell function and mood.It was postulated that estrogen could help delay age-related cognitive decline or help prevent Alzheimer’s disease, and small studies on animals appearedto confirm this.138However, two large-scale humanstudies failed to demonstrate any significant benefitof estrogen supplementation on cognitive function.

The Atherosclerosis Risk in Communities(ARIC) study evaluated the effects of estrogen onmemory and cognitive function in 2,000 women participants ages 48-67 over a 10-year period and foundno correlation (either positive or negative) betweenestrogen and cognitive function.138

The WHIMS also failed to demonstrate acognitive benefit for estrogen alone. In fact, resultsdemonstrated an increased risk for dementia in women using estrogen alone, although not as great a riskas combined synthetic HRT.12It should be noted thatthe WHIMS utilized equine estrogens with or without MPA, while the prospective ARIC study did not denote estrogens utilized.

Conclusion

The use of bioidentical hormone therapy iswell tolerated, provides symptom relief, and can address many of the health needs as well as the individual preferences of menopausal and perimenopausalwomen. Physicians are encouraged to take the timeand effort to help women determine the regimen thatbest suits their needs, including testing hormone levels directly prior to supplementation and using theleast amount necessary to achieve the desired results.This effort will undoubtedly pay off in fewer unwanted side effects and greater quality of life.

References

1. Wetzel W. Human identical hormones: real people,real problems, real solutions. Nurse Pract Forum1998;9:227-334.

2. Andrist LC. The impact of media attention, familyhistory, politics and maturation on women’sdecisions regarding hormone replacement therapy.Health Care Women Int 1998;19:243-260.

3. Hunter MS, O’Dea I, Britten N. Decision-makingand hormone replacement therapy: a qualitativeanalysis. Soc Sci Med 1997;45:1541-1548.

4. Rossouw JE, Anderson GL, Prentice RL, et al.Risks and benefits of estrogen plus progestin inhealthy postmenopausal women: principal resultsFrom the Women’s Health Initiative randomizedcontrolled trial. JAMA 2002;288:321-333.

5. Johannes CB, Crawford SL. Menstrual bleeding,hormones, and the menopausal transition. SeminReprod Endocrinol 1999;17:299-309.

6. Richardson SJ. The biological basis of themenopause. Baillieres Clin Endocrinol Metab1993;7:1-16.

7. Burger HG. The endocrinology of the menopause. JSteroid Biochem Mol Biol 1999;69:31-35.

8. Klein NA, Soules MR. Endocrine changes of theperimenopause. Clin Obstet Gynecol 1998;41:912-920.

9. Burger HG. Diagnostic role of folliclestimulating hormone (FSH) measurementsduring the menopausal transition – an analysisof FSH, oestradiol and inhibin. Eur J Endocrinol1994;130:38-42.

10. Burger HG. The endocrinology of the menopause.Maturitas 1996;23:129-136.

11. Speroff L, Glass RH, Kase NG. ClinicalGynecologic Endocrinology and Infertility. 6th ed.Philadelphia, PA: Lippincott, Williams & Wilkins;1999.

12. Shumaker SA, Legault C, Rapp SR, et al. Estrogenplus progestin and the incidence of dementia andmild cognitive impairment in postmenopausalwomen: the Women’s Health Initiative MemoryStudy: a randomized controlled trial. JAMA2003;289:2651-2662.

13. Vihtamaki T, Savilahti R, Tuimala R. Why dopostmenopausal women discontinue hormonereplacement therapy? Maturitas 1999;33:99-105.

14. Newton KM, LaCroix AZ, Leveille SG, et al.Women’s beliefs and decisions about hormonereplacement therapy. J Womens Health 1997;6:459-465.

15. Legare F, Godin G, Guilbert E, et al. Determinantsof the intention to adopt hormone replacementtherapy among premenopausal women. Maturitas2000;34:211-218.

16. den Tonkelaar I, Oddens BJ. Determinants of longterm hormone replacement therapy and reasons forearly discontinuation. Obstet Gynecol 2000;95:507-512.

17. Ettinger B, Pressman A. Continuation ofpostmenopausal hormone replacement therapy in alarge health maintenance organization: transdermalmatrix patch versus oral estrogen therapy. Am JManag Care 1999;5:779-785.

18. Bjorn N, Backstrom T. Compliance to HRT: thesignificance of negative side effects and moodsymptoms. Abstract: Eighth Annual Meeting ofNAMS. Menopause 1997;4:283.

19. Ettinger B, Pressman A, Silver P. Effect of ageon reasons for initiation and discontinuationof hormone replacement therapy. Menopause1999;6:282-289.

20. Perrone G, Capri O, Borrello M, Galoppi P.Attitudes toward estrogen replacement therapy.Study conducted on a sample population ofwomen attending an ambulatory care center forthe treatment of menopause. Minerva Ginecol1993;45:603-608. [Article in Italian]

21. Leake R. Contents of HRT and mechanismsof action. J Epidemiol Biostat 1999;4:129-133;discussion 133-139.

22. Huber JC, Campagnoli C, Druckmann R, et al.Recommendations for estrogen and progestinreplacement in the climacteric and postmenopause.European Progestin Club. Maturitas 1999;33:197-209.

23. Kabuto M, Akiba S, Stevens RG, et al. Aprospective study of estradiol and breast cancer inJapanese women. Cancer Epidemiol BiomarkersPrev 2000;9:575-579.

24. Miyoshi Y, Tanji Y, Taguchi T, et al. Association ofserum estrone levels with estrogen receptor-positivebreast cancer risk in postmenopausal Japanesewomen. Clin Cancer Res 2003;9:2229-2233.

25. Ursin G, Palla SL, Reboussin BA, et al. Posttreatment change in serum estrone predictsmammographic percent density changes inwomen who received combination estrogenand progestin in the postmenopausal estrogen/progestin interventions (PEPI) trial. J Clin Oncol2004;22:2842-2848.

26. van der Vies J. The pharmacology of oestriol.Maturitas 1982;4:291-299.

27. Follingstad AH. Estriol, the forgotten estrogen?JAMA 1978;239:29-30.

28. Head KA. Estriol: safety and efficacy. Altern MedRev 1998;3:101-113.

29. Mashchak CA, Lobo RA, Dozono-Takano R, etal. Comparison of pharmacodynamic propertiesof various estrogen formulations. Am J ObstetGynecol 1982;144:511-518.

30. http://www.pharmafocus.com/cda/focusH/1,2109,21-0-0-JUN_2004-focus_news_detail-0-225648,00.html [Accessed July 26, 2006]

31. Hudson T. Wild yam, natural progesterone:unraveling the mystery. The Townsend Letter forDoctors and Patients 1996;July:156.

32. Hirvonen E. Progestins. Maturitas 1996;23:S13-S18.

33. Gompel A. Progestin treatments of menopause. RevPrat 1993;43:2645-2650. [Article in French]

34. Belaisch J. Chemical classification of syntheticprogestogens. Rev Fr Gynecol Obstet 1985;80:473-477. [Article in French]

35. Fuhrmann U, Krattenmacher R, Slater EP,Fritzemeier KH. The novel progestin drospirenoneand its natural counterpart progesterone:biochemical profile and antiandrogenic potential.Contraception 1996;54:243-251.

36. Ojasoo T. Multivariate preclinical evaluation ofprogestins. Menopause J North Am Menopause Soc1995;2:97-107.

37. Kamada M, Irahara M, Aono T. Action of syntheticprogestin. Nippon Rinsho 1994;52:593-599.[Article in Japanese]

38. Jordan VC, Jeng MH, Catherino WH, Parker CJ.The estrogenic activity of synthetic progestins usedin oral contraceptives. Cancer 1993;71:1501-1505.

39. Negro-Vilar A. New progestins and potentialactions. J Soc Gynecol Investig 2000;7:S53-S54.

40. http://www.acog.org/from_home/publications/press_releases/nr10-01-04.cfm [Accessed July 26,2006]

41. Chambon Y. Synergism and antagonism betweenestrogens and progestins: an update. Bull Acad NatlMed 1993;177:177-186. [Article in French]

42. Hargrove JT, Osteen KG. An alternative methodof hormone replacement therapy using the naturalsex steroids. Infertility Reprod Med Clin North Am1995;6:653-674.

43. Saffran J, Loeser BK, Faber LE. Effects ofprogestins on the progesterone receptor in guineapig uterus. Adv Exp Med Biol 1979;117:223-239.

44. Cato AC, Ponta H. Different regions of the estrogenreceptor are required for synergistic action withthe glucocorticoid and progesterone receptors. MolCell Biol 1989;9:5324-5330.

45. Bradshaw MS, Tsai SY, Leng XH, et al. Studies onthe mechanism of functional cooperativity betweenprogesterone and estrogen receptors. J Biol Chem1991;266:16684-16690.

46. Schmidt IU, Wakley GK, Turner RT. Effectsof estrogen and progesterone on tibiahistomorphometry in growing rats. Calcif Tissue Int2000;67:47-52.

47. Casper RF. Estrogen with interrupted progestinHRT: a review of experimental and clinical studies.Maturitas 2000;34:97-108.

48. Casper RF, MacLusky NJ, Vanin C, Brown TJ.Rationale for estrogen with interrupted progestin asa new low-dose hormonal replacement therapy. JSoc Gynecol Investig 1996;3:225-234.

49. DeSombre ER, Kuivanen PC. Progestin modulationof estrogen-dependent marker protein synthesis inthe endometrium. Semin Oncol 1985;12:6-11.

50. http://www.fda.gov/bbs/topics/NEWS/2003/NEW00938.html [Accessed July 26, 2006]

51. Nahoul K, Dehennin L, Jondet M, Roger M.Profiles of plasma estrogens, progesterone and theirmetabolites after oral or vaginal administration ofestradiol or progesterone. Maturitas 1993;16:185-202.

52. Lyrenas S, Carlstrom K, Backstrom T, von SchoultzB. A comparison of serum oestrogen levels afterpercutaneous and oral administration of oestradiol-17 beta. Br J Obstet Gynaecol 1981;88:181-187.

53. Selby P, McGarrigle HH, Peacock M. Comparisonof the effects of oral and transdermal oestradioladministration on oestrogen metabolism, proteinsynthesis, gonadotrophin release, bone turnover andclimacteric symptoms in postmenopausal women.Clin Endocrinol (Oxf) 1989;30:241-249.

54. Palacios S, Menendez C, Jurado AR, Vargas JC.Effects of oestradiol administration via differentroutes on the lipid profile in women with bilateraloophorectomy. Maturitas 1994;18:239-244.

55. Pattison NS, Uptin T, Knox B, France J.Transdermal oestrogen for postmenopausal women:a double blind crossover comparative study withethinyl oestradiol. Aust N Z J Obstet Gynaecol1989;29:62-65.

56. Warren MP, Shantha S. Uses of progesteronein clinical practice. Int J Fertil Womens Med1999;44:96-103.

57. de Lignieres B, Dennerstein L, BackstromT. Influence of route of administration onprogesterone metabolism. Maturitas 1995;21:251-257.

58. Hermann AC, Nafziger AN, Victory J, et al.Over-the-counter progesterone cream producessignificant drug exposure compared to a food anddrug administration-approved oral progesteroneproduct. J Clin Pharmacol 2005;45:614-619.

59. Pouly JL, Bassil S, Frydman R, et al. Luteal phasesupport after vaginal progesterone: comparativestudy with micronized oral progesterone.Contracept Fertil Sex 1997;25:596-601. [Article inFrench]

60. Mahesh VB, Brann DW, Hendry LB. Diversemodes of action of progesterone and itsmetabolites. J Steroid Biochem Mol Biol1996;56:209-219.

61. Dusterberg B, Nishino Y. Pharmacokinetic andpharmacological features of oestradiol valerate.Maturitas 1982;4:315-324.

62. McAuley JW, Kroboth FJ, Kroboth PD. Oraladministration of micronized progesterone: areview and more experience. Pharmacotherapy1996;16:453-457.

63. Burry KA, Patton PE, Hermsmeyer K.Percutaneous absorption of progesterone inpostmenopausal women treated with transdermalestrogen. Am J Obstet Gynecol 1999;180:1504-1511.

64. Mircioiu C, Perju A, Griu E, et al.Pharmacokinetics of progesterone inpostmenopausal women: 2. Pharmacokineticsfollowing percutaneous administration. Eur J DrugMetab Pharmacokinet 1998;23:397-402.

65. Mircioiu C, Perju A, Neagu A, et al.Pharmacokinetics of progesterone inpostmenopausal women: 1. Pharmacokineticsfollowing intravaginal administration. Eur J DrugMetab Pharmacokinet 1998;23:391-396.

66. Cicinelli E, Nahoul K, Sabatelli S, et al.Administration of unmodified progesterone bynasal spray in fertile women. Gynecol Endocrinol1995;9:289-293.67. Levy T, Gurevitch S, Bar-Hava I, et al.Pharmacokinetics of natural progesteroneadministered in the form of a vaginal tablet. HumReprod 1999;14:606-610.

