Posted By Mark Hyman, MD,
Wednesday, February 29, 2012
Updated: Thursday, January 30, 2014
| Comments (0)
What life threatening, life sapping, energy
robbing condition affects one in every two Americans (that is EVERY
OTHER person) including 80% of those overweight and up to 40% of normal
weight people? What condition is responsible for more deaths from heart
disease, cancer, high blood pressure, diabetes and dementia than
anything else? What condition also causes acne, infertility, sexual
dysfunction and depression?
What condition accounts for more then
70% of our $2.4 trillion annual health care bill and will account for
most of the $47 trillion we will spend globally over the next 20 years
to deal with chronic disease? What is responsible for nearly twice as
many deaths every year as infectious disease, even in the developing
And what condition is not even diagnosed in over 90% of those who suffer from it?
condition are doctors not trained or reimbursed to diagnose, treat or
prevent, yet makes up the majority of health care visits and costs?
And what condition is nearly 100% preventable, treatable and reversible?
It is the single biggest health challenge facing us individually, as a nation and as a global community.
Diabesity is the continuum of metabolic disturbances from mild
blood sugar and insulin imbalances to pre-diabetes to full blown type 2
diabetes. It occurs in about 40% of people of normal weight – these are
the skinny fat people who look thin but are metabolically fat and have
all the same risk factors for disease and death as those who are
overweight. And it occurs in 80% of overweight people.
Since it affects every other American, watch this video to see if you have it
solution is not coming from our health care system or doctors, not from
our government, or from most corporations. There are too many people
vested in maintaining the status quo or worse profiting from making us
fat and sick. We need a solution.
That is why I wrote, The Blood Sugar Solution
It has a bold central goal: to address and begin to reverse a global
epidemic. It is a personal guide and plan, as well as a program for
helping people get healthy together, based on functional medicine, and
it is a blueprint for us to take back our health as a society.
pre-diabetes and diabetes or what I call diabesity, which now affects
one in two Americans arises out of existing social, economic and
political conditions. In fact obesity and diabetes are social diseases
and need a social cure and collective action on many levels to reverse
Over 10 years, these conditions will cost America over
$3.5 trillion in direct costs, not including lost productivity and the
costs in quality of life. From 1983 to 2008, worldwide diabetes rates
increased seven fold from 35 million to 240 million. In just 3 years
from 2008 to 2011, the roll call for diabetes increased another 110
Children less than 10 years old now get type 2 (or adult
onset) diabetes, and have strokes and heart attacks by age 15 or 20.
One in three children born today will have diabetes unless we do
I wrote The Blood Sugar Solution
to tackle this problem head on.
is a personal plan that breaks through myths about obesity and diabetes
that keep us sick and fat. And lays out the seven key steps to
preventing, treating and reversing diabesity by dealing with the
underlying causes. It is an eight-week plan that takes you through step
by step how to reboot your metabolism, lose weight, reverse type 2
It is a plan for us to be more successful by working
together to get healthy. We do twice as well and lose twice as much
weight when we get support from others in community. We are better
We recently did a "beta test” of this program with about 150 people. Their results were astounding:
- The group lost a total of 1,536 pounds in just eight weeks. That’s an average weight loss of over ten pounds per person!
- More than half the group lost more than ten pounds. Some lost as much as 28 pounds.
- Average waist size decreased by 1.5 inches, and some people lost so
much of their waist that they had to go out and buy new clothes. One
woman lost eight inches from her waist. Imagine, eight inches in eight
weeks. No medication can help you do that.
But The Blood Sugar Solution is about far more than weight
loss; it’s about taking back your health and your life. People who
completed the program reported an average reduction of 14 points on
their systolic blood pressure, their fatigue evaporated and they had
more energy than they had felt in years, their joint and muscle pain
vanished; the program improved their mood and sleep, eliminated their
brain fog, and a provided a deep sense of well being. The Blood Sugar Solution gave these people a new lease on life, here are a few of their stories.
Blood Sugar Solution is a plan for each of us to take back our health
as a society. Our health has been hijacked from us, taken from us
slowly, quietly, over the past century. Our current food, social,
family, school, work, faith-based, and community environments, health
care institutions, and government policies make it hard for us to make
healthy choices. We are presented with choices that foster bad habits.
together, getting and staying healthy is possible given the right
information, tools, support, and collective action to take back our
Navigating the Terrain of Disease: Getting to the Root of the Problem
effectively treat diabesity we must shift our focus away from the
symptoms or risk factors of the disease and begin taking a hard look at
the causes. All of our attention is on treatments that lower blood sugar
(diabetes drugs and insulin), lower high blood pressure
(anti-hypertensive drugs), improve cholesterol (statins), and thin the
blood (aspirin). But we never ever ask the most important question:
Why is your blood sugar, blood pressure, or blood cholesterol too high and why is your
blood too sticky and likely to clot?
Put another way: What are the root causes of diabesity?
that question must be the focus of our diagnosis and treatment of the
disease if we are going to solve this global epidemic.
The good news is that the answer is shockingly simple.
The Real Causes of Diabesity
entire spectrum of diabesity including all of its
complications—diabetes, elevated blood sugar, blood pressure, and
cholesterol—are simply downstream symptoms that result from problems
with diet, lifestyle, and environmental toxins interacting with our
unique genetic susceptibilities.
Those are the real causes of diabesity.
And the reason these dietary and lifestyle factors lead to diabesity is because they create a condition known as insulin resistance.
Contrary to what most people think, type 2 diabetes is a disease of too
much, not too little, insulin. Insulin is the real driver of problems
When your diet is full of empty calories and an
abundance of quickly absorbed sugars, liquid calories, and carbohydrates
(like bread, pasta, rice, and potatoes), your cells slowly become
resistant to the effects of insulin and needs more and more to do the
same job of keeping your blood sugar even. Thus you develop insulin resistance. A high insulin level is the first sign of a problem. The higher your insulin levels are, the
your insulin resistance. Your body starts to age and deteriorate. In
fact, insulin resistance is the single most important phenomenon that
leads to rapid and premature aging and all its resultant diseases,
including heart disease, stroke, dementia, and cancer.
insulin levels increase it leads to an appetite that is out of control,
increasing weight gain around the belly, more inflammation and oxidative
stress, and myriad downstream effects including high blood pressure;
high cholesterol; low HDL, high triglycerides; weight gain around the
middle; thickening of the blood; and increased risk of cancer,
Alzheimer’s, and depression. These are all a result of insulin resistance
and too much insulin. Elevated blood sugar is not the source of the
problem. And because insulin resistance (and diabesity) are a direct
outcome of diet and lifestyle, the condition is 100 percent reversible
in the vast majority of cases. Most people just need to eliminate the
things that are sending their biology out of balance and include what’s
needed to help the body rebalance itself. For most the interventions
required are extremely simply and extraordinarily effective.
8 Steps to Reversing Diabesity
In my new book The Blood Sugar Solution
I outline a comprehensive 8-week plan for overcoming diabesity in all
its forms. Here is a sneak preview of the steps outlined in the book:
1. Get the right tests.
Most doctors focus on fasting blood sugar. This is actually a poor
indicator of diabesity. The best test to tease out the condition is an
insulin response test where insulin levels are measured fasting and then
1 and 2 hours after a glucose drink. Demand this test from your doctor.
