Portland Oregon Bioidentical Doctors Seminar - Bioidentical Hormones

Bioidentical Hormones Replacement Therapy

Portland Oregon Doctors Seminar

Part 1

Part 2

What are Bioidentical Hormones?

Dr. Kathryn Retzler, HormoneSynergy Clinic LLC

Bioidentical hormones are plant-derived, and are structurally identical to hormones produced by your body. Bioidentical hormone delivery methods and dosages are chosen based on testing and your individual symptoms and specific needs. There are many types of bioidentical hormones including pharmaceuticals such as patches and gels, as well as compounded options including sustained-release capsules, topical creams or gels, sublingual lozenges, and subcutaneous pellet implants.

Historically, hormone replacement has involved the use of synthetic hormones, especially synthetic estrogen, progestins (e.g., Premarin® and Provera® or PremPro®) and testosterone (methyltestosterone in Estratest®). These synthetic hormones have been shown to increase the risk for health problems including breast cancer, heart disease, stroke, and liver problems.

Bioidentical hormones are prescribed in individualized dosages (based on clinical symptoms and lab results). Because bioidentical hormones are identical in structure as those hormones produced by the human body, they are safer and more effective than synthetic hormones (this is especially true for bioidentical progesterone and testosterone).

Dr. Barry Ritz responds to the Omega-3 Fatty Acid and Prostate Cancer headlines

Literature Watch: Omega-3 Fatty Acids and Prostate Cancer

7/11/2013

Author:  Barry W. Ritz, PhD

Commentary:

Observational case-cohort study reports an association between increased blood concentrations of omega-3 fatty acids and risk for prostate cancer among men involved in an intervention study designed to examine prostate cancer risk in subjects supplemented with vitamin E and/or selenium. 

In an analysis of data generated from the SELECT trial (Selenium and Vitamin E Cancer Prevention Trial), Brasky and colleagues have reported that men with the highest quartile of serum long-chain omega-3 polyunsaturated fatty acids were at a 43% increased risk for prostate cancer, including a 44% increased risk of low-grade cancer and a 71% increased risk for clinically-significant, high-grade cancer.  The authors conclude that these data “confirm” the link between omega-3 fatty acid intake and increased risk for prostate cancer and, in both the original paper and subsequent media interviews, specifically emphasize the risks of consuming omega-3 (fish oil) supplements.  The current study effectively adds to a body of inconsistent literature regarding the role of dietary fatty acids and prostate cancer risk, which is an area that does indeed require further study with appropriate, controlled trials.  However, the authors greatly overstate their conclusions, especially in attributing increased risk to fish oil supplementation, such that a more thorough discussion on the study design, a review of the results in context, and illumination of the limitations of their analysis are clearly warranted.

The SELECT trial enrolled 35,533 men between 2001 and 2004 at average risk for developing prostate cancer and assigned them to intervention groups providing selenium, vitamin E, selenium + vitamin E, or placebo.  The trial was discontinued in 2008 due to no observed evidence of a protective effect.  Subsequent analysis, several years after the discontinuation of the intervention, reported a 17% increased risk for prostate cancer among men who had been previously supplemented with vitamin E.  Although the SELECT study was not designed to evaluate an association between fatty acid status and cancer outcome, baseline blood samples were available for the analysis of fatty acid composition, making the current study possible. 