68. Rylance PB, Brincat M, Lafferty K, et al. Naturalprogesterone and antihypertensive action. Br Med J(Clin Res Ed) 1985;290:13-14.

69. Armstrong JG. Hypotensive action of progesteronein experimental and human hypertension. Proc SocExp Biol Med 1959;102:452-455.

70. Oelkers WK. Effects of estrogens and progestogenson the renin-aldosterone system and blood pressure.Steroids 1996;61:166-171.

71. Elkik F, Mauvais-Jarvis P. The role of progesteroneand progestins in hydroelectrolytic metabolism(author’s transl). Nouv Presse Med 1980;9:35-38.[Article in French]

72. Tollan A, Oian P, Kjeldsen SE, et al. Progesteronereduces sympathetic tone without changing bloodpressure or fluid balance in men. Gynecol ObstetInvest 1993;36:234-238.

73. Molinari C, Battaglia A, Grossini E, et al. Effectof progesterone on peripheral blood flow inprepubertal female anesthetized pigs. J Vasc Res2001;38:569-577.

74. Tsuda K, Kinoshita Y, Nishio I. Synergistic role ofprogesterone and nitric oxide in the regulation ofmembrane fluidity of erythrocytes in humans: anelectron paramagnetic resonance investigation. AmJ Hypertens 2002;15:702-708.

75. Toy JL, Davies JA, Hancock KW, McNicol GP. Thecomparative effects of a synthetic and a ‘natural’oestrogen on the haemostatic mechanism in patientswith primary amenorrhoea. Br J Obstet Gynaecol1978;85:359-362.

76. Orwoll ES, Stribrska L, Ramsey EE, Keenan EJ.Androgen receptors in osteoblast-like cell lines.Calcif Tissue Int 1991;49:183-187.

77. Stephenson K, Price C, Kurdowska A, et al.Progesterone cream does not increase thromboticand inflammatory factors in postmenopausalwomen. Blood 2004;104:16.

78. Cheng W, Lau OD, Abumrad NA. Twoantiatherogenic effects of progesterone onhuman macrophages; inhibition of cholesterylester synthesis and block of its enhancementby glucocorticoids. J Clin Endocrinol Metab1999;84:265-271.

79. Fahraeus L, Larsson-Cohn U, Wallentin L.L-norgestrel and progesterone have differentinfluences on plasma lipoproteins. Eur J Clin Invest1983;13:447-453.

80. Ottosson UB. Oral progesterone and estrogen/progestogen therapy. Effects of natural andsynthetic hormones on subfractions of HDLcholesterol and liver proteins. Acta Obstet GynecolScand Suppl 1984;127:1-37.

81. No authors listed. Effects of estrogen or estrogen/progestin regimens on heart disease risk factorsin postmenopausal women. The PostmenopausalEstrogen/Progestin Interventions (PEPI) Trial.The Writing Group for the PEPI Trial. JAMA1995;273:199-208.

82. Ottosson UB, Johansson BG, von Schoultz B.Subfractions of high-density lipoprotein cholesterolduring estrogen replacement therapy: a comparisonbetween progestogens and natural progesterone.Am J Obstet Gynecol 1985;151:746-750.

83. Warren MP, Biller BM, Shangold MM. A newclinical option for hormone replacement therapyin women with secondary amenorrhea: effectsof cyclic administration of progesterone fromthe sustained-release vaginal gel Crinone (4%and 8%) on endometrial morphologic featuresand withdrawal bleeding. Am J Obstet Gynecol1999;180:42-48.

84. Williams JK, Honore EK, Washburn SA, ClarksonTB. Effects of hormone replacement therapy onreactivity of atherosclerotic coronary arteriesin cynomolgus monkeys. J Am Coll Cardiol1994;24:1757-1761.

85. Wagner JD, Martino MA, Jayo MJ, et al. Theeffects of hormone replacement therapy oncarbohydrate metabolism and cardiovascular riskfactors in surgically postmenopausal cynomolgusmonkeys. Metabolism 1996;45:1254-1262.

86. Wallace JM, Shively CA, Clarkson TB. Effects ofhormone replacement therapy and social stress onbody fat distribution in surgically postmenopausalmonkeys. Int J Obes Relat Metab Disord1999;23:518-527.

87. Beck P. Effect of progestins on glucose and lipidmetabolism. Ann N Y Acad Sci 1977;286:434-445.

88. Carmody BJ, Arora S, Wakefield MC, et al.Progesterone inhibits human infragenicular arterialsmooth muscle cell proliferation induced by highglucose and insulin concentrations. J Vasc Surg2002;36:833-838.

89. Lee WS, Harder JA, Yoshizumi M, et al.Progesterone inhibits arterial smooth muscle cellproliferation. Nat Med 1997;3:1005-1008.

90. Minshall RD, Stanczyk FZ, Miyagawa K, etal. Ovarian steroid protection against coronaryartery hyperreactivity in rhesus monkeys. J ClinEndocrinol Metab 1998;83:649-659.

91. Miyagawa K, Rosch J, Stanczyk F, HermsmeyerK. Medroxyprogesterone interferes with ovariansteroid protection against coronary vasospasm. NatMed 1997;3:324-327.

92. Hermsmeyer RK, Mishra RG, Pavcnik D, etal. Prevention of coronary hyperreactivity inpreatherogenic menopausal rhesus monkeys bytransdermal progesterone. Arterioscler ThrombVasc Biol 2004;24:955-961.

93. Otsuki M, Saito H, Xu X, et al. Progesterone, butnot medroxyprogesterone, inhibits vascular celladhesion molecule-1 expression in human vascularendothelial cells. Arterioscler Thromb Vasc Biol2001;21:243-248.

94. Dubey RK, Gillespie DG, Jackson EK, Keller PJ.17Beta-estradiol, its metabolites, and progesteroneinhibit cardiac fibroblast growth. Hypertension1998;31:522-528.

95. Ottosson UB, Carlstrom K, Johansson BG, vonSchoultz B. Estrogen induction of liver proteins andhigh-density lipoprotein cholesterol: comparisonbetween estradiol valerate and ethinyl estradiol.Gynecol Obstet Invest 1986;22:198-205.

96. Suvanto-Luukkonen E, Sundstrom H, PenttinenJ, Kauppila A. Lipid effects of an intrauterinelevonorgestrel device or oral vs. vaginal naturalprogesterone in post-menopausal women treatedwith percutaneous estradiol. Arch Gynecol Obstet1998;261:201-208.

97. Schairer C, Lubin J, Troisi R, et al. Menopausalestrogen and estrogen-progestin replacementtherapy and breast cancer risk. JAMA2000;283:485-491.

98. Mauvais-Jarvis P, Kuttenn F, Gompel A,Benotmane A. Antiestrogen action of progesteronein the breast. Pathol Biol (Paris) 1987;35:1081-1086. [Article in French]

99. Mauvais-Jarvis P, Kuttenn F, Gompel A. Estradiol/progesterone interaction in normal and pathologicbreast cells. Ann N Y Acad Sci 1986;464:152-167.

100. Gorins A, Denis C. Effects of progesterone andprogestational hormones on the mammary gland.Arch Anat Cytol Pathol 1995;43:28-35. [Article inFrench]

101. Inoh A, Kamiya K, Fujii Y, Yokoro K. Protectiveeffects of progesterone and tamoxifen inestrogen-induced mammary carcinogenesis inovariectomized W/Fu rats. Jpn J Cancer Res1985;76:699-704.

102. Wren BG, Eden JA. Do progestogens reduce therisk of breast cancer? A review of the evidence.Menopause J North Am Menopause Soc 1996;3:4-12.

103. Cowan LD, Gordis L, Tonascia JA, Jones GS.Breast cancer incidence in women with a historyof progesterone deficiency. Am J Epidemiol1981;114:209-217.

104. Chang KJ, Lee TT, Linares-Cruz G, et al.Influences of percutaneous administration ofestradiol and progesterone on human breastepithelial cell cycle in vivo. Fertil Steril1995;63:785-791.

105. Formby B, Wiley TS. Progesterone inhibits growthand induces apoptosis in breast cancer cells:inverse effects on Bcl-2 and p53. Ann Clin Lab Sci1998;28:360-369.

106. Desreux J, Kebers F, Noel A, et al. Progesteronereceptor activation – an alternative to SERMs inbreast cancer. Eur J Cancer 2000;36:S90-S91.

107. Malet C, Spritzer P, Guillaumin D, Kuttenn F.Progesterone effect on cell growth, ultrastructuralaspect and estradiol receptors of normal humanbreast epithelial (HBE) cells in culture. J SteroidBiochem Mol Biol 2000;73:171-181.

108. Plu-Bureau G, Le MG, Thalabard JC, et al.Percutaneous progesterone use and risk of breastcancer: results from a French cohort study ofpremenopausal women with benign breast disease.Cancer Detect Prev 1999;23:290-296.

109. de Lignieres B, de Vathaire F, Fournier S, et al.Combined hormone replacement therapy and riskof breast cancer in a French cohort study of 3175women. Climacteric 2002;5:332-340.

110. Fournier A, Berrino F, Riboli E, et al. Breast cancerrisk in relation to different types of hormonereplacement therapy in the E3N-EPIC cohort. Int JCancer 2005;114:448-454.

111. Lemon HM, Wotiz HH, Parsons L, MozdenPJ. Reduced estriol excretion in patients withbreast cancer prior to endocrine therapy. JAMA1966;196:1128-1136.

112. Lemon HM. Pathophysiologic considerations in thetreatment of menopausal patients with oestrogens;the role of oestriol in the prevention of mammarycarcinoma. Acta Endocrinol Suppl (Copenh)1980;233:17-27.

113. Lemon HM. Estriol prevention ofmammary carcinoma induced by 7,12-dimethylbenzanthracene and procarbazine. CancerRes 1975;35:1341-1353.

114. Lippert C, Seeger H, Mueck AO. The effectof endogenous estradiol metabolites on theproliferation of human breast cancer cells. Life Sci2003;72:877-883.

115. de Lignieres B. Oral micronized progesterone. ClinTher 1999;21:41-60;discussion 1-2.

116. Sitruk-Ware R, Bricaire C, De Lignieres B, et al.Oral micronized progesterone. Bioavailabilitypharmacokinetics, pharmacological andtherapeutic implications – a review. Contraception1987;36:373-402.

117. Wilson KJ. Private communication.

118. Schiff I. The effects of progestins on vasomotorflushes. J Reprod Med 1982;27:498-502.

119. Leonetti HB, Longo S, Anasti JN. Transdermalprogesterone cream for vasomotor symptomsand postmenopausal bone loss. Obstet Gynecol1999;94:225-228.

120. Montplaisir J, Lorrain J, Denesle R, Petit D. Sleepin menopause: differential effects of two formsof hormone replacement therapy. Menopause2001;8:10-16.

121. Ryan N, Rosner A. Quality of life and costsassociated with micronized progesterone andmedroxyprogesterone acetate in hormonereplacement therapy for nonhysterectomized,postmenopausal women. Clin Ther 2001;23:1099-1115.

122. van der Linden MC, Gerretsen G, Brandhorst MS,et al. The effect of estriol on the cytology of urethraand vagina in postmenopausal women with genitourinary symptoms. Eur J Obstet Gynecol ReprodBiol 1993;51:29-33.

123. Heimer GM. Estriol in the postmenopause. ActaObstet Gynecol Scand Suppl 1987;139:1-23.

124. Takahashi M, Kushida K, Hoshino H, et al.Biochemical markers of bone turnover do notdecline after menopause in healthy women. Br JObstet Gynaecol 1999;106:427-431.

125. Bland R. Steroid hormone receptor expression andaction in bone. Clin Sci (Lond) 2000;98:217-240.

126. Liang M, Liao EY, Xu X, et al. Effects ofprogesterone and 18-methyl levonorgestrel onosteoblastic cells. Endocr Res 2003;29:483-501.

127. Barengolts EI, Gajardo HF, Rosol TJ, et al. Effectsof progesterone on postovariectomy bone loss inaged rats. J Bone Miner Res 1990;5:1143-1147.

128. Bowman BM, Miller SC. Elevated progesteroneduring pseudopregnancy may prevent bone lossassociated with low estrogen. J Bone Miner Res1996;11:15-21.

129. Fujimaki T, Kurabayashi T, Yamamoto Y, et al.Effects of progesterone on the metabolism ofcancellous bone in young oophorectomized rats. JObstet Gynaecol 1995;21:31-36.

130. Burnett CC, Reddi AH. Influence of estrogen andprogesterone on matrix-induced endochondral boneformation. Calcif Tissue Int 1983;35:609-614.

131. Ikram Z, Dulipsingh L, Prestwood KM. Lackof effect of short-term micronized progesteroneon bone turnover in postmenopausal women. JWomens Health Gend Based Med 1999;8:973-978.

132. Yamamoto Y, Kurabayashi T, Tojo Y, et al. Effectsof progestins on the metabolism of cancellous bonein aged oophorectomized rats. Bone 1998;22:533-537.