2. Get smart about nutrition.
Despite the media hype and the seeming confusion amongst doctors, the
basics of nutrition are extremely simply. Eliminate sugar and processed
carbohydrates, include whole real foods like lean protein (chicken or
fish), veggies, nuts, seeds, beans and whole grains.
3. Get the right supplements.
There has recently been a frenzy of negative reports about supplements.
Most of them are unfounded. Supplements are an essential part of
treating diabesity. A good multivitamin, vitamin D, fish oil, and
special blood sugar balancing nutrients like alpha lipoic acid, chromium
polynicotinate, biotin, cinnamon, green tea catechins, and PGX (a super
fiber) should also be included.
4. Get relaxed.
Stress is a major unrecognized contributor to insulin resistance and
blood sugar imbalance. Push your pause button every day with deep
breathing, visualization, yoga, and other relaxation techniques.
5. Get moving.
Aside from changing your diet, exercise is probably the single best
medication for diabesity. Walk for at least 30 minutes every day. For
some, 30-60 minutes of more vigorous aerobic exercise 4-6 times a week
may be necessary.
6. Get clean and green.
Environmental toxins also contribute to diabesity. Filter your water,
look for green cleaning products, and avoid plastics when you can.
7. Get personal.
While the steps above will address 80 percent of the problems with
diabesity, some may need to take additional steps to optimize key areas
of their biology. Remember, the medicine of the future is personal
medicine. Seek out your own biological imbalances and look for ways to
8. Get connected. Research is
beginning to show that we get better more effectively when we get
together. Invite your friends, families, and neighbors to change their
diets and lifestyle along with you. Together we can all take back our
I hope that my book The Blood Sugar Solution
will be the beginning of a larger transformation – for individuals,
communities and for society. In the book I outline all of the social,
economic, biological, and medical underpinnings of this health epidemic
and provide an 8-week, step-by-step system that will allow you to dig
deep into your own biology and heal even the most severe cases of
Get a book, get two and give one to someone you love – you might be saving their life. When
you purchase the book from this link you will automatically receive access to the following special bonuses:
- Special Report—Diabetes and Alzheimer’s: The Truth About "Type 3 Diabetes” and How You Can Avoid It.
- More Delicious Recipes: 15 Additional Ways to Make The Blood Sugar Solution as Tasty as It’s Healthy!
- Dr. Hyman’s UltraWellness Nutrition Coaching – FREE for 30 days!
- Hour 1 of The Blood Sugar Solution Workshop DVD
For more on diabesity, join us on www.drhyman.com
Posted By Administration,
Friday, March 4, 2011
Updated: Friday, April 18, 2014
| Comments (0)
by Zina Kroner, DO
As a nutritionally-oriented internist, I have seen air travel take quite a toll on the health and well-being of many of my friends and patients. With the excitement of traveling to a new destination, the new food, the change in schedule, the stress, the hassle; it is easy to neglect one’s health. My patients are frequently asking me for health travel advice. While practicing in a city where both business and leisure travel are staples in the lives of many of my patients, I have developed a nutritional and lifestyle plan to help optimize health while traveling.
Drink 2 large glasses of water on an empty stomach in the morning of travel. This will hydrate you effectively. Have a high protein breakfast.
Stress plays a significant role in air travel. Aside from a healthy diet, restorative sleep, regular exercise, and the addition of key nutritional supplements to the regime are helpful. One mineral that helps to combat stress is magnesium. It is one of the first nutrients to be depleted in the setting of stress. Your adrenal glands depend on magnesium, as do over 300 different enzyme reactions in the body. I recommend my patients take 100mg of magnesium-taurate the morning of the flight, and then another 100mg just before the flight.
It is not uncommon for travelers to contract a respiratory infection, the flu, or other infection while flying. The poor air circulation in the cabin compounded by the proximity to other passengers who may potentially be sick poses a double threat. Those with weak sinuses are at a heightened risk, as well, due to the periodic changes in air pressure. Washing hands and using hand sanitizers in the plane may be of benefit. Hydration and optimal nutrition are integral components, as well. I recommend my patients take several key nutrients to help boost the immune system in the setting of travel. I recommend taking oleuropin before the flight, which is the active ingredient in the olive leaf that has potent antibacterial, antifungal, and antiviral properties. In addition, beta 1,3 glucans and the prickly pear are cutting edge nutrients that I recommend that have been studied for their anti-microbial effects. Vitamin C and a combination of immune boosting mushrooms, such as cordyceps, reishi, and maitake, may help to prevent colds and other respiratory ailments in flight.
Boosting the immune system by addressing the gut is essential. It is an established fact that over sixty percent of the immune system is in the gut, referred to as the gut associated lymphoid tissue (GALT). In addition to a healthy diet, intake of a probiotic (beneficial gastrointestinal flora) is imperative to optimizing function. I strongly recommend taking a probiotic a week before the date of travel and to continue for a week thereafter.
Constipation is common in the setting of travel. The change in food, regime, stress level, and diet are contributors to this phenomenon. Probiotics can help deal with this. Magnesium plays a crucial role as well, being that it is a muscle relaxor that can relax the muscles of the colon wall and therefore improve regularity. Hydration, exercise and healthy fiber intake are important as well.
It is not uncommon to get a muscle cramp during the flight. Magnesium, a natural muscle relaxer, can help to prevent this. Be careful, because what feels like a cramp may actually be a blood clot. I highly recommend taking natural supplements that improve circulation before the flight. Natural vitamin E and omega-3 fish oil have been shown to optimize the cardiovascular system. Their mild blood thinning effect may help to prevent a clot. I also recommend the use of nattokinase for clot prevention. There is a lot of research supporting nattokinase’s role as an anti-clotting agent. It is an enzyme extracted from natto, which is derived from fermented soybeans.
To make it more user-friendly, I have put together all the supplements described above into prearranged packets. I have blended the highest quality nutrients into the “Flight Pack,” the only physician-grade supplement pack on the market used to optimize health and well-being while flying. I hope you find them helpful. Take one packet with a meal before your flight. Each Flight Pack contains 8 supplements. If it is okay with your physician, you can take this packet daily while traveling. Do not take if you are pregnant, are taking a blood thinner, have kidney or liver disease, or a bleeding disorder. Living smarter, living longer… (The product can be ordered online at www.advanced-medicine.com.)
Posted By Administration,
Wednesday, February 16, 2011
Updated: Friday, April 18, 2014
| Comments (0)
by Allan Magaziner, DO
It’s nothing to sneeze at: 54 million Americans suffer from seasonal allergies. Until now, many have either wearily resigned themselves to the watery eyes, runny nose, sneezing, wheezing and hives associated with the condition, or have opted to try to combat these symptoms with allergy shots that can be costly and inconvenient. That’s been the bad news. The good news is that a recent study of more than 60 patients allergic to pollen, dust mites and cat allergens has shown that an approach known as sublingual desensitization is indeed a safe and effective alternative to traditional immunotherapy injections. The study findings have prompted researchers to strongly recommend its use, especially in children. In the study, the practice was shown to significantly reduce the symptoms of hay fever and nasal allergies, as well as the need for medication, compared to placebo.