The analysis of blood samples for fatty acid composition was conducted on a sub-sample of the original study population including 1364 subjects who did not develop cancer and 834 total subjects who had developed prostate cancer.  The authors created the case cohort by selecting subjects who had developed prostate cancer during a specific period of time during the study and for which there were baseline blood samples available.  They then created a control subgroup by selecting subjects from the trial that could be matched for the basic demographics of the case cohort but who had not developed prostate cancer.  Fatty acid compositions were then reported for total omega-3, alpha-linolenic, EPA, DHA, DPA, the omega-6 fatty acids linoleic and arachadonic, and a selection of trans-fatty acids as a percentage of total fatty acids, and each group was split up into quartiles from the highest to the lowest percentages.  The authors then analyzed the relative risk of developing prostate cancer by comparing the lowest quartile to the highest for each fatty acid.  It is important to note that these quartiles of fatty acid composition from high to low represented fatty acid composition at BASELINE, not during the course of the study or at the time point at which the subjects were known to develop prostate cancer.  In many cases, the blood sample from which fatty acids were analysis would have been drawn years before the development of cancer.  Although the development of cancer is considered a long-term process, there is absolutely no way to determine whether the baseline fatty acid levels were reflective of typical values for that individual or whether they were reflective of fatty acid intakes or fatty acid status during the time period when cancer was developing or at the time point at which cancer was detected.

The authors report an increase in prostate cancer risk associated with elevations in total omega-3, as well as elevated concentrations of the fatty acids DPA and DHA, specifically.  The omega-3 fatty acids alpha-linolenic and EPA were not associated with increased risk.  The authors also provide a meta-analysis in which they put the current results into the context of previous reports.  According to the meta-analysis of seven studies, EPA was not associated with prostate cancer risk.  An analysis of alpha-linolenic was not provided, but the authors note that results from other studies have consistently demonstrated no relationship.  Results for the fatty acid DHA were mixed.  One trial in the analysis reported a protective effect against total prostate cancer outcomes, three trials reported an increased risk (including both the current study and Brasky 2011), and three studies demonstrated no effects.  The meta-analysis concluded a 16% increased risk for total prostate cancer.  Results for low- and high-grade cancer risks were also mixed, with the overall outcomes being a 20% and 48% increased risk, respectively.  The meta-analysis concluded no association between total omega-3 intake and total or low-grade prostate cancer risk, although high-grade prostate cancer risk was increased by 51%.  This elevated risk came from only one trial, also by Brasky and colleagues (2011), while the other three studies in the meta-analysis yielded null results.  Indeed, much of the data supporting a positive association between omega-3 status and cancer risk have been generated by Brasky and colleagues.  Further, numerous studies appear to be missing from the Brasky meta-analysis (Berquin 2007, Terry 2001, Augustsson 2003, Leitzmann 2004), possibly related to incompatible methodologies, and a previous meta-analysis reporting no association between omega-3 fatty acids intake and prostate cancer risk but a 63% decreased risk of prostate cancer-related mortality with increased omega-3 intake was excluded (Szymanski 2010).  Taken together, the collective literature clearly does not provide definitive evidence associating omega-3 fatty acid status with prostate cancer risk.

In addition to reporting an increased risk for prostate cancer associated with increased omega-3s, the authors reported a decreased risk of prostate cancer of about 25-30% associated with an increase in the omega-6 fatty acid linoleic acid.  Arachadonic acid was not associated with an increased or decreased risk.  In addition, in a previous study using data in a similar manner but obtained from the Prostate Prevention Trial, the same authors reported a decreased risk for prostate cancer associated with increased trans-fats.  It is unknown why generally recognized pro-inflammatory omega-6 and trans-fatty acids might be associated with a protective effect against prostate cancer.  Given this unknown and the inconsistency in results, the authors conclude that it is unlikely that omega-6 or trans-fats are associated either positively or negatively with prostate cancer risk.  However, while the authors concede that a coherent mechanism is also missing for why anti-inflammatory omega-3s would be associated with increased prostate cancer risk, they conclude that their data are definitive in establishing a relationship between increased omega-3 fatty acids and increased prostate cancer risk.  This conclusion is clearly overstated.