133. Wang C, Eyre DR, Clark R, et al. Sublingualtestosterone replacement improves muscle massand strength, decreases bone resorption, andincreases bone formation markers in hypogonadalmen – a clinical research center study. J ClinEndocrinol Metab 1996;81:3654-3662.

134. Baulieu E, Schumacher M. Progesterone as aneuroactive neurosteroid, with special reference tothe effect of progesterone on myelination. Steroids2000;65:605-612.

135. Gibson CL, Murphy SP. Progesterone enhancesfunctional recovery after middle cerebral arteryocclusion in male mice. J Cereb Blood Flow Metab2004;24:805-813.

136. Grossman KJ, Goss CW, Stein DG. Effects ofprogesterone on the inflammatory response to braininjury in the rat. Brain Res 2004;1008:29-39.

137. Schumacher M, Guennoun R, Robert F, et al. Localsynthesis and dual actions of progesterone in thenervous system: neuroprotection and myelination.Growth Horm IGF Res 2004;14:S18-S33.

138. de Moraes SA, Szklo M, Knopman D, Park E.Prospective assessment of estrogen replacementtherapy and cognitive functioning: atherosclerosisrisk in communities study. Am J Epidemiol2001;154:733-739.

Source:Altern Med Rev.2006 Sep;11(3):208-23.

This post has not been tagged.

Share |
PermalinkComments (0)
 

Market Your Practice with Facebook

Posted By Michelle Schiavo, Thursday, August 11, 2011
Updated: Thursday, January 30, 2014
Social Media is a great tool for health care providers to reach out to their patients and the public beyond their practices. Leading the way in Social Media is Facebook with over 750 million active users.

While some physicians and health care practitioners may be wary of creating a Facebook presence, it’s really a great way to disseminate information, connect with patients, and even grow your practice. Should Your Doctor Be On Facebook? is an article written by an NYC doctor about Facebook etiquette for physicians and is a great reference for practitioners new to Social Media.

Your Facebook page should represent your brand and the best way to do this is with a "Fan Page”. You may have heard of Facebook "Groups”, but they are a bit limited in terms of security and messaging capabilities and you’ll find a fan page to be more beneficial for marketing purposes. When visitors become fans of your page it displays on their "Wall” informing their "Friends” who may then also become a fan of your page. Additionally, fan pages are indexed by external search engines such as Google, whereas group pages are not.

ACAM member, Shira Miller, MD, has done exemplary work with her Facebook page. Shortly after its creation, her page boasted over 5,000 fans. How did she do it? By creating a unique page, communicating with her fans, and sharing her expertise on a consistent basis. Dr. Miller’s practice focuses on menopause and andropause, so that is the information she shares on her page. By providing a certain niche, in Dr. Miller’s case female and male hormone information, she’s setting herself apart and attracting a segment of the population that could potentially come into her practice and become new patients. Visit Dr. Miller’s Facebook fan page here.

There are over 900 million objects (pages, groups, events, and community pages) that people interact with on Facebook. The average user is connected to 80 community pages, groups, and events. With so many brands and companies represented on Facebook, how do you make yourself stand out? You’ll notice on some pages, for example on Dr. Miller’s page, there are unique elements that are not found on other Facebook pages. When you arrive at Dr. Miller’s page, you don’t see the standard Facebook wall showing updates and conversations, you see a large picture of Dr. Miller, a description of who she is and what she does, and a request to "like” her page. In order to gain access to her page, visitors must click the like button and become fans. This fan-gating feature is called a "Landing Page” and is a great way to increase your fan count.

You can create a landing page as well as many other unique touches with the use of apps. ACAM’s Facebook page is a prime example of a page that’s utilized apps to add more creativity and functionality to a page. Through custom apps, fans of ACAM may connect to ACAM doctors on Facebook, the ACAM website, ACAM Integrative Medicine Blog, and more all right from our Facebook page. Visit our page here and see the different elements we’ve added that you too can add to your page.

There are apps already built into Facebook that you can access at no charge. Or for a fee you can partner with a company that has designed customized apps for Facebook in user-friendly formats. Most of these companies have various price plans depending on the number of fans a page has.

Companies to consider:

NorthSocial
SocialAppsHQ

Questions? Or looking for a little assistance with your page? ACAM’s Marketing Team is happy to help! Please contact Michelle Schiavo - Social Impact Coordinator for ACAM at: michelle.schiavo@acam.org.

Tags:  practice marketing 

Share |
PermalinkComments (0)
 

How is Your Glutatione?

Posted By Matt Angove, ND, NMD, Thursday, August 11, 2011
Updated: Tuesday, February 4, 2014

In 1994, theJournal of Nutritional Biochemistrystated, "Disease states due to glutathione deficiency are not common.”

Well, 25 years and 90 thousand journal articles later we have found this statement to be false on all levels. Glutathione is recognized as an extremely important intracellular antioxidant that also plays a central role in the detoxification and elimination of potential carcinogens and toxins. Studies have found that glutathione synthesis and tissue glutathione levels become significantly lower with age, leading to decreased ability to respond to oxidative stress or toxin exposure.

The higher the glutathione peroxidasein the plasma or red blood cells, the more your body is running through and out of glutathione. Now consider the follow…

Total glutathione peroxidase activity was elevated in females 65 years of age or older. Cigarette smoking significantly elevated glutathione peroxidase. Alcohol elevated glutathione peroxidase, with the highest levels seen in drinkers who also smoked. Increased glutathione peroxidase was also seen in vigorous exercise, especially triathletes and marathoners.

According to the National Cancer Institute, dairy products, cereals and breads are low in glutathione. Fruit and vegetables have moderate to high amounts of glutathione. Frozen versus fresh foods had similar amounts of glutathione. Processing and preservation resulted in considerable loss of glutathione.

A 27% reduction in glutathionehas been reported in the cerebrospinal fluid of schizophrenic patients.

Studies have shown that dietary glutathione enhances the metabolic clearance and reduces net absorption of dietary peroxidized lipids, which cause intense cellular damage.

High altitude exposurereduces glutathione levels.

Glutathione functions as an antioxidant and can maintain vitamin C in its reduced and functional form.

Chronically low glutathione levelsare seen in premature infants,alcoholic cirrhotics and individuals with HIV.

Glutathione increases sperm motility patterns and sperm morphology. In a double-blind, placebo-controlled crossover trial of infertile patients, patients were randomly and blindly assigned to treatment with one injection every other day of either glutathione at 600 mg or an equal volume of placebo. All the glutathione selected patients showed an increase in sperm concentration and a highly statistically significant improvement in sperm motility, sperm kinetic parameters and sperm morphology. Want to get pregnant? Make sure your husband has optimal levels of glutathione.

From the journal of Digestion: Glutathione is extremely important in normal functioning of the pancreas, being needed for normal folding of the proteins that will ultimately form key digestive enzymes when the pancreas is stimulated after a meal. In patients with chronic pancreatitis, it has been found that glutathione is often significantly depleted, suggesting that lack of glutathione has a role in the generation and/or maintenance of the disease. In addition, many patients suffering from chronic pancreatitis appear to be under xenobiotic or oxidant stress, creating an evengreater need for glutathione. Since the pancreas is under relative glutathione "stress” during the normal process of packing and secreting digestive enzymes, it is easy to see how the lack of glutathione could have a role in chronic pancreatitis.

From the Journal of Brain Research Reviews:Glutathione depletioncan enhance oxidative stress and may increase levels of excitotoxic (toxins that excite neurons to the point of death) molecules, which may initiate cell death in specific nerve cell populations. Evidence of oxidative stress andreduced glutathione statusis found in Lou Gehrig’s disease, Parkinson’s disease and Alzheimer’s disease.

From the Annals of Pharmacotherapy:Glutathione is importantin DNA synthesis and repair, protein and prostaglandin synthesis, amino acid transport, metabolism of toxins and carcinogens, enhancement of immune function, prevention of oxidative cell damage and enzyme activation.

From the Journal Acta Dermato-Venereologica:Low levels of blood glutathionewere found in patients with pemphigoid, acne conglobata, polymyositis, rheumatoid arthritis, scleroderma, systemic lupus erythematosus, atopic dermatitis, eczema and psoriasis.

From the Journal of the Federation of American Societies for Experimental Biology:Intracellular glutathione enhances the immunologic function of lymphocytes (perhaps the most important immune cell line in preventing infection and cancer).Low levels of glutathionelimit the optimal functioning of T cells. Cytotoxic T cell (necessary to eliminate cancer) responses and interleukin-II-dependent functions are inhibited even by a partialdepletion of the intracellular glutathionepool.

From the journal of Ocular Pharmacological Therapy:Susceptibility of the lens nucleus to oxidative damage and loss of transparency has been shown in experimental animal models, including exposure to hyperbaric oxygen, x-ray and UVA light.Depletion of glutathioneallows the levels of oxidant to damage lens tissue and structure.

From the Journal of Laboratory and Clinical Science:An increased incidence oflow glutathione levelsin apparently healthy subjects suggests a decreased capacity to maintain metabolic and detoxification reactions that are stimulated by glutathione. The authors stated thatglutathione status, physical health, and longevity are closely related.

From the Lancet: The plasma glutathione in young, healthy adults was 0.54 umol/L; in healthy elderly it was 0.29 umol/L; in elderly outpatients it was 0.24 umol/L; and in elderly inpatients it was 0.17 umol/L. Aging results in a decrease in plasma glutathione and an increase in oxidative damage in apparently healthy individuals.

Simply put, if you want young cells and the ability to overcome disease you need to work on getting your glutathione levels up!


Tags:  food and drink  nutrition 

Share |
PermalinkComments (0)
 

Enhance Your Practice with E-billing

Posted By Michelle Schiavo, Tuesday, August 9, 2011
Updated: Tuesday, February 4, 2014
As technology continues to advance the healthcare industry, physicians are discovering the benefits of electronic billing. Reduce your staff's billing administration time and consider switching to electronic billing. Kareo, an Irvine CA based company can help.
What is Kareo?

Kareo is a web-based medical billing and practice management software program. CEO, Dan Rodrigues founded the company in 2004 and had two goals: to create a software that is affordable and easy to use.

In the past, software companies sold a ‘client-server model’ where a physician would have to buy hardware, plus the server, have a representative come to the office for a demo, and come back again to install and train. This process was very time and cost-intensive. At the time, this process was acceptable, because most people were not highly educated consumers in terms of purchasing technology, including physicians.

Then came the release of the iPhone and people started to really understand what a consumer-oriented engagement is with technology. Many doctors got the iPhone and started developing a taste for what technology should be like. This is when Kareo came into the picture and decided to mimic this new experience.

What makes Kareo different?

When you visit the Kareo website, 90 to 95 percent of what a consumer wants to understand and needs to know is right there and easily accessible. The buying experience is done online, sign-up takes about 30 to 45 seconds, you receive your log in information and you’re ready to go.

Additionally, Kareo’s software is delivered in the ‘cloud’ versus on a web server, which means physicians can use their existing software, get into a browser, download the app, and they’re in. No matter where physicians are, they can access data from Kareo.

Kareo’s website also offers thought leadership content. They’ve partnered with experts that write content specifically for Kareo regarding not only medical billing, but other issues physicians are concerned about such as HIIPA, meaningful use and other items of interest that have come out of health care reform and stimulus. This content goes on the Kareo blog and they also incorporate that information into their thinking about product perspective, delivery, and sales experience.

How can Kareo help integrative physicians?

Kareo makes it simple for doctors to get paid. Whether it’s billing patients and being able to accept payments via credit card online or filing insurance claims, Kareo’s goal is to get the doctor maximum reimbursement in the quickest possible amount of time.

Kareo’s software allows physicians to keep track of finances, look at and analyze their client base and schedule appointments. From Kareo’s Dashboard, which users see when they log in, there are short-cuts that link to key functions, a list of tasks that need to be completed and a snapshot of financial metrics. Part of the financial metrics is the Payment Velocity feature. This number is featured in a large orange display and tells the number of days on average it’s taking the practitioner to receive payment from the time of service to the time payment has been posted.

Many practitioners use programs where only 60 to 70 percent of the features apply to them and the remaining 30 to 40 percent is almost always work-arounds. Kareo specializes their software specifically for physical therapists, chiropractors, dermatologists, etc. They understand that there are nuances in certain practices regarding the way they have to bill and how they have to document and one standard program will not work for every practice.

What’s next for Kareo?

They’ve made it easy for doctors to get paid, now they’re finding ways for physicians to connect with their patients beyond the office. Since data is stored in the cloud and can be accessed from anywhere, there are an endless amount of possibilities for physician-patient interaction.

Patients could have an app that connects to their medical records (stored in Kareo’s platform in the cloud) and input what they ate that day, then the app will tell them according to their data that they should watch their sugar intake or eat more iron-rich foods, etc. etc.

If a physician finds a fantastic article on diabetes and has a percentage of patients that are diabetic, he or she can send that article to the diabetic patients through an app.