The study finally validates what we’ve been practicing at the Magaziner Center for Wellness with great success for more than 24 years. During this time, we’ve found sublingual desensitization (which is defined as immunotherapy using drops or pills) to be:
- Less invasive
- More convenient – as it can be self-administered by the patient
- Without risk of anaphylactic shock, a potential side effect of immunotherapy injections.
- Less taxing mentally and physically
This last bullet has been an important one for our patients who are children whose parents wisely sought a natural therapy. Sublingual desensitization is great for kids – it’s the difference between taking a drop or a pill orally versus being stuck with a needle. And, let’s face it, how many children do you know that aren’t a little upset at the sight of a needle?
Like all treatments at the Magaziner Center for Wellness, our patients first undergo a thorough evaluation. We test patients’ reactions to common, as well as unexpected, allergens, including:
- Cat/dog dander
- Pollens (grass, trees and weeds)
- Dust/dust mites
- Chemicals (perfumes, paint, carpets, etc.)
Why? Because, simply put, allergies are additive. If a person suffers from seasonal allergies, what he or she eats and breathes throughout the year affects his or her reaction during the documented allergy season. In fact, we have found that food allergies and food sensitivities have more to do with chronic complaints than almost any other factors.
After patients’ reactions are tested, we use injection therapy to place tiny amounts of the allergen into the bloodstream to assess clinical symptoms and behavioral reactions (i.e., change in frequency of headaches, even handwriting samples). When we get to the point that triggers a response, we give successive dosages until the symptoms that have been created disappear. Once the level is identified, we make up a vial of antigens that patients place as drops under their tongue on a daily basis.
In the simplest terms, we are naturally treating the immune system and getting it to respond appropriately to the allergens. This takes time, of course, so it is recommended that anyone who suffers from seasonal allergies receive treatment in mid-March so that the immune system’s response can be built well in advance of the blossoming of trees and flowers between April and October.
Posted By Administration,
Thursday, December 23, 2010
Updated: Friday, April 18, 2014
| Comments (0)
by Ronald L. Hoffman, MD, CNS
Although diets rich in marine lipids and fish-oil supplements have staked a claim to heart disease prevention, controversy remains. A recent study examining the role of omega-3-enriched margarine as a functional food for secondary prevention of heart attacks yielded negative results;1 publication of the study spawned skeptical and even derisive headlines in the popular press: Omega-3 Fats Offer No Protection Against Heart Disease—Study and Low Doses of Omega-3s Don't Help with Heart Disease: Say it Ain't So, Fish Oil!.
Are the results of this study (perhaps somewhat prematurely titled "The Alpha Omega Trial") definitive? How do clinicians reconcile these negative findings with the vast body of references that support the cardiovascular benefits of fish consumption and omega-3 supplementation? And most important, what are the implications for consumers and for potential advocacy by health-care professionals?
The current regulatory climate for fish-oil claims underscores this uncertainty. Lovaza (omega-3-acid ethyl esters), the only FDA-approved fish-oil supplement, is indicated only for its pharmacologic effect of lowering elevated triglycerides. FDA labeling specifically qualifies that "The effect of Lovaza on cardiovascular mortality and morbidity in patients with elevated triglyceride levels has not been determined."2
No comparable approval, either explicit or tacit, exists in the United States for the application of fish-oil supplements to primary or secondary prevention of cardiovascular disease (CVD). But a considerable proportion of the population consumes these supplements, and a high percentage of health-care providers embrace such recommendations—if not for their patients, then for themselves and their families.
While the exact proportions are not known, a recent investigation showed that 62% of U.S. doctors surveyed agreed that one of their roles as a health-care professional is to provide information to patients about appropriate dietary supplements.3 The most popular supplements among cardiologists were multivitamins, omega-3s/fish oil, and vitamin C.
Even regulatory language governing claims for cardioprotection via consumption of omega-3-rich foods remains highly circumscribed. In September 2004, the FDA announced permission for "qualified health claims on omega-3 fatty acids" to the effect that, "Supportive but not conclusive research shows that consumption of eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA] omega-3 fatty acids may reduce the risk of coronary heart disease."4
Compounding the controversy are international discrepancies vis a vis the prescription of fish-oil supplements. A front-page article in The New York Times pointed out that while 57% of family clinicians in Washington State acknowledged fish oil's potential benefits in preventing a second heart attack, only 17% identified themselves as frequent prescribers of fish oil.5
The situation in the United States stood in contrast with that in Europe where, according to Dr. Massimo Santini, chief of cardiology at Rome's San Filippo Neri hospital, a doctor's failure to prescribe fish oil to a heart patient "would be considered tantamount to malpractice."5
The article concluded that in the United States, "community doctors do not learn how to use [fish oil]," while insurers will not pay for cardiovascular prevention via fish-oil supplementation because it is not specifically approved by the FDA for that indication.5
In its scientific statement on fish consumption, fish oil, omega-3 fatty acids, and CVD, the American Heart Association (AHA) acknowledges that: "[Randomized controlled trials] have demonstrated that omega-3 fatty acid supplements can reduce cardiac events (e.g., death, nonfatal MI, nonfatal stroke) and decrease progression of atherosclerosis in coronary patients. However, additional studies are needed to confirm and further define the health benefits of omega-3 fatty acid supplements for both primary and secondary prevention."6
After some equivocation to the effect that dietary approaches to omega-3 supplementation are preferable, the AHA allows that certain individuals, whose dietary preferences preclude adequate intake from natural sources, "in consultation with their physician, could consider supplements for coronary heart disease [CHD] risk reduction."6
What lines of evidence support fish-oil supplementation for cardiovascular prevention? Early impetus came from epidemiologic studies. As early as 1944, Sinclair noted the decreased prevalence of CVD in Arctic Eskimos who subsisted largely on omega-3-rich fish and aquatic mammals.7 In the 1970s, Danish researchers noted improved cardiovascular profiles and lower MI mortality among Greenland Eskimos consuming a low-carbohydrate, fat-rich diet when compared with subjects consuming a Western diet on the Danish mainland.8
Three large randomized trials have documented the effects of omega-3 polyunsaturated fatty acid (PUFA) in primary and especially in secondary prevention of CHD.9 More than twenty years ago, the Diet and Reinfarction Trial demonstrated a 29% reduction in mortality—almost entirely attributable to decreased cardiovascular death—in subjects consuming high amounts of omega-3 from fish sources or supplements.10The reduction in cardiovascular events was particularly impressive in individuals consuming fish-oil capsules.
A subsequent prevention trial corroborated the benefits of fish-oil supplementation for secondary prevention in MI survivors, namely with one Lovaza capsule per day delivering
850 mg of EPA/DHA in a 1.2:1 ratio. Researchers demonstrated a 21% and a 30% reduction, respectively, in total death and cardiovascular death over the one-year duration of the study.11 These results were driven by an impressive 46% reduction in sudden cardiac death. Reductions in major clinical events continued to be demonstrated at 3.5-year follow-up.12
Additional evidence for the protective effects of omega-3 supplementation comes from the Japan EPA Lipid Intervention Study, published in 2007. In a mixed trial of primary and secondary prevention, 18,645 patients with hypercholesterolemia (70% women) were randomized to statin alone or statin and highly purified EPA 1,800 mg/day. At the end of the five-year study, those randomized to statin plus EPA had a 19% reduction in major cardiovascular events.13
How do clinicians reconcile these results with those of the Alpha Omega Trial, which demonstrated no secondary prevention benefits of supplementation with an omega-3-enriched margarine spread?