Importantly, the authors go on to explain their results in the context of “other” clinical trials in which nutritional supplements have reported increases in cancer risk despite a complex association between nutrients and chronic disease.  This is the salient error in the authors’ analysis and conclusion—they implicate supplemental omega-3 fats without any data related to supplemental intake.  The study was not designed to look at omega-3 intake.  Remember, outcomes were compared to the subjects’ fatty acid status at baseline, possibly years before cancer was detected.  Further, no data on dietary or supplemental nutrient intakes was provided.  In the original study design, an intervention trial looking at selenium and vitamin E, subjects were asked to avoid consumption of any multivitamin or supplemental selenium or E.  Instead, a special multi-vitamin was provided for free to account for subjects who might wish to consume a multi and would otherwise confound the results.  There were apparently no restrictions or recommendations on diet or supplements related to omega-3 fatty acids (fish intake or fish oils).  As a result of the lack of any intervention related to fish or fish oil intake, the resultant quartiles of fatty acid status were quite close together.  As noted by the senior author on the study Dr. Alan Kristal and reported in Science Daily, the difference in blood concentrations between the lowest and highest quartiles for total omega-3 was quite small and reflects a difference of about 2 fish meals per week.  The range in total omega-3 as a percentage of total fatty acids was only about 1.6%, from 3.7% in the lowest group to 5.3% in the highest quartile.  (Note: the percentages and range reported in Science Daily and commented on by Dr. Kristal are incorrect.)  While methodologies differ, the literature suggests that a fatty acid percentage of approximately 4% is indicative of a normal, unsupplemented population (Skulas-Ray 2011, Carney 2009).  Therefore, the current study even at the highest quartile is probably not reflective of a generally supplemented population.  According to Atrium’s our own data (unpublished, in press), we have observed a baseline fatty acid status of 6% in a healthy population regularly consuming fish oil supplements.  This exceeds the highest fatty acid quartile in the current study.  In conclusion, any association between fatty acid status and prostate cancer cannot be attributed to supplementation.  Notably, the authors appear to be eager to recommend against the use of fish oil supplements, despite their established health benefits, but stop short of calling for a reduction in dietary fish intake.

Despite these limitations and the gross overextension of the results by the study authors and media, the current study does make an important contribution to the overall body of literature investigating the potential association between fatty acid status and prostate cancer risk.  As currently available data are inconsistent and a plausible mechanism remains unknown, further studies are warranted.  These should be of proper design and account for omega-3 intake from dietary and supplemental sources. 

Citation:

Brasky TM, Darke AK, Song X, et al. Plasma phospholipid fatty acids and prostate cancer risk in the SELECT trial. J Nat Cancer Inst. 2013

Additional references:

Brasky TM, Till C, White E, et al. Serum phospholipid fatty acids and prostate cancer risk: results from the prostate cancer prevention trial. Am J Epidemiol. 2011;173(12):1429-39.

Berquin IM, Min Y, Wu R, et al. Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. J Clin Invest. 2007;117:1866-75.

Terry P, Lichtenstein P, Feychting M, Ahlbom A, Wolk A. Fatty fish consumption and risk of prostate cancer. Lancet. 2001;357:1764-6.

Augustsson K, et al. A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer Epidemiol Biomarkers Prev. 2003;12(1):64-7.

Leitzmann MF, Stampfer MJ, Michaud DS, et al. Dietary intake of n-3 and n-6 fatty acids and the risk of prostate cancer. Am J Clin Nutr. 2004;80(1):204-16.

Szymanski KM, Wheeler DC, Mucci LA. Fish consumption and prostate cancer risk: a review and meta-analysis. Am J Clin Nutr. 2010;92(5):1223-33.

Skulas-Ray AC, Kris-Etherton PM, Harris WS, et al. Dose-response effects of omega-3 fatty acids on triglycerides, inflammation, and endothelial function in healthy persons with moderate hypertriglyceridemia. Am J Clin Nutr. 2011;93:243-52.

Carney RM, Freedland KE, Rubin EH, et al. Omega-3 augmentation of sertraline in the treatment of depression in patients with coronary heart disease: a randomized controlled trial. JAMA. 2009;302(15):1651-7.