If a patient is running low on a supplement or medication and does not need to see the doctor, an app could alert that patient, ask if he or she would like to order more, provide the ability to pay right there on the app and then the supplement or medication gets delivered to the patient.

Kareo has the ecosystem to be able to do these things and more. Look to Kareo for more innovative ways for physicians to live with their patients outside the office.

Visit www.kareo.com to watch a free demo and to view their various plans and pricing.

Tags:  practice marketing 

Share |
PermalinkComments (0)
 

Metabolic Syndrome, Heart Health, and Risk Factors

Posted By John Gannage, MD, MCFP, DH, Monday, August 8, 2011
Updated: Tuesday, February 4, 2014
The medical community has recently seen a raft of literature instructing "aggressive” management of hypertension, diabetes and high cholesterol (the Big Three). The basic premise is to diagnose early and treat early, while at the same time lowering the upper limits of acceptability for these conditions. The aggressive intervention leads to polypharmacy, where a single one of these conditions is best managed with more than one medication, as conventional medical literature now recommends. In other words, if you have high blood pressure, your doctor has been instructed that control best comes from prescribing two medications. The goal is to reduce risk of death and morbidity due to heart disease, stroke and other complications.

The same literature often addresses lifestyle change, including nutrition considerations, as a footnote usually towards the end of a long article (similar to the proportion allocated to this topic when I was a medical student 25 years ago). Make no mistake: these three conditions do require the respect they deserve as risk factors for heart disease, the number one killer in North American society. But what do they have in common beyond the espoused aggressive management, and cardiac risk?

DIET, INSULIN AND METABOLIC SYNDROME

First line therapy in the management of these conditions comes through alteration of lifestyle habits - related to diet, exercise, and stress management. The fact that these conditions can be managed with a similar unifying approach tells us something about their commonality related to cause and biochemistry. The average North American diet, self-indulgent and high glycemic, triggers an insulin response that is self-destructive in many aspects. Consistently high levels of insulin, in and of itself, are damaging to the walls of arteries, leading to hardening and degeneration. Insulin is a fat-making hormone, explaining the relationship of each of the Big Three to obesity in many cases. In fact, diabetes, hypertension, obesity and heart disease, along with gout and hormone disturbances, can all be categorized into one syndrome: The Metabolic Syndrome.

At the core of Metabolic Syndrome is the high glycemic (sugar)-insulin connection, which leads to a cascade of biochemical disturbances. White sugar (and brown), white potatoes, white rice and white flour are all high glycemic foods that require restriction. The Glycemic Index of foods, gaining popularity worldwide in Westernized nations, was conceived by Toronto's Dr. David Jenkins. Food lists can be consulted to ensure a low glycemic diet, aiming for carbohydrates that are below 55 on the glycemic index scale.

HEALTHY BODY COMPOSITION, EXERCISE AND STRESS

Of course, successful management of excess weight is imperative. The hallmark of a good weight loss program, in my opinion, is not to achieve loss of the greatest amount of weight in the shortest time possible as the goal, but rather, with an emphasis on patient education and involvement, establishing HEALTH as the focus.

Obesity is indeed related to the aforementioned high glycemic diet, but also linked are exposures to toxins, lack of healthy bowel flora and sleep disturbances. The approach to weight management requires a comprehensive approach - with a low glycemic diet, incorporated beyond a temporary period, the foundation. Of importance is getting an early start to healthy body composition - studies link later heart disease to obesity beginning in adolescence, as an independent risk factorhttp://bit.ly/iCA1A6. Indeed, pediatric obesity is one of the significant public health issues of our time.

Also of importance is the lack of exercise that aggravates the picture of Metabolic Syndrome. Exercise allows for better response of healthy cells to insulin itself, thereby improving blood sugar, fat and cholesterol metabolism. Exercise leads to the development of lean muscle mass, which has a higher level of cellular activity. Increased lean muscle is associated with decreased risk of acute and chronic illness, and healthier body composition long term due to less likelihood of regaining any lost weight. Simply put, exercise expends calories, lowers weight, increases muscle, lowers blood pressure, regulates blood sugar and improves the cholesterol profile, in addition to improving mood and sleep.

Stress chronically alters biochemistry as well, with increased output of cortisol long-term causing blood sugar disturbances and fat storage. Stress can heighten cholesterol levels through similar pathways, and is likely the single most important risk factor for heart disease.


HIGH CHOLESTEROL

High cholesterol is also an aspect of Metabolic Syndrome, and as a marker of the syndrome has been targeted for aggressive management mostly from a pharmacologic perspective. Sadly, when it comes to nutrition and cholesterol, if mentioned at all, the existence of myths remains pervasive in the medical mainstream.

Firstly, I am familiar with the school of thought that suggests cholesterol is misplaced as a dangerous chemical; that excessive lowering of cholesterol, which comprises 2 % of brain mass, is detrimental to neurologic health; that as a natural antioxidant substance, raised cholesterol is a programmed protective response to toxin exposure (suggesting a role for detoxification and antioxidant supplementation). Nonetheless, high cholesterol remains an entity most patients are not comfortable with, insomuch that treatment is desirable and requested.

Returning to the discussion of nutrition misperceptions, dietary cholesterol has virtually no effect on circulating levels of cholesterol in the bloodstream. Eggs are an excellent source of protein and nutrients, and should not be avoided for their cholesterol content. The lecithin that naturally occurs in the whole egg (with emphasis on whole) exists coincidentally with the egg's cholesterol for good reason. Mother Nature once again gets it right.

The myth that cholesterol can only be lowered a small percentage solely through dietary management has also been dispelled. This was the mainstay of medical thinking for decades, seemingly necessitating drug research and application. Dr. Jenkins and his colleagues at St. Michael's hospital constructed the Portfolio Diet, and showed results equal to the financially successful statin drugs in a study published by the prestigious Journal of the American Medical Association (JAMA) http://jama.ama-assn.org/content/290/4/502.full.pdf.http://bit.ly/iVcqqd.Statins lowered LDL by 30-33 percent and the Portfolio Diet lowered LDL by nearly 30 percent. The portfolio was rich in soymilk, soy burgers, almonds, oats, barley, psyllium seeds, okra and eggplant.

Interestingly, Reuters News agency reported: "… people who cannot tolerate the statin drugs because of side-effects can turn to the diet, which they [the researchers] said their volunteers could easily follow.” A worthwhile question might be why not use the diet as first line therapy, as has always been footnoted. We now have a study with clear results supporting dietary management of a common condition, and the advice is to consider it a secondary intervention.

THE BOTTOM LINE

Eat whole, choose low glycemic foods, exercise regularly, supplement thoughtfully and maintain healthy body composition. Your heart will be thankful.

Tags:  health 

Share |
PermalinkComments (0)
 

Case Study on Link Between Sleep & Diabetes

Posted By Carol Touma, MD and Silvana Pannain, MD, Friday, August 5, 2011
Updated: Tuesday, February 4, 2014
Published in the Cleveland Clinic Journal of Medicine.

by Carol Touma, MD and Silvana Pannain, MD

Abstract

Several lines of evidence indicate that chronic lack of sleep may contribute to the risk of type 2 diabetes mellitus. Adequate sleep and good sleep hygiene should be included among the goals of a healthy lifestyle, especially for patients with diabetes. We urge clinicians to recommend at least 7 hours of uninterrupted sleep per night as part of a healthy lifestyle.

Key Points

  • Sleep loss and sleep disturbances have become very common in our society, and so have obesity and type 2 diabetes.
  • In epidemiologic studies, people who reported sleeping less were at higher risk of diabetes or disordered glucose metabolism.
  • In laboratory studies, short-term sleep deprivation caused measurable changes in glucose metabolism, hormone levels, autonomic nervous system activity, and other variables, which are plausible mechanisms by which loss of sleep could contribute to diabetes.
  • Obstructive sleep apnea is very common in people with diabetes and may be directly linked to diabetes risk and worse diabetes control. Diabetic patients should be systematically assessed for obstructive sleep apnea, and patients with known obstructive sleep apnea should be screened for diabetes.

ADULTS ARE SLEEPING LESS AND LESS in our society. Yet sleep is no longer thought of as strictly a restorative process for the body. The importance of sleep for metabolic function and specifically glucose homeostasis is now widely accepted, as many studies have shown a correlation between sleep deprivation or poor sleep quality and an increased risk of diabetes.

Obesity and aging are both associated with worse sleep. As the prevalence of obesity and diabetes increases, and as the number of elderly people increases, it is imperative to target sleep in the overall treatment of our patients.

In the pages that follow, we examine the evidence of a link between sleep loss (both short sleep duration and poor-quality sleep) and the risk of diabetes. (For evidence linking short sleep duration and the related problem of obesity, we invite the reader to refer to previous publications on the topic.)

SLEEP LOSS, OBESITY, AND DIABETES ARE ALL ON THE RISE

The prevalence of obesity and, consequently, of type 2 diabetes mellitus has increased alarmingly worldwide and particularly in the United States in the past few decades. Such a rapid increase cannot be explained simply by an alteration in the genetic pool; it is more likely due to environmental, socioeconomic, behavioral, and demographic factors and the interaction between genetics and these factors. Besides traditional lifestyle factors such as high-calorie diets and sedentary habits, other, nontraditional behavioral and environmental factors could be contributing to the epidemic of obesity and diabetes.

At the same time, people are sleeping less, and sleep disorders are on the rise. According to recent polls from the US Centers for Disease Control and Prevention, approximately 29% of US adults report sleeping less than 7 hours per night, and 50 to 70 million have chronic sleep and wakefulness disorders.

The sleep curtailment of our times probably is partly self-imposed, as the pace and the opportunities of modern society place more demands on time for work and leisure activities and leave less time for sleep.

The quality of sleep has also declined as the population has aged and as the prevalence of obesity and its related sleep disorders has increased. Furthermore, patients with type 2 diabetes tend to sleep less, and to sleep poorly. Poor sleep quality generally results in overall sleep loss.

 


 

GLUCOSE TOLERANCE HAS A CIRCADIAN RHYTHM

The human body regulates blood levels of glucose within a narrow range.

Glucose tolerance refers to the ability to maintain euglycemia by disposing of exogenous glucose via insulin-mediated and non–insulin-mediated mechanisms. Normal glucose tolerance depends on the ability of the pancreatic beta cells to produce insulin. As insulin sensitivity declines, insulin secretion increases to maintain normal glucose levels. Diabetes becomes manifest when the pancreatic beta cells fail to compensate for the decreased insulin sensitivity.

Glucose tolerance varies in a circadian rhythm, including during the different stages of sleep.

HOW SLEEP AFFECTS METABOLISM AND HORMONES

Sleep has often been thought of as a "restorative” process for the mind and the body; however, many studies have shown that it also directly affects many metabolic and hormonal processes.

Sleep has five stages: rapid eye movement (REM) sleep and stages 1, 2, 3, and 4 of non-REM sleep. The deeper stages of non-REM sleep, ie, stages 3 and 4, are also known as slow-wave sleep and are thought to be the most restorative.

Additionally, the onset of slow-wave sleep is temporally associated with transient metabolic, hormonal, and neurophysiologic changes, all of which can affect glucose homeostasis. The brain uses less glucose, the pituitary gland releases more growth hormone and less corticotropin, the sympathetic nervous system is less active, and conversely, vagal tone is increased.

As a result, in the first part of the night, when slow-wave sleep predominates, glucose metabolism is slower. These effects are reversed in the second part of the night, when REM sleep, stage 1, and awakening are more likely.

In view of these important changes in glucose metabolism during sleep, it is not surprising that getting less sleep or poorer sleep on a regular basis could affect overall glucose homeostasis.

SHORT SLEEP DURATION AND RISK OF DIABETES

Laboratory and epidemiologic evidence supports an association between short sleep duration (< 7 hours per night) and the risk of diabetes, and also between poor sleep quality and the risk of diabetes. We will explore putative mechanisms for these relationships.

Laboratory studies of short sleep duration and glucose metabolism

Studies in small numbers of healthy volunteers who underwent experimental sleep restriction or disruption have revealed mechanisms by which sleep loss might increase the risk of diabetes.

Kuhn et al performed the very first laboratory study of the effect of sleep deprivation on metabolism. Published in 1969, it showed that total sleep deprivation led to a marked increase in glucose levels.

A caution in extrapolating such results to real-life conditions is that total sleep deprivation is uncommon in humans and is inevitably followed by sleep recovery, with normalization of glucose metabolism. However, people in modern society are experiencing recurrent partial sleep deprivation, and its effect on glucose metabolism may be different.

Spiegel et al, in landmark laboratory studies of partial sleep deprivation in healthy, lean adults, found that restricting sleep to 4 hours per night for 6 nights resulted in a 40% decrease in glucose tolerance, to levels similar to those seen in older adults with impaired glucose tolerance. This metabolic change was paralleled by an increase in the activity of the sympathetic nervous system, and both of these effects reversed with sleep recovery.

A criticism of these initial studies is that they restricted sleep to 4 hours, a restriction more severe than that seen in real life.