Researchers leading the Alpha Omega Trial assigned 4,837 MI survivors to one of four experimental groups. For 40 months, participants consumed either (1) placebo margarine, (2) margarine with a combined total of 400 mg of EPA/DHA, (3) margarine with 2 g of alpha-linolenic acid (ALA), a plant-derived precursor to EPA/DHA, or (4) a margarine containing a combination of EPA/DHA and ALA. State-of-the-art antihypertensive, antithrombotic, and lipid-modifying therapy was implemented in all four groups.
The results showed that neither the EPA/DHA nor the ALA (nor a combination of both) proved more beneficial than placebo. Does this constitute a repudiation of the omega-3 CVD prevention hypothesis?
Critics of the Alpha Omega Trial were quick to point out specific objections to its methodology. First, aggressive pharmacologic management may have masked some of the advantages conferred by fish oil. Additionally, it was thought that the results did not disqualify a putative benefit of omega-3-enriched margarines in primary prevention.
Some have claimed that the choice of a margarine-like spread as a delivery system might have compromised the efficacy of the active omega-3 component. The caloric load provided by daily consumption of 18.8 g of omega-6-rich vehicle and the attendant consumption of multiple slices of high glycemic index bread on which the margarine-like substance was spread, might have acted as confounders.
But most important, the low-dose of EPA/DHA (400 mg) employed in the trial is well below the threshold noted in some studies to influence cardiovascular outcome. The study might best be viewed as merely contravening the hoped-for cardio-protective role of a specific functional food—with inherent limitations to palatability attributable to fish oil's inability to being disguised in neutral vehicles. Therefore, it would be an overstatement to claim, as some have, that the Alpha Omega Trial is the death knell for omega-3 supplementation in CVD.
How then are omega-3 PUFAs thought to influence CVD progression and reduce mortality? Several pathways have been investigated.
Hypolipidemic. It is well established that omega-3s reduce lipid levels, and this is the basis for the approved indication for use of Lovaza in hypertriglyceridemia. It is generally acknowledged that doses >3-4 g/day are required. The mechanism of omega-3's triglyceride reduction relates to its favorable effects on reducing hepatic production and secretion of very-low-density lipoprotein (VLDL) and VLDL apo B particles, its favorable effects on plasma lipolytic activity through lipoprotein lipase-mediated clearance, and its ability to stimulate beta-oxidation of other fatty acids in the liver.14
Generally, omega-3s produce no significant improvements in LDL, except in patients with elevated triglycerides, in whom modest improvements in LDL and HDL are sometimes seen. Even when absolute LDL levels are not significantly impacted by fish-oil supplementation (or even when they increase, as has occasionally been reported), there is evidence that omega-3s may shift particle size to a more benign, "fluffier" LDL, thus favorably impacting the atherogenic profile.
Antithrombotic. Fish oils produce platelet inhibition and reduce fibrinogen. Although some experts contend that higher doses (>3-4 g/day) are required, others argue for a lower threshold. Epidemiologic evidence of fish oil's anti-clotting effects comes from several studies that link higher intake of fish oil to a reduction in ischemic strokes with coincident increased risk of hemorrhagic strokes. This leads to a net gain in protection, since ischemic strokes outnumber hemorrhagic strokes by 85% to 15%.
Antihypertensive. Fish oil is thought to exert an antihypertensive effect in several ways. It supports flow-mediated vasodilation, enhances vascular reactivity, and may balance autonomic tone by reducing adrenergic drive.
An analysis of randomized trials revealed that consumption of approximately 4.0 g/day of omega-3 fatty acid was associated with a significant 1.7- and 1.5-mm Hg reduction in systolic and diastolic BP, respectively; these reductions were more pronounced in older patients and in individuals with higher BP. Evidence suggests that lowering systolic BP by as little as 2 mm Hg can yield reductions of 4% in CAD mortality.15
Adiponectin. A hormone produced by fat cells, adiponectin plays a role in regulating lipids and glucose. Low levels of this hormone are associated with obesity, and higher levels have been shown to confer protection against heart disease. When administered to obese individuals, 1.8 g/day of EPA increased the level of adiponectin.16
Insulin regulator. To date, research in the area of insulin regulation has been inconclusive. While numerous studies support a role for EPA/DHA in attenuating insulin resistance, and omega-3 deficiency has been associated with the metabolic syndrome, the Agency for Healthcare Research and Quality reports, "Among 18 studies of type 2 diabetes or the metabolic syndrome, omega-3 fatty acids . . . had no effect on fasting blood sugar, or glycosylated hemoglobin, by meta-analysis. Omega-3 fatty acids had no effect on plasma insulin or insulin resistance in type 2 diabetics or patients with the metabolic syndrome, by qualitative analysis of four studies."17
Antiarrhythmic. The principle cause of sudden cardiac death (SCD) is sustained ventricular arrhythmia. Considerable evidence supports an antiarrhythmic role for omega 3s, probably via autonomic pathways. Studies show that EPA/DHA enhances sympatho-vagal tone, leading to slower heart rates and fewer arrhythmias, and in some studies, reduced incidence of SCD. Omega 3s have also been shown to favorably impact heart rate variability, a marker of autonomic adaptability.
Knowledge of fish oil's beneficial effects on arrhythmias recently prompted a trial of omega-3 supplementation in patients with implantable cardioverter defibrillators (ICDs). The results—which showed a higher incidence of ICD discharges in consumers of fish-oil supplements—and the consequent negative publicity have dampened enthusiasm over fish oil for this indication.
Some studies have shown impressive results for fish oil in prophylaxis of atrial fibrillation, particularly in patients at risk after coronary artery bypass grafting.18
Anti-inflammatory. Omega-3 fatty acids act as eicosanoid precursors to reduce inflammation. This may impact cardiovascular risk in several ways.
First, chronic inflammation is thought to play a critical role in endothelial damage that leads to compromised vascular reactivity and atherosclerotic changes. Additionally, inflammation promotes unstable plaque, a harbinger of thrombotic events.
Next, it is now commonly acknowledged that elevated high-sensitivity C-reactive protein (hs-CRP), a selective marker of intra-arterial inflammation, is a robust risk factor for CVD. Research on the potential for fish oil to lower this cardiospecific parameter has produced mixed results. One study found that atorvastatin (Lipitor), but not fish oil, reduced hs-CRP in obese, at-risk subjects.19 In other research, omega-3 supplements did not reduce hs-CRP in healthy subjects.20 Another set of findings showed that EPA/DHA reduced hs-CRP in patients on dialysis, a population known to be at higher risk for inflammation and CVD.21
Finally, fish oil has a less equivocal effect on other inflammatory mediators, specifically such cytokines as tumor necrosis factor-alpha, elevations of which are hallmarks of chronic congestive heart failure (CHF). Studies show improvement in cytokine levels in CHF patients taking EPA/DHA, with corresponding improvements in clinical outcomes.9
Prevention of restenosis. Accelerated restenosis following angioplasty or stenting is one of the thorniest problems in medicine, associated with numerous failed strategies. Because of fish oil's acknowledged antiatherosclerotic effects, it became a likely candidate for restenosis prevention. Early meta-analyses showed modest benefit and provided reason to be hopeful.22 Unfortunately, the Coronary Angioplasty Restenosis Trial demonstrated no reduction in restenosis rates with 5 g/day of Omacor, a precursor to Lovaza.23
Other benefits. Ancillary benefits of fish-oil supplementation are thought to be considerable. Therapeutic effects have been investigated, with various degrees of evidence, in such diverse conditions as bipolar disorder, depression, dementia, psychosis, certain cancers (including breast, colon, and prostate) cancer cachexia, rheumatoid arthritis, cystic fibrosis, inflammatory bowel disease, dysmenorrhea, IgA nephropathy, systemic lupus, asthma, chronic obstructive pulmonary disease, psoriasis, eczema, dry eye, macular degeneration, pre-eclampsia, and prevention of organ-transplant rejection.24
With regard to fish oil's role in secondary prevention of CVD, studies suggest potential amelioration of depression in heart attack survivors who take omega-3s. Depression is a known comorbidity following MI. It is also a negative prognostic, so, if proven, fish oil's antidepressant effects would be a valuable ancillary benefit.
A recent trial compared fish oil plus sertraline with sertraline alone in a group of post-MI patients. Mood improved in all the patients, but no difference was seen in depression scores between fish-oil-supplemented patients vs. controls.
"Whether higher doses of EPA, DHA, or sertraline, a longer duration of treatment, or the use of omega-3 as monotherapy can improve depression in patients with stable heart disease remains to be determined," the authors concluded.25
ADVERSE EFFECTS AND CONTRAINDICATIONS
The most commonly observed adverse effects of omega-3 PUFA supplementation are nausea, GI upset, and "fishy" burp. These problems can sometimes be ameliorated through the use of flavored, emulsified omega-3 formulations that are palatable even to children. Alternatively, enteric-coated forms of fish oil are designed to dissolve distal to the stomach, reducing the potential for oily reflux.
Because of fish oil's antiplatelet effects, concerns have been raised over the possibility that higher intakes will lead to an increase hemorrhagic complications. However, a comprehensive review concluded that no increased risk of clinically significant bleeding was noted with omega-3 PUFA doses of up to 7 g of combined DHA and EPA per day, even when coupled with antiplatelet therapy or warfarin.26 Results may vary in clinical practice, and such clotting disorders as Von Willebrand disease or thrombocytopenia may pose relative contraindications to high-dose fish-oil supplementation.
A recent study explored fish-oil supplements' synergy with aspirin and clopidogrel in post-stenosis patients. Resistance to platelet inhibition was overcome with no concomitant increase in adverse hemorrhagic events.27
To prevent excessive perioperative bleeding, patients undergoing elective surgery are typically advised to forgo fish-oil supplementation for several weeks, but some studies actually support a role for fish oil in improving surgical outcomes. Some researchers have credited fish oil with offering circulatory benefits, or alternatively with modulating immunity, perhaps by blunting the exaggerated cytokine response to surgery.28
Lately, concerns have been raised over fish oil's potential to down-regulate immunity in detrimental ways. One study observed that fish oil decreased resistance to influenza virus in a murine model,29 but the observation has not been extended to humans.
FISH-OIL SUPPLEMENTS ON THE MARKET
Fish-oil supplements come in a variety of forms. Cod-liver oil is the original article, but its disadvantages relative to omega-3 capsules include low ratio of EPA/DHA to overall calories, greater risk of mercury and PCB contamination, and potential for vitamin A and D toxicity with high levels of supplementation.
Most fish-oil capsules are free of significant mercury and PCB contamination, and industry standards for monitoring and disclosure are relatively stringent. Disparities exist, however, in the amount of active EPA and DHA delivered per capsule, and some ultra-discounted brands may be of dubious benefit due to the sheer number of capsules required to achieve clinically meaningful supplementation.
Manufacturers sometimes use the term "pharmaceutical grade" to imply greater potency or purity, but the claim is not regulated and almost meaningless. Also, controversy persists over relative advantages of two competing technologies for enhancing the EPA/DHA concentration: triglyceride substitution vs. ethyl esterification (used in Lovaza). Each camp claims superior bioavailability, but evidence remains inconclusive.
Finally, new formulation technology permits the offering of EPA/DHA in variable ratios designed to target specific clinical goals. EPA and DHA may have differing effects on desirable cardioprotective endpoints. The precise "optimal" ratio of EPA/DHA for heart disease prevention, if such a thing exists, has not yet been determined.
Uncertainty remains among health-care professionals as to the potential therapeutic application of fish-oil supplements in heart disease. A wide range of mechanistic, epidemiologic, and controlled-trial evidence substantiates a role for omega-3 fatty-acid supplementation in both primary and secondary cardiovascular prevention. An extensive margin of safety has been confirmed in most settings. More work remains to be done in studying the effects of fish oil in specific subpopulations and circumstances as well as in clarifying optimal dosage regimens and EPA/DHA ratios. Only then can specific guidelines for administration of omega-3 supplements coalesce into consistent and clear recommendations from health-care professionals.
Dr. Hoffman is founder and medical director of the Hoffman Center in New York City. The author has no relationships to disclose relating to the content of this article.
1. Kromhout D, Giltay EJ, Geleijnse JM; Alpha Omega Trial Group. n-3 fatty acids and cardiovascular events after myocardial infarction. N Engl J Med. 2010;363:2015-2026.
2. GlaxoSmithKline. Lovaza prescribing information. Available at us.gsk.com/products/assets/us_lovaza.pdf.
3. Natural Products Insider. Cardiologists recommend dietary supplements for a healthy heart. Available at multivu.prnewswire.com/mnr/lifesupplemented/36723/.
4. U.S. Food and Drug Administration. FDA announces qualified health claims for omega-3 fatty acids. Available at www.fda.gov/NewsEvents
5. Rosenthal E. In Europe it's fish oil after heart attacks, but not in U.S. The New York Times. October 3, 2006: A1. Available at www.nytimes
6. Kris-Etherton PM, Harris WS, Appel LJ; American Heart Association. Nutrition Committee. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002;106:2747-2757. Available at circ
7. Sinclair HM. The diet of Canadian Indians and Eskimos. Proc Nutr Soc. 1953;12:69-82.
8. Dyerberg J, Bang HO, Hjorne N. Fatty acid composition of the plasma lipids in Greenland Eskimos. Am J Clin Nutr. 1975;28:958-966. Available at www.ajcn.org/cgi/reprint/28/9/958.pdf.
9. Lavie CJ, Milani RV, Mehra MR, Ventura HO. Omega-3 polyunsaturated fatty acids and cardiovascular diseases. J Am Coll Cardiol. 2009;54:585-594.
10. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART). Lancet. 1989;2:757-761.
11. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico. Lancet. 1999;354:447-455.