Nedeltcheva et al more recently examined the effects of less-severe sleep curtailment (5.5 hours per night for 14 nights) in sedentary middle-aged men and women. This degree of bedtime restriction led to a decrease in glucose tolerance due to decreased insulin sensitivity in the absence of adequate beta cell compensation.

Such recurrent bedtime restriction is closer to the short sleep duration experienced by many people in everyday life, and in people at risk it may facilitate the development of insulin resistance, reduced glucose tolerance, and ultimately diabetes. Indeed, epidemiologic studies suggest that people who sleep less than 6 hours per night are at higher risk of type 2 diabetes.

Epidemiologic studies of short sleep duration and glucose metabolism

Multiple cross-sectional epidemiologic studies have suggested an association between short sleep duration and diabetes, and several prospective epidemiologic studies have suggested that short sleep actually plays a causative role in diabetes.

The landmark observations of Spiegel et al led to a number of epidemiologic studies examining the relationships between sleep duration and sleep disturbances and diabetes risk.

The Sleep Heart Study was a large, cross-sectional, community-based study of the cardiovascular consequences of sleep-disordered breathing. The authors assessed the relationship between reported sleep duration and impaired glucose tolerance or type 2 diabetes in more than 1,400 men and women who had no history of insomnia. After adjustment for age, sex, race, body habitus, and apnea-hypopnea index, the prevalence of impaired glucose tolerance and type 2 diabetes was higher in those who reported sleeping 6 hours or less per night—or 9 hours or more per night (more below about the possible effect of too much sleep on the risk of diabetes).

The major limitations of the study were that it was cross-sectional in design, sleep duration was self-reported, the reasons for sleep curtailment were unknown, and possible confounding variables as physical activity, diet, and socioeconomic status were not measured.

Knutson et al, in our medical center, examined the association between self-reported sleep duration and sleep quality on the one hand and hemoglobin A1c levels on the other in 161 black patients with type 2 diabetes. In patients without diabetic complications, glycemic control correlated with perceived sleep debt (calculated as the difference between self-reported actual and preferred weekday sleep duration); the authors calculated that a perceived sleep debt of 3 hours per night predicted a hemoglobin A1cvalue 1.1 absolute percentage points higher than the median value. The analyses controlled for age, sex, body mass index, insulin use, and the presence of major complications; it excluded patients whose sleep was frequently disrupted by pain. The effect size was comparable to (but opposite) that of oral antidiabetic drugs. However, the direction of causality cannot be confirmed from this association, as it is possible that poor glycemic control in diabetic patients could impair their ability to achieve sufficient sleep.

To date, several major prospective studies have looked at the association between short sleep duration and sleep problems and the risk of developing type 2 diabetes in adults.

The Nurses Health Study followed 70,000 nondiabetic women for 10 years. Compared with nurses who slept 7 to 8 hours per 24 hours, those who slept 5 hours or less had a relative risk of diabetes of 1.34 even after controlling for many covariables, such as body mass index, shift work, hypertension, exercise, and depression.

The first National Health and Nutrition Examination Survey (NHANES I) examined the effect of sleep duration on the risk of incident diabetes in roughly 9,000 men and women over a period of 8 to 10 years. The statistical model included body mass index and hypertension and adjusted for physical activity, depression, alcohol consumption, ethnicity, education, marital status, and age. Findings: those who slept 5 hours or less per night were significantly more likely to develop type 2 diabetes than were those who slept 7 hours per night (odds ratio 1.57, 95% confidence interval [CI] 1.11–2.22), and so were those who slept 9 or more hours per night (odds ratio 1.57, 95% CI 1.10–2.24).

Kawakami et al followed 2,649 Japanese men for 8 years. Those who had difficulty going to sleep and staying asleep, which are both likely to result in shorter sleep duration, had higher age-adjusted risks of developing type 2 diabetes, with hazard ratios of 2.98 and 2.23, respectively.

Björkelund et al followed 6,599 nondiabetic Swedish men for an average of 15 years. Self-reported difficulty sleeping predicted the development of diabetes with an odds ratio of 1.52 even after controlling for age, body mass index at screening, changes in body mass index at follow-up, baseline glucose level, follow-up time, physical activity, family history of type 2 diabetes, smoking, social class, and alcohol intake.

Interestingly, the authors found that the resting heart rate was higher at baseline in the men who later developed diabetes. This finding could be interpreted as reflecting greater sympathetic nervous system activity, a putative mediator of the metabolic dysfunction associated with both short sleep duration and obstructive sleep apnea.

Meisinger et al, in a study of more than 8,000 nondiabetic German men and women 25 to 74 years old, found a hazard ratio of developing diabetes of 1.60 (95% CI 1.05–2.45) in men and 1.98 (95% CI 1.20–3.29) in women who reported difficulty staying asleep, who thus would have shortened sleep duration. This effect was independent of other risk factors for diabetes.

Yaggi et al, in a prospective study of 1,139 US men, also found a U-shaped relationship between sleep duration and the incidence of diabetes, with higher rates in people who slept less than 5 or more than 8 hours per night.

Cappuccio et al performed a meta-analysis of all the prospective studies published to date. Their review included 10 prospective studies, with 107,756 participants followed for a median of 9.5 years. Sleep duration and sleep disturbances were self-reported in all the studies. They calculated that the risk of developing diabetes was 28% higher with short sleep duration (≤ 5 or < 6 hours in the different studies), 48% higher with long sleep duration (> 8 hours), 57% higher with difficulty going to sleep, and 84% higher with difficulty staying asleep.

Limitations of these studies. A consideration when trying to interpret the relationship between length of sleep and the incidence of diabetes is that sleep duration in these studies was self-reported, not measured. If a patient reports sleeping more than 8 hours per night, it could mean that he or she is not truly getting so much sleep, but rather is spending more time in bed trying to sleep.

Another possibility is that the higher incidence of type 2 diabetes in people who slept longer is due to undiagnosed obstructive sleep apnea, which is associated with daytime sleepiness and possibly longer sleep time to compensate for inefficient sleep.

Finally, depressive symptoms, unemployment, a low level of physical activity, and undiagnosed health conditions have all been associated with long sleep duration and could affect the relationship with diabetes risk.

In summary, epidemiologic studies from different geographic locations have consistently indicated that short sleep or poor sleep may increase the risk of developing type 2 diabetes mellitus and suggest that such an association spans different countries, cultures, and ethnic groups.

Therefore, there is a need for additional prospective epidemiologic studies that use objective measures of sleep. Furthermore, studies need to determine whether the cause of sleep restriction (eg, insomnia vs lifestyle choice) affects this relationship. Randomized, controlled, interventional studies would also be useful to determine whether lengthening sleep duration affects the development of impaired glucose tolerance or type 2 diabetes mellitus.

Putative mechanisms linking short sleep duration and the risk of diabetes

The effects of sleep loss on glucose metabolism are likely multifactorial, involving several interacting pathways.

Decreased brain glucose utilization has been shown on positron emission tomography in sleep-deprived subjects.

Hormonal dysregulation. Sleep deprivation is associated with disturbances in the secretion of the counterregulatory hormones growth hormone and cortisol.

Young, healthy volunteers who were allowed to sleep only 4 hours per night for 6 nights showed a change in their patterns of growth hormone release, from a normal single pulse to a biphasic pattern. They were exposed to a higher overall amount of growth hormone in the sleep-deprived condition, which could contribute to higher glucose levels.

Also, evening cortisol levels were significantly higher in young, healthy men who were allowed to sleep only 4 hours per night for 6 nights, as well as in young, healthy women who were allowed to sleep only 3 hours for 1 night. A cross-sectional analysis that included 2,751 men and women also demonstrated that short sleep duration and sleep disturbances are independently associated with more cortisol secretion in the evening.Elevated evening cortisol levels can lead to morning insulin resistance.

Inflammation. Levels of inflammatory cytokines, inflammation, or both increase as sleep duration decreases, which in turn can also increase insulin resistance.

Sympathetic nervous system activity. Patients who have been sleep-deprived have been shown to have higher sympathetic nervous system activity, lower parasympathetic activity, or both. The sympathetic nervous system inhibits insulin release while the parasympathetic system stimulates it, so these changes both increase glucose levels.Moreover, overactivity of the sympathetic nervous system results in insulin resistance.

Excess weight is a well-established risk factor for type 2 diabetes mellitus, and several epidemiologic studies have suggested that sleep loss may increase the risk of becoming overweight or obese, which would ultimately increase the risk of type 2 diabetes.

A primary mechanism linking sleep deprivation and weight gain is likely to be hyperactivity of the orexin system. Orexigenic neurons play a central role in wakefulness, but, as suggested by the name, they also promote feeding. Studies in animals have indicated that the orexin system is overactive during sleep deprivation, and this could be in part mediated by the increase in sympathetic activity.

Increased sympathetic activity also affects the levels of peripheral appetite hormones, inhibiting leptin release and stimulating ghrelin release. Lower leptin levels and higher ghrelin levels act in concert to further activate orexin neurons, resulting in increased food intake.

One could also argue that less time sleeping also allows more opportunity to eat.

Reduced energy expenditure. Sleep loss and its associated sleepiness and fatigue may result in reduced energy expenditure, partly due to less exercise but also due to less nonexercise activity thermogenesis. To date, reduced energy expenditure is an unexplored pathway that could link short sleep, the risk of obesity, and ultimately diabetes. In many overweight and obese people, this cascade of negative events is likely to be accelerated by sleep-disordered breathing, a reported independent risk factor for insulin resistance.

SLEEP QUALITY AND THE RISK OF DIABETES

Slow-wave sleep and diabetes

Slow-wave sleep, the most restorative sleep, is associated with metabolic, hormonal, and neurophysiologic changes that affect glucose homeostasis. Its disturbance may have deleterious effects on glucose tolerance.

Shallow slow-wave sleep occurs in elderly people and in obese people, even in the absence of obstructive sleep apnea. Both groups are also at higher risk of diabetes. One wonders if the decreased slow-wave sleep could in part contribute to the risk of diabetes in these groups.

A few studies specifically tested the effect of experimental suppression of slow-wave sleep on glucose homeostasis.

Tasali et al evaluated nine young, lean, nondiabetic men and women after 2 consecutive nights of undisturbed sleep and after 3 consecutive nights of suppressed slow-wave sleep without a change in total sleep duration or in REM sleep duration. Slow-wave sleep was disturbed by "delivering acoustic stimuli of various frequencies and intensities” whenever the subjects started to go into stage 3 or stage 4 sleep. This decreased the amount of slow-wave sleep by nearly 90%, which is comparable to the degree of sleep fragmentation seen in moderate to severe obstructive sleep apnea. After 3 nights of slow-wave sleep suppression, insulin sensitivity decreased by 25%, without a compensatory increase in insulin release, which resulted in a reduction in glucose tolerance of 23%, a value seen in older adults with impaired glucose tolerance.

Stamatakis et al confirmed these findings in a similar study of 11 healthy, normal volunteers whose sleep was fragmented for 2 nights across all stages of sleep using auditory and mechanical stimuli. Insulin sensitivity significantly decreased, as did glucose effectiveness (ability of glucose to dispose itself independently of an insulin response) after the 2 nights of disturbed sleep quality.

These results support the hypothesis that poor sleep quality with short durations of slow-wave sleep, as seen with aging and obesity, could contribute to the higher risk of type 2 diabetes in these populations. These data also suggest that more studies are needed to look at the relationship between amount and quality of slow-wave sleep and diabetes risk.

Obstructive sleep apnea and diabetes

The most robust evidence that not only short sleep duration but also poor sleep quality affects diabetes risk comes from studies of metabolic function in patients with obstructive sleep apnea, an increasingly common condition.

Obstructive sleep apnea is characterized by recurrent episodes of partial or complete upper airway obstruction with intermittent hypoxia and microarousals, resulting in low amounts of slow-wave sleep and overall decreased sleep quality.

Obstructive sleep apnea is common in patients with type 2 diabetes, and several clinical and epidemiologic studies suggest that, untreated, it may worsen diabetes risk or control.

The Sleep AHEAD (Action for Health in Diabetes) study revealed, in cross-sectional data, that more than 84% of obese patients with type 2 diabetes had obstructive sleep apnea (with an apnea-hypopnea index ≥ 5).

Aronsohn et al, in a study conducted in our laboratory in 60 patients with type 2 diabetes, found that 46 (77%) of them had obstructive sleep apnea. Furthermore, the worse the obstructive sleep apnea, the worse the glucose control. After controlling for age, sex, race, body mass index, number of diabetes medications, level of exercise, years of diabetes, and total sleep time, compared with patients without obstructive sleep apnea, the adjusted mean hemoglobin A1c was increased in a linear trend by (in absolute percentage points):

  • 1.49% in patients with mild obstructive sleep apnea (P = .0028)

  • 1.93% in patients with moderate obstructive sleep apnea (P = .0033)

  • 3.69% in patients with severe obstructive sleep apnea (P < .0001).

Other epidemiologic studies. A growing number of epidemiologic studies, in various geographic regions, have suggested an independent link between obstructive sleep apnea and risk of type 2 diabetes. Most of the studies have been cross-sectional, and while most had positive findings, a criticism is that the methodology varied among the studies, both in how obstructive sleep apnea was assessed (snoring vs polysomnography) and in the metabolic assessment (oral glucose tolerance test, homeostatic model assessment, hemoglobin A1c, medical history, physician examination, or patient report).

So far, 14 population studies (TABLE 1) have assessed obstructive sleep apnea with polysomnography, but only two of them were prospective. Of the cross-sectional studies, all but the earliest study, which also was the smallest, found an association between the increased severity of obstructive sleep apnea and alterations in glucose metabolism consistent with an increased risk of diabetes. The one retrospective study and the first published prospective study did not find an independent relationship between the severity of obstructive sleep apnea at baseline and the incidence of diabetes. Of note, the duration of follow-up in the prospective study was only 4 years, which may not be sufficient.

Table 1

Studies linking obstructive sleep apnea to altered glucose metabolism and diabetes

Author & Year No. of Patients Findings

Cross-Sectional Studies

Stoohs et al,62 1996 50 Increase in insulin resistance in obstructive sleep apnea (OSA) was entirely dependent on body mass index.

Elmasry et al,66 2001 116 Prevalence of severe OSA in people with diabetes was 36% vs. 14% in those without diabetes (P < .05)

Punjabi et al,55, 2002 150 Quartiles of OSA severity (apnea-hypopnea index [AHI] 5-40) had dose effect on 2-hour glucose and insulin levels.

IP et al,452002 270 One unit increase in AHI increased fasting insulin or homeostasis model

Reichmuth et al,64 2005 1,382 Odds ratio of diabetes with AHI > 15 vs. < 5 was 2.30 (95% confidence interval [CI] 1.28-4.11

Lam et al,67 2006 255 AHI greater than or equal to 5 (vs < 5) increased the odds of fasting glucose greater than or equal to 110 mg/dL, with an odds ratio of 2.74 (95% CI 1.16-6.49)

Okada et al,68 2006 207 12% of subjects with sleep-disordered breathing had hemoglobin A1c > 5.8%, vs. only 4% of those without sleep-disordered breathing (P < .05)

Sulit et al,69 2006 394 Subjects with oxygen saturation < 90% greater than or equal to 2% of time had odds ratio of 2.33 (95% CI 1.38-3.94) of impaired glucose tolerance.

Seicean et al,70 2008 2,588 Respiratory disturbance index greater than or equal to 10 events/hour was associated with odds ratio of 1.3 (95% CI 1.1-1.6) for impaired fasting glucose, 1.2 (1.0-1.4) for impaired glucose tolerance, 1.4 (1.1-2.7) for both impaired fasting glucose and impaired glucose tolerance, and 1.7 (1.1-2.7) for occult type 2 diabetes mellitus.

Punjabi et al,71 2009 118 26.7% reduction in insulin sensitivity with mild sleep-disordered breathing, 36.5% with moderate, and 43.7% with severe.

Steiropoulos et al,72 2009 56 Fasting glucose and hemoglobin A1c were not correlated with AHI or average oxygen saturation (P = .008).

Aronsohn et al,5 2010 60 Mean hemoglobin A1c significantly increased by 1.49% with mild OSA, 1.93% with moderate OSA, and 3.69% with severe OSA.

Prospective Studies

Reichmuth et al,64 2005 987 No change in odds ratio of type 2 diabetes with higher AHI when adjusted for waist girth.

Botros et al,65 2009 544 For every quartile of severity of OSA, there was a significant 43% increased incidence of type 2 diabetes.

Retrospective Study

Mahmood et al,63 2009 1,088 OSA was not independently associated with type 2 diabetes.

A more recent prospective study of 544 nondiabetic patients showed that the risk of developing type 2 diabetes over an average of 2.7 years of follow-up was a function of the severity of obstructive sleep apnea expressed in quartiles: for each increased quartile of severity there was a 43% increase in the incidence of diabetes. Additionally, in patients with moderate to severe sleep apnea, regular use of continuous positive airway pressure (CPAP) was associated with an attenuated risk.

Two prospective studies (not included in TABLE 1) used snoring as a marker of obstructive sleep apnea; at 10 years of follow-up, snoring was associated with a higher risk of developing diabetes in both men and women.

Does CPAP improve glucose metabolism? Other studies have specifically examined the effects of CPAP treatment on glucose metabolism, in both diabetic and nondiabetic populations. Accumulating evidence suggests that metabolic abnormalities can be partially corrected by CPAP treatment, which supports the concept of a causal link between obstructive sleep apnea and altered glucose control. This topic is beyond the scope of this review; please see previously published literature for further information. Whether treating obstructive sleep apnea may delay the development or reduce the severity of type 2 diabetes is another important unanswered question.

Is obstructive sleep apnea a cause or consequence of diabetes? It may be a novel risk factor for type 2 diabetes, and its association with altered glucose metabolism is well supported by a large set of cross-sectional studies, but there are still insufficient longitudinal studies to indicate a direction of causality.

If obstructive sleep apnea is the cause, what is the mechanism? There are likely many. High levels of sympathetic nervous system activity, intermittent hypoxia, sleep fragmentation, and sleep loss in obstructive sleep apnea may all lead to dysregulation of the hypothalamic-pituitary axis, endothelial dysfunction, and alterations in cytokine and adipokine release and are all potential mechanisms of abnormal glucose metabolism in this population.

WHAT TO TELL PATIENTS

Taken together, the current evidence suggests that strategies to improve the duration and the quality of sleep should be considered as a potential intervention to prevent or delay the development of type 2 diabetes mellitus in at-risk populations. While further studies are needed to better elucidate the mechanisms of the relationship between sleep loss and diabetes risk and to determine if extending sleep and treating obstructive sleep apnea decreases the risk of diabetes, we urge clinicians to recommend at least 7 hours of uninterrupted sleep per night as a goal in maintaining a healthy lifestyle. Additionally, clinicians should systematically evaluate the risk of obstructive sleep apnea in their patients who have type 2 diabetes mellitus and the metabolic syndrome, and conversely, should assess for diabetes in patients with known obstructive sleep apnea.

REFERENCES

    1. Pannain S,
    2. Van Cauter E
    . Sleep loss, obesity and diabetes: prevalence, association and emerging evidence for causation. Obesity Metab 2008; 4:28–41.
    1. Van Cauter E,
    2. Knutson KL
    . Sleep and the epidemic of obesity in children and adults. Eur J Endocrinol 2008; 159(suppl 1):S59–S66.
     
    1. US Centers for Disease Control and Prevention (CDC)
    . Perceived insufficient rest or sleep among adults—United States, 2008. MMWR Morb Mortal Wkly Rep 2009;58:1175–1179.
     
    1. Knutson KL,
    2. Ryden AM,
    3. Mander BA,
    4. Van Cauter E
    . Role of sleep duration and quality in the risk and severity of type 2 diabetes mellitus. Arch Intern Med 2006;166:1768–1774.
     
    1. Aronsohn RS,
    2. Whitmore H,
    3. Van Cauter E,
    4. Tasali E
    . Impact of untreated obstructive sleep apnea on glucose control in type 2 diabetes. Am J Respir Crit Care Med 2010; 181:507–513.
     
    1. Broussard J,
    2. Knutson KL
    . Sleep and metabolic risk and disease. In: CappuccioFP, Miller MA, Lockley SW, editors. Sleep, Health and Society: From Aetiology to Public Health. Cary, NC: Oxford University Press; 2010:111–140.
    1. Zoccoli G,
    2. Walker AM,
    3. Lenzi P,
    4. Franzini C
    . The cerebral circulation during sleep: regulation mechanisms and functional implications. Sleep Med Rev 2002;6:443–455.
     
    1. Pannain S,
    2. Van Cauter E
    . Modulation of endocrine function by sleepwake homeostasis and circadian rhythmicity. Sleep Med Clin 2007; 2:147–159.
     
    1. Somers VK,
    2. Dyken ME,
    3. Mark AL,
    4. Abboud FM
    . Sympathetic-nerve activity during sleep in normal subjects. N Engl J Med 1993; 328:303–307.
     
    1. Kuhn E,
    2. Brodan V,
    3. Brodanová M,
    4. Rysánek K
    . Metabolic reflection of sleep deprivation. Act Nerv Super (Praha) 1969; 11:165–174.
     
    1. Spiegel K,
    2. Leproult R,
    3. Van Cauter E
    . Impact of sleep debt on metabolic and endocrine function. Lancet 1999; 354:1435–1439.
     
    1. Nedeltcheva AV,
    2. Kessler L,
    3. Imperial J,
    4. Penev PD
    . Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance. J Clin Endocrinol Metab2009; 94:3242–3250.
     
    1. Zizi F,
    2. Jean-Louis G,
    3. Brown CD,
    4. Ogedegbe G,
    5. Boutin-Foster C,
    6. McFarlane SI
    . Sleep duration and the risk of diabetes mellitus: epidemiologic evidence and pathophysiologic insights. Curr Diab Rep 2010; 10:43–47.
     

    1. Gottlieb DJ,
    2. Punjabi NM,
    3. Newman AB,
    4. et al.
    Association of sleep time with diabetes mellitus and impaired glucose tolerance. Arch Intern Med 2005; 165:863–867.
     
    1. Ayas NT,
    2. White DP,
    3. Al-Delaimy WK,
    4. et al.
    A prospective study of selfreported sleep duration and incident diabetes in women. Diabetes Care 2003;26:380–384.

    1. Gangwisch JE,
    2. Heymsfield SB,
    3. Boden-Albala B,
    4. et al.
    Sleep duration as a risk factor for diabetes incidence in a large U.S. sample. Sleep 2007; 30:1667–1673.
     
    1. Kawakami N,
    2. Takatsuka N,
    3. Shimizu H
    . Sleep disturbance and onset of type 2 diabetes. Diabetes Care 2004; 27:282–283.
     
    1. Björkelund C,
    2. Bondyr-Carlsson D,
    3. Lapidus L,
    4. et al.
    Sleep disturbances in midlife unrelated to 32-year diabetes incidence: the prospective population study of women in Gothenburg. Diabetes Care 2005; 28:2739–2744.
     
    1. Nilsson PM,
    2. Rööst M,
    3. Engström G,
    4. Hedblad B,
    5. Berglund G
    . Incidence of diabetes in middle-aged men is related to sleep disturbances. Diabetes Care 2004;27:2464–2469.
    1. Spiegel K,
    2. Tasali E,
    3. Penev P,
    4. Van Cauter E
    . Brief communication: sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 2004; 141:846–850.
     
    1. Punjabi NM,
    2. Polotsky VY
    . Disorders of glucose metabolism in sleep apnea. J Appl Physiol 2005; 99:1998–2007.
    1. Meisinger C,
    2. Heier M,
    3. Loewel H,
    4. MONICA/KORA Augsburg Cohort Study
    .Sleep disturbance as a predictor of type 2 diabetes mellitus in men and women from the general population. Diabetologia 2005; 48:235–241.
    1. Yaggi HK,
    2. Araujo AB,
    3. McKinlay JB
    . Sleep duration as a risk factor for the development of type 2 diabetes. Diabetes Care 2006; 29:657–661.
     
    1. Cappuccio FP,
    2. D’Elia L,
    3. Strazzullo P,
    4. Miller MA
    . Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis. Diabetes Care 2010; 33:414–420.
     
    1. Thomas M,
    2. Sing H,
    3. Belenky G,
    4. et al.
    Neural basis of alertness and cognitive performance impairments during sleepiness. I. Effects of 24 h of sleep deprivation on waking human regional brain activity. J Sleep Res 2000; 9:335–352.
     
    1. Spiegel K,
    2. Leproult R,
    3. Colecchia EF,
    4. et al.
    Adaptation of the 24-h growth hormone profile to a state of sleep debt. Am J Physiol Regul Integr Comp Physiol 2000;279:R874–R883.
     
    1. Omisade A,
    2. Buxton OM,
    3. Rusak B
    . Impact of acute sleep restriction on cortisol and leptin levels in young women. Physiol Behav 2010; 99:651–656.
     
    1. Kumari M,
    2. Badrick E,
    3. Ferrie J,
    4. Perski A,
    5. Marmot M,
    6. Chandola T
    . Selfreported sleep duration and sleep disturbance are independently associated with cortisol secretion in the Whitehall II study. J Clin Endocrinol Metab 2009; 94:4801–4809.
     
    1. Van Cauter E,
    2. Polonsky KS,
    3. Scheen AJ
    . Roles of circadian rhythmicity and sleep in human glucose regulation. Endocr Rev 1997; 18:716–738.
     