12. Marchioli R, Barzi F, Bomba E, et al. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002;105(16):1897-1903. Available at circ.ahajournals.org/cgi/content/full/105/16/1897.
13. Yokoyama M, Origasa H, Matsuzaki M, et al. Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis.Lancet. 2007;369:1090-1098.
14. Jacobson TA. Role of n-3 fatty acids in the treatment of hypertriglyceridemia and cardiovascular disease. Am J Clin Nutr. 2008;87:1981S-1990S. Available at www.ajcn.org/cgi/content/full/87/6/1981S.
15. Geleijnse JM, Giltay EJ, Grobbee DE, et al. Blood pressure response to fish oil supplementation: metaregression analysis of randomized trials.
J Hypertens. 2002;20:1493-1499.
16. Itoh M, Suganami T, Satoh N, et al. Increased adiponectin secretion by highly purified eicosapentaenoic acid in rodent models of obesity and human obese subjects. Arterioscler Thromb Vasc Biol. 2007;27:1918-1925. Available at atvb.ahajournals.org/cgi/content/full/27/9/1918.
17. MacLean CH, Mojica WA, Morton SC, et al. Effects of omega-3 fatty acids on lipids and glycemic control in type II diabetes and the metabolic syndrome and on inflammatory bowel disease, rheumatoid arthritis, renal disease, systemic lupus erythematosus, and osteoporosis. Evid Rep Technol Assess (Summ). 2004;89:1-4. Available at www.ahrq.gov/downloads/pub/evidence/pdf/o3lipid/o3lipid.pdf.
18. Calò L, Bianconi L, Colivicchi F, et al. N-3 Fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery: a randomized, controlled trial. J Am Coll Cardiol. 2005;45:1723-1728.
19. Chan DC, Watts GF, Barrett PH, et al. Effect of atorvastatin and fish oil on plasma high-sensitivity C-reactive protein concentrations in individuals with visceral obesity. Clin Chem. 2002;48:877-883. Available at www.clinchem.org/cgi/content/full/48/6/877.
20. Geelen A, Brouwer IA, Schouten EG, et al. Intake of n-3 fatty acids from fish does not lower serum concentrations of C-reactive protein in healthy subjects. Eur J Clin Nutr. 2004;58:1440-1442. Available at www.nature.com/ejcn/journal/v58/n10/full/1601986a.html.
21. Saifullah A, Watkins BA, Saha C, et al. Oral fish oil supplementation raises blood omega-3 levels and lowers C-reactive protein in haemodialysis patients—a pilot study. Nephrol Dial Transplant. 2007;22):3561-3567. Available at ndt.oxfordjournals.org/content/22/12/3561.long.
22. O'Connor GT, Malenka DJ, Olmstead EM, et al. A meta-analysis of randomized trials of fish oil in prevention of restenosis following coronary angioplasty. Am J Prev Med. 1992;8:186-192.
23. Johansen O, Brekke M, Seljeflot I, et al. N-3 fatty acids do not prevent restenosis after coronary angioplasty: results from the CART study. Coronary Angioplasty Restenosis Trial. J Am Coll Cardiol.1999;33:1619-1626.
24. National Library of Medicine. Fish Oil. Available at www.nlm.nih.gov/medlineplus/druginfo/natural/993.html.
25. Carney RM, Freedland KE, Rubin EH, et al. Omega-3 augmentation of sertraline in treatment of depression in patients with coronary heart disease: a randomized controlled trial. JAMA. 2009;302:1651-1657. Available at jama.ama-assn.org/cgi/content/full/302/15/1651.
26. Harris WS. Expert opinion: omega-3 fatty acids and bleeding-cause for concern? Am J Cardiol.2007;99:44C-46C.
27. Gajos G, Rostoff P, Undas A, Piwowarska W. Effects of polyunsaturated omega-3 fatty acids on responsiveness to dual antiplatelet therapy in patients undergoing percutaneous coronary intervention: the OMEGA-PCI (OMEGA-3 fatty acids after PCI to modify responsiveness to dual antiplatelet therapy) study.J Am Coll Cardiol. 2010;55:1671-1678.
28. Tsekos E, Reuter C, Stehle P, Boeden G. Perioperative administration of parenteral fish oil supplements in a routine clinical setting improves patient outcome after major abdominal surgery. Clin Nutr.2004;23:325-330.
29. Schwerbrock NM, Karlsson EA, Shi Q, et al. Fish oil-fed mice have impaired resistance to influenza infection. J Nutr. 2009;139:1588-1594. Available at www.ncbi.nlm.nih.gov/pmc/articles/PMC2709305/.
All electronic documents accessed November 15, 2010.
Posted By Administration,
Thursday, December 16, 2010
Updated: Friday, April 18, 2014
| Comments (0)
by Zina Kroner, DO
Menopause has been grabbing all the headlines lately, but half the world faces a comparable syndrome that is more insidious and less predictable. This disease entity is andropause.
Unlike menopause which usually occurs at a predictable time, men's testosterone levels decline at different ages and different rates, sometimes slowly, and sometimes precipitously. Testosterone production by the testes reaches adult levels by age 17 (300-1000 ng/dL). The testosterone level remains constant until the fifth decade at which point it declines at a rate of 1.2 percent per year. But in some men, testosterone can drop prematurely and precipitously.
In the Baltimore Longitudinal Study of Aging (2001), it was demonstrated that free testosterone decreased at a constant rate with age and this decline was not related to other causes. Another study demonstrated that poor health may accelerate the natural age-associated decline in testosterone concentrations. One interesting finding is that studies that measured testosterone in the morning were more likely to show a decline in testosterone when compared to studies that measured testosterone in the afternoon. The logic behind this is that older men have little variation in their levels of testosterone throughout the day, unlike young men, who have peaks in their testosterone levels in the morning and troughs in the evenings.
As one ages, there is an increase in fat cells, which in turn causes an elevation in an enzyme called aromatase. This enzyme transforms testosterone to estrogen in the body. Secondarily, estrogen can indirectly cause an increase in a protein called sex-hormone-binding-globulin (SHBG), which binds to free testosterone and prevents its action. This protein will ultimately cause a decrease in testosterone.
At this point you should be asking "Does this apply to me or to my spouse/partner?"
There are theories that demonstrate that a decline in testosterone can cause a decline in mental function. In a study published in the Journal Of Clinical Endocrinological Metabolism in 2002, 407 men were studied ages 50-91 and subsequently demonstrated that those classified as having a low testosterone had lower scores on memory and visuo-spacial performance. The results of several pilot studies have tied low testosterone levels to Alzheimer's disease, in which there is a build-up of a toxic peptide called beta-amyloid. These studies showed that the toxic effects of this peptide are reduced by testosterone. Interestingly, testosterone levels were lower in Alzheimer's patients as compared to controls. It is unknown if these low levels cause or are caused by Alzheimer's disease. According to Dr. Jonathan Wright (co-author of Maximize Your Vitality and Potency), low testosterone levels are associated with moodiness, feeling weak, passivity, and reduced interest in one's surroundings.
In addition to having an effect on cognitive function, studies have shown correlations between a declining testosterone level and a decline in sexual function as measured by frequency of orgasm or intercourse or by sexual satisfaction (Journal of Clinical Endoclinology 1983). Studies also show that muscle mass, muscle strength and bone mineral density decline with age.
The first step in diagnosing andropause starts with a thorough evaluation at your physician's office. First, your doctor will obtain a complete medical history from you and perform a series of blood tests to see if you have testosterone deficiency and what may be causing it. Before starting any treatment, however, it is imperative to rule out underlying prostate cancer, just as we would rule out breast cancer in a woman contemplating estrogen therapy. The following are some examples of causes of low testosterone and approaches to them.
First, as discussed, in obese patients, there is excess aromatase enzyme activity causing the testosterone to convert to estradiol causing estrogen overload and testosterone deficiency. Poor liver function is another entity that causes excess estrogen because the liver then cannot detoxify the small amounts of estrogen that even men have. In this case, total testosterone levels would be normal and estrogen levels would be high as much of the testosterone is being changed into estradiol, and the free or usable testosterone levels would be low. This often occurs with excess alcohol consumption.
If you fall into the above category, you should maintain an appropriately high level of aromatase inhibitors in your diet. The recommendation is zinc 80mg daily. A supplement call chrysin, a flavonoid, together with piperine for enhance absorption into the bloodstream, functions as a mild aromatase inhibitor as well. There is a more potent aromatase- inhibiting drug called Arimidex (anastrozole), which can only be prescribed by your doctor. Arimidex is prescribed to estrogen receptor positive breast cancer patients to prevent hormones in the body from aromatizing into estrogen. It has not yet been FDA approved for other indications.
A diet that does not adversely affect liver function should be adhered to. This will of course include an alcohol-free diet, since even small amounts of alcohol are shown to augment estrogen in both men and women. Special attention should be paid to medications affecting the liver and should be reviewed with your doctor in detail. As estrogen excess may be a problem in the setting of liver dysfunction, a substance called indole-3-carbinol (or diindole methane or DIM)) found in special supplements or cruciferous vegetables can help to neutralize the excess estrogen. Most importantly, it is essential that you lose weight as it is the excess aromatase enzyme that is produced by the fat cells that convert the testosterone into the estrogen.
Second, an excess of sex-hormone-binding-globulin can bind much of the free- testosterone and therefore inactivates it. In this case, one will have low free testosterone, normal or even high total testosterone and normal estradiol levels. In addition to following the protocol that inhibits aromatase activity, take saw palmetto which can block the estrogen receptor sites in the prostate cells and therefore reduce the effects of excess estrogen. Saw palmetto also blocks the conversion of testosterone into a hormone, DHT, which has been directly linked to the development of prostate disease.
Methanolic extract of nettle can also inhibit SHBG. It binds to SHBG and therefore blocks its testosterone binding effects, thus allowing more testosterone to be in its natural free state. This root has also been used for benign prostatic hyperplasia. It inhibits the binding of dihydrotestosterone ( DHT), a prostate growth stimulator, to the prostate.
A third cause of low testosterone is failure of the pituitary gland to produce a hormone called leutenizing hormone (LH). One of the functions of LH is to stimulate testosterone production by the testes. In this case, the levels of total testosterone would be low as there is a problem with production.
Fourth, if the testes themselves lose their ability to produce testosetrone, there would be an elevated LH, which would act as a stimulant to produce testosterone. Total testosterone would be low. Patients like these are candidates for testosterone replacement.
Lastly, DHEA, a precursor hormone to testosterone and estrogen, may be low and worsen the consequences of borderline testosterone. The solution here is to supplement DHEA under a doctor's supervision.
Physicians have prescribed testosterone administered via creams, tablets, patches, lozenges and injections. Such preparations can lead to normalization of testosterone and improvements in muscle strength, libido, mood and bone density. They may also be associated with side effects, so care must be taken to use the right form of replacement and dosage. There is no "one size fits all" approach.
After initiating testosterone, during the first few months, some men may note effects seen in normal puberty, such as acne and gynecomastia. In men over the age of 50, worsening of prostate symptoms may occur, although sometimes they improve. If, however, the testosterone is not taken in excess and used to maintain a normal serum testosterone, there is no reason to believe that these men are more likely to develop these conditions than men who produce their own natural testosterone. Nevertheless, a PSA and a digital rectal exam and close monitoring of hormone levels must be adhered to.
Posted By Administration,
Monday, November 22, 2010
Updated: Friday, April 18, 2014
| Comments (0)
by Fiona McCulloch, ND
Sometimes I am asked – is Polycystic Ovarian Syndrome (PCOS) caused by eating too much sugar, unhealthy fat and our sedentary lifestyle? Interestingly, the disease of PCOS does not appear to increase in areas of the world where obesity is more prevalent. This indicates that this disease is not caused primarily by obesity. There are many ancient medical records describing women with PCOS conditions (including prolonged menstrual cycles, infertility, acne, abdominal fat, and hirsutism). A recent article in Fertility and Sterility proposes that PCOS is actually an ancient genetic condition that has persisted over thousands of years in women. But why would PCOS persist in our gene pool when it leads to infertility or decreased reproduction in women?
Ancient Hunter-Gatherer communities and women with PCOS
There are several reasons why PCOS variants may have persisted in women over thousands of years. In ancient hunter gatherer communities those who had metabolisms which conserved energy and stored fat had definite survival benefits. Women with PCOS do carry these metabolic advantages. They tend to be metabolic energy conservers – something which is of great advantage in times of low food supply. Because women with PCOS generally had fewer children due to reduced fertility rates, they often had the survival advantage of caring for only one young child at a time and had greater resources for themselves and their families. Childbirth related complications were a common cause of death, so women with PCOS were also at a survival advantage due to decreased maternal mortality. In ancient cultures, there was less food supply, more physical activity and therefore less obesity, so women with PCOS generally had a lower BMI (Body Mass Index) compared to modern women. At times when food was in short supply, women with PCOS would tend to have more normal BMIs (leading to more normal levels of fertility). At these same times, women without PCOS would have lower BMIs and may have been more prone to have subfertility themselves.
Generally, fertility is lower amongst women with PCOS at all BMI levels. In times when BMIs are on average lower in the population, women with PCOS will have more normal reproductive rates. This illustrates the importance of achieving a healthy BMI for women with PCOS and that the condition actually is one of subfertility rather than infertility.
Another point to consider is that PCOS genes are also carried through males, who also carry these metabolic survival advantages and do not experience subfertility. PCOS genetic variants include greater lean muscle mass and bone density and these males could pass on these beneficial genes to their offspring. This explains how this genetic type could persist through thousands of years even though it is related to subfertility.
How this translates to modern women
In general, BMI levels tend to be increased with the modern western diet and lifestyle, so the effects on reproduction of PCOS are amplified compared to those in ancient times. Women with this condition must pay extra attention to achieving a healthy BMI. Although having a high BMI does not cause PCOS, it will definitely cause lower fertility levels. For those women who have a high level of insulin resistance (which is aggravated by the western diet), extra attention must be paid to working with insulin balance in the body. This can be done very effectively with the right diet and supplements.