    1. Vgontzas AN,
    2. Papanicolaou DA,
    3. Bixler EO,
    4. et al.
    Circadian interleukin-6 secretion and quantity and depth of sleep. J Clin Endocrinol Metab 1999; 84:2603–2607.
  1. 31.
    1. Vgontzas AN,
    2. Zoumakis E,
    3. Bixler EO,
    4. et al.
    Adverse effects of modest sleep restriction on sleepiness, performance, and inflammatory cytokines. J Clin Endocrinol Metab 2004; 89:2119–2126.
     
    1. Spiegel K,
    2. Leproult R,
    3. L’hermite-Balériaux M,
    4. Copinschi G,
    5. Penev PD,
    6. Van Cauter E
    . Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab 2004; 89:5762–5771.
     
    1. Teff KL
    . Visceral nerves: vagal and sympathetic innervation. JPEN J Parenter Enteral Nutr 2008; 32:569–571.
     
    1. Esler M,
    2. Rumantir M,
    3. Wiesner G,
    4. Kaye D,
    5. Hastings J,
    6. Lambert G
    .Sympathetic nervous system and insulin resistance: from obesity to diabetes. Am J Hypertens 2001; 14:304S–309S.
     
    1. Cappuccio F,
    2. Miller MA
    . The epidemiology of sleep and cardiovascular risk and disease. In: Cappuccio FP, Miller MA, Lockley SW, editors. Sleep, Health and Society: From Aetiology to Public Health. Cary, NC: Oxford University Press;2010:111–140.

    1. Sakurai T
    . Roles of orexin/hypocretin in regulation of sleep/wakefulness and energy homeostasis. Sleep Med Rev 2005; 9:231–241.
    1. Wu MF,
    2. John J,
    3. Maidment N,
    4. Lam HA,
    5. Siegel JM
    . Hypocretin release in normal and narcoleptic dogs after food and sleep deprivation, eating, and movement. Am J Physiol Regul Integr Comp Physiol 2002; 283:R1079–R1086.
     
    1. Estabrooke IV,
    2. McCarthy MT,
    3. Ko E,
    4. et al.
    Fos expression in orexin neurons varies with behavioral state. J Neurosci 2001; 21:1656–1662.
     
    1. Zeitzer JM,
    2. Buckmaster CL,
    3. Lyons DM,
    4. Mignot E
    . Increasing length of wakefulness and modulation of hypocretin-1 in the wake-consolidated squirrel monkey. Am J Physiol Regul Integr Comp Physiol 2007; 293:R1736–R1742.
     
  2. Rayner DV,
    1. Trayhurn P
    . Regulation of leptin production: sympathetic nervous system interactions. J Mol Med 2001; 79:8–20.
    1. van der Lely AJ,
    2. Tschöp M,
    3. Heiman ML,
    4. Ghigo E
    . Biological, physiological, pathophysiological, and pharmacological aspects of ghrelin. Endocr Rev 2004;25:426–457.
    1. Samson WK,
    2. Taylor MM,
    3. Ferguson AV
    . Non-sleep effects of hypocretin/orexin. Sleep Med Rev 2005; 9:243–252.
    1. Willie JT,
    2. Chemelli RM,
    3. Sinton CM,
    4. Yanagisawa M
    . To eat or to sleep? Orexin in the regulation of feeding and wakefulness. Annu Rev Neurosci 2001;24:429–458.
    1. Qin LQ,
    2. Li J,
    3. Wang Y,
    4. Wang J,
    5. Xu JY,
    6. Kaneko T
    . The effects of nocturnal life on endocrine circadian patterns in healthy adults. Life Sci 2003; 73:2467–2475.
     
    1. Ip MS,
    2. Lam B,
    3. Ng MM,
    4. Lam WK,
    5. Tsang KW,
    6. Lam KS
    . Obstructive sleep apnea is independently associated with insulin resistance. Am J Respir Crit Care Med2002; 165:670–676.
    1. Punjabi NM,
    2. Shahar E,
    3. Redline S,
    4. Gottlieb DJ,
    5. Givelber R,
    6. Resnick HE,
    7. Sleep Heart Health Study Investigators
    . Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study. Am J Epidemiol 2004;160:521–530.
     
    1. Van Cauter E,
    2. Leproult R,
    3. Plat L
    . Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men. JAMA 2000; 284:861–868.
     
    1. Resta O,
    2. Foschino Barbaro MP,
    3. Bonfitto P,
    4. et al.
    Low sleep quality and daytime sleepiness in obese patients without obstructive sleep apnoea syndrome. J Intern Med 2003; 253:536–543.
    1. Vgontzas AN,
    2. Tan TL,
    3. Bixler EO,
    4. Martin LF,
    5. Shubert D,
    6. Kales A
    . Sleep apnea and sleep disruption in obese patients. Arch Intern Med 1994; 154:1705–1711.
     
    1. Mokdad AH,
    2. Ford ES,
    3. Bowman BA,
    4. et al.
    Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA 2003; 289:76–79.
     

    1. Tasali E,
    2. Leproult R,
    3. Ehrmann DA,
    4. Van Cauter E
    . Slow-wave sleep and the risk of type 2 diabetes in humans. Proc Natl Acad Sci U S A 2008; 105:1044–1049.
     
    1. Prigeon RL,
    2. Kahn SE,
    3. Porte D Jr.
    . Changes in insulin sensitivity, glucose effectiveness, and B-cell function in regularly exercising subjects. Metabolism 1995;44:1259–1263.
    1. Stamatakis KA,
    2. Punjabi NM
    . Effects of sleep fragmentation on glucose metabolism in normal subjects. Chest 2010; 137:95–101.
     
    1. Caples SM,
    2. Gami AS,
    3. Somers VK
    . Obstructive sleep apnea. Ann Intern Med2005; 142:187–197.
     
    1. Punjabi NM,
    2. Sorkin JD,
    3. Katzel LI,
    4. Goldberg AP,
    5. Schwartz AR,
    6. Smith PL
    .Sleep-disordered breathing and insulin resistance in middle-aged and overweight men. Am J Respir Crit Care Med 2002; 165:677–682.
    1. Tassone F,
    2. Lanfranco F,
    3. Gianotti L,
    4. et al.
    Obstructive sleep apnoea syndrome impairs insulin sensitivity independently of anthropometric variables. Clin Endocrinol (Oxf) 2003; 59:374–379.

    1. Coughlin SR,
    2. Mawdsley L,
    3. Mugarza JA,
    4. Calverley PM,
    5. Wilding JP
    . Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J 2004; 25:735–741.
     

    1. Svatikova A,
    2. Wolk R,
    3. Gami AS,
    4. Pohanka M,
    5. Somers VK
    . Interactions between obstructive sleep apnea and the metabolic syndrome. Curr Diab Rep 2005; 5:53–58.
     

    1. Budhiraja R,
    2. Quan SF
    . Sleep-disordered breathing and cardiovascular health. Curr Opin Pulm Med 2005; 11:501–506.
    1. Foster GD,
    2. Sanders MH,
    3. Millman R,
    4. et al.,
    5. Sleep AHEAD Research Group
    .Obstructive sleep apnea among obese patients with type 2 diabetes. Diabetes Care2009; 32:1017–1019.
    1. Tasali E,
    2. Mokhlesi B,
    3. Van Cauter E
    . Obstructive sleep apnea and type 2 diabetes: interacting epidemics. Chest 2008; 133:496–506.

    1. Stoohs RA,
    2. Facchini F,
    3. Guilleminault C
    . Insulin resistance and sleep-disordered breathing in healthy humans. Am J Respir Crit Care Med 1996; 154:170–174.
     
    1. Mahmood K,
    2. Akhter N,
    3. Eldeirawi K,
    4. et al.
    Prevalence of type 2 diabetes in patients with obstructive sleep apnea in a multi-ethnic sample. J Clin Sleep Med 2009;5:215–221.
     
    1. Reichmuth KJ,
    2. Austin D,
    3. Skatrud JB,
    4. Young T
    . Association of sleep apnea and type II diabetes: a population-based study. Am J Respir Crit Care Med 2005;172:1590–1595.
    1. Botros N,
    2. Concato J,
    3. Mohsenin V,
    4. Selim B,
    5. Doctor K,
    6. Yaggi HK
    . Obstructive sleep apnea as a risk factor for type 2 diabetes. Am J Med 2009; 122:1122–1127.
     
    1. Elmasry A,
    2. Lindberg E,
    3. Berne C,
    4. et al.
    Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study. J Intern Med 2001;249:153–161.
     
    1. Lam JC,
    2. Lam B,
    3. Lam CL,
    4. et al.
    Obstructive sleep apnea and the metabolic syndrome in community-based Chinese adults in Hong Kong. Respir Med 2006;100:980–987.
     
    1. Okada M,
    2. Takamizawa A,
    3. Tsushima K,
    4. Urushihata K,
    5. Fujimoto K,
    6. Kubo K
    .Relationship between sleep-disordered breathing and lifestyle-related illnesses in subjects who have undergone health-screening. Intern Med 2006; 45:891–896.
     
    1. Sulit L,
    2. Storfer-Isser A,
    3. Kirchner HL,
    4. Redline S
    . Differences in polysomnography predictors for hypertension and impaired glucose tolerance. Sleep 2006; 29:777–783.
     
    1. Seicean S,
    2. Kirchner HL,
    3. Gottlieb DJ,
    4. et al.
    Sleep-disordered breathing and impaired glucose metabolism in normal-weight and overweight/obese individuals: the Sleep Heart Health Study. Diabetes Care 2008; 31:1001–1006.
    1. Punjabi NM,
    2. Beamer BA
    . Alterations in glucose disposal in sleep-disordered breathing. Am J Respir Crit Care Med 2009; 179:235–240.
     
    1. Steiropoulos P,
    2. Papanas N,
    3. Nena E,
    4. et al.
    Markers of glycemic control and insulin resistance in non-diabetic patients with obstructive sleep apnea hypopnea syndrome: does adherence to CPAP treatment improve glycemic control? Sleep Med2009; 10:887–891.
    1. Al-Delaimy WK,
    2. Manson JE,
    3. Willett WC,
    4. Stampfer MJ,
    5. Hu FB
    . Snoring as a risk factor for type II diabetes mellitus: a prospective study. Am J Epidemiol 2002;155:387–393.
    1. Elmasry A,
    2. Janson C,
    3. Lindberg E,
    4. Gislason T,
    5. Tageldin MA,
    6. Boman G
    . The role of habitual snoring and obesity in the development of diabetes: a 10-year follow-up study in a male population. J Intern Med 2000; 248:13–20.
     
    1. Steiropoulos P,
    2. Papanas N,
    3. Nena E,
    4. Maltezos E,
    5. Bouros D
    . Continuous positive airway pressure treatment in patients with sleep apnoea: does it really improve glucose metabolism? Curr Diabetes Rev 2010; 6:156–166.

Cleve Clin J Med. 2011 Aug;78(8):549-58. Does lack of sleep cause diabetes? Touma, C. Pannain, S.

Tags:  diabetes  sleep 

Share |
PermalinkComments (0)
 

New Thyroid Guideliens for Pregnancy (and Fertility!)

Posted By ona McCulloch, BSc, ND, Wednesday, August 3, 2011
Updated: Tuesday, February 4, 2014

The American Thyroid Association has updated their guidelines for the management of thyroid concerns in pregnancy, the details of which were published in the journal Thyroid this past month. Many of us who work in the field of fertility have long been aware of research suggesting that ranges for TSH should be lower in pregnancy. It is truly great to see that this has been formally recognized. Although these guidelines were written for pregnancy, I also apply these to women with fertility concerns who are preparing for pregnancy. Prevention is always best when it comes to avoiding miscarriage.

Thyroid disease is very common in pregnancy. One of the reasons is thatone of the main thyroid hormones (free T4) decreases in pregnancy.Another reason is that TBG (thyroxine binding globulin) increases during pregnancy – TBG is a hormone that binds to the circulating thyroid hormone, making it unavailable to act on receptors. This aggravates cases of hypothyroidism by binding up the thyroid hormone that would normally be available to work in the body.

hCG, the pregnancy hormone, has a profound effect on thyroid function too. Normally in pregnancy, hCG causes TSH (Thyroid stimulating hormone) to decrease. TSH is produced by the pituitary gland and causes the thyroid gland to make thyroid hormones. So in a healthy pregnancy, we expect a woman to have a lower TSH than she usually would . This makes high levels of TSH in pregnancy to be of even more concern and gives us a lower "normal” reference range for pregnancy. When TSH levels are high, this indicates that the thyroid function is low, as the pituitary is attempting to stimulate more thyroid hormone production from the thyroid gland.

Autoimmune thyroiditisis very common in pregnancy as well. 1 in 10 pregnant women will develop antibodies to the thyroid. Hypothyroidism develops in 16% of women with thyroid antibodies. Thyroid antibodies are also associated with lower success rates in IVF cycles, and increased miscarriage rates, even if there is no hypothyroidism in the patient. Postpartum thyroiditis can occur in around 50% of women who develop antibodies during pregnancy.