Integrative medicine assessments
PCOS variants should be screened for in all women seeking fertility treatment who have a long cycle, acne, hirsutism, or abdominal fat accumulation (even in slimmer women). Many traditional assessments can miss mild cases of this condition or “leanings” towards the condition. Restoring pituitary and metabolic function in these women can effectively restore fertility and often heavy medical intervention is not required.
The following tests should be completed :
1) glucose to insulin ration and oral glucose tolerance testing
3) day 3 LH to FSH ratio
4) full early am androgen panel – (androstenedione, free testosterone, DHEA-S, 17-OH Progesterone)
5) am cortisol or diurnal cortisol
6) transvaginal pelvic ultrasound to check for cystic ovaries
In a women who has an elevated LH to FSH ratio we can assume much of the PCOS is related to hypothalamic pituitary dysfunctions. With a normal LH to FSH ratio other metabolic disorders are often more prevalent and contributing factors should be identified. Androgen balance is of great importance, and elevated levels should be identified. It is also important to note that PCOS variants can be closely mimicked or aggravated by adrenal conditions so assessment of the adrenal function including diurnal cortisol, and DHEA-S testing is very important.
Treatment very much depends on the individual characteristics of each woman’s condition. There are many different PCOS variants as this is a syndrome involving reduced frequency of ovulation and is not a discrete disease with one cause. A patient does not have to have all of the diagnostic criteria of PCOS to have her fertility affected by a milder variant of this disease. Each patient will require different treatment based on her lab values, metabolic characteristics, body type, severity of disease and level of inflammation.
Hunter-Gatherer diets and PCOS
Returning the patient to a healthy BMI is much more important for fertility than in women without PCOS. Thus, healthy diets with attention to glycemic index are of great effectiveness. I always counsel patients with PCOS extensively on nutrition and diet as this is an area of special need for them even if they are a “lean” type. A hunter-gatherer diet is often the best type of diet for PCOS. This diet is high in healthy proteins such as lean meats, seafood, fruits and berries, vegetables, and nuts and low in grains. Most especially of course, the diet should be low in sugar since hunter gatherer cultures had very low sugar intake overall.
A simple one day hunter-gatherer diet for PCOS variants:
Breakfast: Omelette made with onions and spinach.
Snack : Ambrosia (pear, avocado and 1/2 unripe banana – blend in blender until smooth and creamy) *Did you know unripe bananas have a glycemic index of 50 whereas a ripe banana has a glycemic index of 82?
Lunch: Tilapia fillet drizzled with olive oil, with brocolli or salad (dressing of fresh lemon, olive oil and fresh herbs)
Snack: Sliced baby cucumber with fresh lemon squeezed on top. 3 tbsp almonds and 1 cup of fresh blueberries
Dinner: Grilled chicken breast with pesto and baby bok choy
This diet would be varied with respect to quantity and calories for differing weight loss or maintenance requirements.
I use supplement therapy as a mainstay along with diet in the treatment of PCOS and have found the combination works wonderfully to restore cycle regularity. Supplements are aimed at restoring normal hypothalamic-pituitary function, increasing antioxidant status, improving insulin resistance, and minimizing excess androgen levels if required. Supplement protocols will vary widely with different “types” and lab results found in different PCOS variants.
Carmina E, Guastella E, Longo RA, Rini GB, Lobo RA. Correlates of increased lean muscle mass in women with polycystic ovary syndrome. Eur J Endocrinol 2009;161:583–9.
Di Carlo C, Shoham Z, MacDougall J, Patel A, Hall ML, Jacobs HS. Polycystic ovaries as a relative protective factor for bone mineral loss in young women with amenorrhea. Fertil Steril 1992;57: 314–9.
Good C, Tulchinsky M, Mauger D, Demers LM, Legro RS. Bone mineral density and body composition in lean women with polycystic ovary syndrome. Fertil Steril 1999;72:21–5.
Ricardo Azziz, Daniel A. Dumesic, Mark O. Goodarzi. Polycystic ovary syndrome: an ancient disorder? Fertility and Sterility – 27 October 2010
To WW, Wong MW. A comparison of bone mineral density in oligomenorrhoeic adolescents with polycystic ovaries and normal ovaries. Gynecol Endocrinol 2005;20:237–42.
Posted By Administration,
Wednesday, October 13, 2010
Updated: Friday, April 18, 2014
| Comments (0)
by Gina Nick, NMD, PhD
A study of 600 nursing facility residents has found that those with adequate zinc levels were about fifty percent less likely to develop pneumonia than those with low body concentrations of zinc. Also, those with sufficient levels of zinc received fewer prescriptions for antibiotics, had shorter durations of pneumonia and had lower mortality rates.
The researchers suggested that zinc supplementation for zinc-deficient elderly persons may result in a lower incidence of pneumonia and that further study is required to determine whether zinc supplements may be an effective and low-cost intervention to reduce pneumonia deaths among vulnerable populations who already have low zinc intakes. (An earlier analysis of the same data had shown that those who consumed 200 international units (IU) of vitamin E were less likely to get upper respiratory infections, such as colds.) The study was released August 10, 2010 and will be published in a future issue of the American Journal of Clinical Nutrition. In the meantime, it can be read online at by subscribers to the journal or those who pay the article access fee.
The evidence is mounting that proper nutrient levels keep us well. In general licensed Naturopathic Medical Doctors will not, however, advise that everyone run out and buy a high potency vitamin and mineral supplement. We are all unique, and what we have discovered at our office is that one person may have toxic levels of zinc in their body, while another may have a deficiency. That is why we are strong proponents for testing to discover what your unique nutrient, amino acid and fatty acid needs are. Armed with objective information on your body, we can then create a plan for you of what supplements to take, in what form, how often, and what dietary and lifestyle changes you can make to keep you healthy, well and safe!
Posted By Administration,
Wednesday, September 29, 2010
Updated: Friday, April 18, 2014
| Comments (0)
by Gina Nick, NMD, PhD
A new study has determined the individual percentages by which a variety of lifestyle changes can reduce the risk of dementia and suggests that these interventions – in the absence of a new treatment for the mind-robbing disease – are likely to have the greatest impact on reducing dementia levels in the future. The study assessed previously identified risk factors such as depression, diet, alcohol consumption, educational level and vascular factors, which include heart disease, stroke, high blood pressure, obesity, diabetes, and high cholesterol. Results found that three changes together – eliminating depression and diabetes and increasing fruit and vegetable consumption – reduced dementia risk by a full 21 percent. Depression alone accounted for a 10 percent risk. Higher education was linked to an 18 percent lower risk. To illustrate the extent of these factors, the genetic tendency towards dementia accounts for seven percent of cases. The study was released August 5, 2010 and will be published in the British Medical Journal. But the journal already has made the full-text version of this important study available to the public, online without the usual requirement of a journal subscription or access fee.
Naturopathic Medicine is an effective approach to preventing and reversing depression and type two diabetes. Paired with diet ad lifestyle recommendations that are based on your unique constitution, licensed Naturopathic Medical Doctors have the tools to prevent and halt the progression of Dementia, even in the face of genetic predisposition. That offers true hope to millions of people! It is time for Naturopathic Medicine, practiced by licensed Naturopathic Medical Doctors, to enter the mainstream and offer simple, genuine solutions to our healthcare crisis worldwide.