As you can see, thyroid conditions are a very common health problem, and have great impact on pregnancies and fertility. Not only is thyroid disease related to miscarriage, but subclinical hypothyroidism or positive thyroid antibodies can impact the brain development of the fetus and have been linked to poor intellectual development in the baby. Hyperthyroidism is related to miscarriage and a host of problems such as intrauterine growth restriction. So this is an issue we must take seriously!

The new guidelines suggest the following:

  1. Trimester specific tighter ranges for TSH:
    TrimesterRange
    First trimester normal range 0.1 to 2.5 mIU/L
    Second trimester 0.2 to 3.0 mIU/L
    Third trimester 0.3 to 3.0 mIU/L
  2. Women who are already receiving thyroid replacement therapy should increase their dose by 25% to 30% when they become pregnant.
  3. The total amount of iodine should be 250 ug from all dietary and supplemental sources.
  4. Monitoring is important to ensure that women with hypothyroidism or subclinical hypothyroidism are not at risk. TSH should be measured once every 4 weeks until 16 to 20 weeks’ gestation and at least once between 26 and 32 weeks’ gestation.

Basic nutrition for thyroid in pregnancy

Of note,although our salt is iodized in developed countries, there is a growing deficiency of iodine.This is because the iodine in our salt supply is not well absorbed and utilized. In pregnancy, there is a 50% increase in iodine requirements. So, choose a prenatal with some iodine content, usually around 150-200ug per day. Do not exceed 500mcg total intake daily, as this can pose an increased risk for hypothyroidism.

Selenium should be part of a prenatal vitamin. Several studies have shown that selenium decreases the levels of thyroid antibodies (anti thyroglobulin (anti TG) and anti thyroidperosidase (anti TPO). A randomized controlled trial found that supplementing with 200mcg of selenium daily during pregnancy and the post partum period reduced the incidence of postpartum thyroiditis in women who were positive for thyroid antibodies. 55 mcg should suffice as prevention in healthy women.

Perinatal thyroid disease is very common and new research is rapidly emerging on this topic. Thyroid disease affects fertility, pregnancy, maternal and fetal health. Women should optimally try to establish healthy thyroid function before conceiving: this way many concerns can be prevented, and the health of both moms and babies will be protected.

References

  • Selenium Supplementation in Patients with Autoimmune Thyroiditis Decreases Thyroid Peroxidase Antibodies Concentrations JCEM 2002 87: 1687-1691
  • Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and Postpartum. The American Thyroid Association Taskforce on Thyroid Disease During Pregnancy and Postpartum. THYROID Volume 21, Number 10, 2011
  • Dietary Iodine: Why Are So Many Mothers Not Getting Enough? Renner R 2010. Environ Health Perspect 118:a438-a442.
    Increased prevalence of thyroid antibodies in euthyroid women with a history of recurrent in-vitro fertilization failure Hum. Reprod. (2000) 15(3): 545-548

Tags:  Infertility  prenatal 

Share |
PermalinkComments (0)
 

5 Questions to Ask a Potential Practice Website Vendor

Posted By Drew McGray, Monday, August 1, 2011
Updated: Tuesday, February 4, 2014

As healthcare continues to be transformed by technology; refreshing or completely re-architecting your practice's website might be on your radar. Unless you have an in-house marketing team, you will probably be outsourcing your website design and production to a third party. How do you know who is going to deliver the most return on your investment? Here are five question to ask any potential vendor.

1.) Have you done this before?A provider that has experience in producing web properties for small business is probably a good fit. However, you want to be sure you are not their "guinea pig" and that they have experience in crafting websites that mesh well with your practice.

2.) What tools will be included for my patients? You want your website to be able to meet several objectives in order to make it relevant to your patient base. These objectives are:

  • Communicate information about your services offered and who you are.
  • Secure your practice's contact information, generate driving directions and provide hours of operation.
  • Allow people to contact your front office easily via web form.

Optionally you can give patients the ability to:

  • Book appointments online
  • Confirm appointments online
  • Cancel appointments online
  • Order supplements from your website

There are numerous companies that provide these optional tools that will transform your website from an information-only page to an interactive website.

3.) I have a change. How do I go about making edits? You don't want to have to call your web designer to make edits to your site and you want the ability to update information instantly. For this reason, its important you select a provider who can implement a Content Management System as opposed to simply building you practice a website. A CMS allows you to edit various parts of your website without having to know any code or programming language. It's basically as simple as editing a Word document and pushing "publish." In the case of CMS, simple is best. Ask your perspective web designer to demo a few systems for you.

4.) Can you work with my budget? A lot pricing in the website production industry is arbitrary. I recommend you be upfront with your website budget and have the provider quote products and services in that budget. Reject any supplementary marketing services they may offer (SEO / SEM) and focus on building a great web property.

5.) What sort of user engagement can I expect from the site?If your potential provider even flinches at this question, drop them. A good website developer knows that the focus of any website is on the visitor. They should answer this question with lots of good information related to engagement, conversion and functionality. If they do, they are probably worthy of further consideration.

Providers to consider:

Questions? Want us to help you? Our member-services team will be glad to provide you with a referral or review a proposal. Send to membership@acam.org

Tags:  member benefit  practice marketing 

Share |
PermalinkComments (0)
 

Healthy Diet, Healthy Skin

Posted By Therese Patterson, NC, Monday, August 1, 2011
Updated: Tuesday, February 4, 2014

Diets rich in fruits and vegetables are good for us, skin included. Healthful foods reduce inflammation and decrease the likelihood of skin breakouts. On the flip side, there are also a few studies that scientifically support the role of two food groups in acne promotion: dairy products and simple carbohydrates (think processed foods and sugary soft drinks).

To keep your skin in tip-top shape, make sure you incorporate these foods into your diet (along with a good skincare routine that features natural skincareproducts):

Vitamin A. Vitamin A helps regulate the skin cycle and is also the main ingredient in Accutane, an effective prescription medicine for acne. Good food sources of vitamin A include fish oil, salmon, carrots, spinach, and broccoli. Too much vitamin A can lead to toxic side effects, however. Limit your daily dose to 10,000 IU and never take it while pregnant or nursing.

Zinc. There is some evidence that people with acne have lower than normal levels of the mineral zinc. Zinc appears to help prevent acne by creating an environment inhospitable to the growth of P. acnes bacteria It also helps calm skin irritated by breakouts. Zinc is found in turkey, almonds, Brazil nuts, and wheat germ.

Vitamins E and C. The antioxidants vitamin E and vitamin C have a calming effect on the skin. Sources of vitamin C include oranges, lemons, grapefruit, papaya, and tomatoes. You can get vitamin E from sweet potatoes, nuts, olive oil, sunflower seeds, avocados, broccoli, and leafy green vegetables.

Selenium. The mineral selenium has antioxidant properties that help protect skin from free radical damage. Food sources of selenium include wheat germ, tuna, salmon, garlic, Brazil nuts, eggs, and brown rice.

Omega-3 fatty acids. Omega-3 fatty acids support the normal healthy skin cell turnover that helps keep acne at bay. You can get omega-3 fatty acids from cold water fish, such as salmon and sardines; flaxseed oil; walnuts; sunflower seeds; and almonds.

Water. Last but definitely not least, water. Many of us have our morning coffee and then drink only one drink during the day and one at night. Water helps hydrate your body and leads to plump, healthy skin. Adequate hydration helps flush out toxins that can cause skin problems. It is also essential for skin metabolism and regeneration.

Sources: Mt. Sinai Medical Center,WebMD

Tags:  food and drink  gut health  health 

Share |
PermalinkComments (0)
 

It's Time to Clean Our Plates

Posted By Administration, Tuesday, July 26, 2011
Updated: Friday, April 18, 2014



Allan Magaziner, DO

In America, where obesity rates continue to increase, it is hard for me to tell anyone to clear their plate – unless I am confident that it is full of fruits, vegetables and whole grains! But, I have no problem urging people to clean their plates, or more specifically, opt for cleaner foods to put on them!

It goes without saying that I’d push for everyone to opt for clean, minimally processed, low sugar, low sodium, unrefined foods that include whole grains, fruits, vegetables, healthy fats, etc. But, this is about more than that. It’s about pushing the government to clean up its act when it comes to the production of our food.

It’s about time that, we, as a society, greatly curtail, and, eventually, eliminate, the use of synthetic, man-made herbicides and pesticides – which continue to be utilized in obscene quantities in both the agricultural and non-agricultural markets. In fact, genetically modified organisms (GMOs) are found in virtually all corn and soy products unless they are organically grown, yet another reason to purchase organic food whenever possible.

That government agencies would think that the use of more than 5.2 billion pounds of pesticides and herbicides each year would have no impact on human health is greatly near-sighted and short minded. Levels of many of these synthetic chemicals are measurable in human tissue at birth as well as in breast milk of mothers who are trying to opt for a healthy, natural, clean way to feed their babies. These chemicals are linked to the rise in chronic fatigue, fibromyalgia, learning disabilities, thyroid and hormone dysregulation, autoimmune disease and many of the inflammatory illnesses that we are seeing more and more in society. They’ve also been found to uncouple mitochondrial phosphorylation causing mitochondrial dysfunction, to stimulate autoimmunity and to increase inflammatory pathways.

The toll on human health and disease of these chemicals is probably more far-reaching than industry has led us to believe. In fact, a comprehensive review of existing data released this month by Earth Open Source, an organization that uses open-source collaboration to advance sustainable food production, suggests that industry regulators in Europe have known for years that the herbicide, glyphosate, causes birth defects in the embryos of laboratory animals, and, that by 1993, the herbicide industry, including the original makers of Roundup, knew that visceral anomalies such as dilation of the heart could occur in rabbits at low and medium-sized doses. The report further suggests that since 2002, regulators with the European Commission have known that glyphosate causes developmental malformations in lab animals. Even so, the commission’s health and consumer division published a final review of glyphosate in 2002 that approved its use in Europe for the next 10 years.


It’s maddening – especially knowing that much of this ingestion of chemicals is coming from the consumption of otherwise healthy foods like apples, celery, strawberries, peaches, spinach, nectarines (imported), grapes (imported), bell peppers, potatoes, blueberries (domestic), lettuce and kale/collard greens. These fruits and vegetables are known as the “dirty dozen,” meaning they are the 12 most contaminated fruits and vegetables and the most important to buy organic.

It’s time we DEMAND that additional independent studies be conducted to demonstrate the real safety of any pesticides or herbicides which affect our air, our food, our water and our future.

It’s time to seek more natural and safe solutions and put an end to this colossal human experiment that has been going on for decades at the expense of our health and the health of our future generations.
Until then, I encourage everyone to keep it clean – try to buy organic versions of the items on the “dirty dozen” list, when possible. When it is not, opt for fruits and vegetables that are grown with the use of less pesticides – as listed on the Environmental Working Group’s (EWG) list of “Clean 15.” These include asparagus, avocado, watermelon, mangoes, onions, sweet corn and pineapple, to name a few. According to the EWG, consumers who choose five servings of fruits and vegetables a day from this list rather than from the “Dirty Dozen” can lower their concentration of pesticides they consume by 92 percent and will also eat fewer types of pesticides, including Bt-Toxin, which has been in the news lately because of a recent study that has “blown” holes in the Environmental Protection Agency’s safety claims around corn grown using this substance.

The study, conducted by doctors at Sherbrooke University Hospital in Quebec found that genetically-modified “Bt” corn (corn grown using the Bt-toxin, a pesticide boasting a gene from soil bacteria that breaks open the stomach of certain insects, killing them instantly, thus protecting the corn crop) is – contrary to safety claims made by the EPA and the pesticide’s developer, Monsanto – harmful, very harmful, to humans.

The study, which has been accepted for publication in Reproductive Toxicology, found the corn's Bt-toxin present in the blood of pregnant women and their babies, as well as in non-pregnant women. (Specifically, the toxin was identified in 93% of 30 pregnant women, 80% of umbilical blood in their babies, and 67% of 39 non-pregnant women.) Bt-Toxin has been linked to allergies, rheumatoid arthritis, inflammatory bowel disease, osteoporosis, MS, cancer, ALS (Lou Gehrig’s Disease) and colitis. And that is the short list.
It is sad that we have to rely on lists to tell us which healthy food choice is, well, healthy. And that we cannot always rely on government agencies to be honest and keep our best interests at heart. Hopefully, though, with our collective voices, we can put pressure on the powers that be to put their money where their mouths are when it comes to the health and wellbeing of their constituents – both of today and tomorrow.

Dr. Allan Magaziner is one of the nation’s leading authorities on nutrition, preventive medicine and environmental illness. He is the founder and director of the Magaziner Center for Wellness in Cherry Hill, New Jersey, where he has treated dozens of patients with ailments resulting from exposure to herbicides and pesticide using medical detoxification. To find out more, contact the Magaziner Center at 856-424-8222 or at info@magazinercenter.com.

This post has not been tagged.

Share |
PermalinkComments (0)
 
Page 9 of 15
 |<   <<   <  4  |  5  |  6  |  7  |  8  |  9  |  10  |  11  |  12  |  13  |  14  |  15
Community Search
Sign In
Sign In securely
Calendar
Latest News