Science Daily: Link between Omega-3 fatty acids and increased prostate cancer risk confirmed, www.sciencedaily.com, July 10, 2013.

NutraIngredients: Omega-3 “confirmed” to increase prostate cancer risk: study, by Nathan Gray, www.nutraingredients-usa.com, July 11, 2013.

Tags:

Literature Watch

Cancer

Omega-3’s

Dr. Barry Ritz

Omega-3 Fish oil and Prostate Cancer study conclusions are overblown

CRN SAYS NEW STUDY ON

OMEGA-3 (Fish Oil and Prostate Cancer) CONCLUSIONS ARE OVERBLOWN

WASHINGTON, D.C., July 11, 2013—In response to a new study, “Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial,” published yesterday online in the Journal of the National Cancer Institute, the Council for Responsible Nutrition (CRN), the leading trade association representing the dietary supplement industry, today issued the following statement: 

“The numerous benefits of omega-3 fatty acids from foods (like salmon and sardines) and dietary supplements are well-established for men and women in all stages of life—and this new study does not change those recommendations about the importance of this nutrient. Hundreds of studies over the past two decades have shown omega-3 fatty acids to have positive effects associated with cardiovascular health, perinatal health, inflammation, cognitive function, or cancer. Collectively, this body of research serves as the basis for numerous recommendations from respected organizations, scientific boards and healthcare practitioners that Americans get omega-3 fatty acids in their diets.

While we encourage researchers to continue to study omega-3 fatty acids with an open mind, it is counterproductive when studying nutrition for researchers to promote their study as if it were the only piece of research that counts. In this case in particular, it is especially disingenuous for the researchers to make the kinds of assertions we’ve seen in the press, given their results are in stark contrast to previous epidemiologic studies¹ that not only demonstrate no correlation between omega-3 consumption through fish and/or supplementation and the risk of prostate cancer, but in many cases also showed a protective effect against prostate cancer.

Further, the researchers were quick to blame dietary supplements even though there is no evidence that anybody in this study took fish oil dietary supplements. In fact, the study demonstrates no cause and effect; it can only purport to show an association between higher plasma levels of omega-3 fatty acids in those whom the researchers advise had an increased rate of prostate cancer.   

One should also consider whether this study could have simply been measuring a biomarker reflecting recent intake of fish or fish oil supplements in a group of high risk cancer patients that had been told to increase their EPA and DHA levels, as compared to a group of non-cancer patients that had not been told to consume more EPA and DHA. Plasma levels of EPA and DHA reflect very recent intake and are considered a poor biomarker of long term omega-3 intake especially when compared to red blood cell levels, which reflect medium term intake. A single fish oil dose (or hearty serving of fish at lunch) results in >100 percent increase in plasma omega-3 levels. So looking at plasma levels in healthy and sick people may only provide insight into the recent habits of these individuals.

Additionally, the study’s conclusions are also limited by the fact that the study was not designed to evaluate the question the researchers sought to confirm.

The American Heart Association, the World Health Organization (WHO), the U.S. Institute of Medicine’s Food Nutrition Board (IOM FNB) and the 2010 Dietary Guidelines all have current policies advising Americans to eat more fatty fish to get the benefits of omega-3 fish oils. It is highly unlikely this one study will change that advice. Omega-3s can also be obtained by taking one of the many supplement products on the market. For those consumers who have concerns about prostate cancer or other questions about omega-3 fatty acids, we recommend speaking with your doctor or other healthcare practitioner.”

Statement by Duffy MacKay, N.D., vice president, scientific and regulatory affairs

References:

Berquin IM, Min Y, Wu R et al. Modulation of prostate cancer genetic risk by omega-3 and omega-6 fatty acids. J Clin Invest 2007; 117: 1866–75

Wang MT, Honn KV, Nie D. Cyclooxygenases, prostanoids, and tumor progression. Cancer Metastasis Rev 2007; 26: 525–34

Terry P, Lichtenstein P, Feychting M, Ahlbom A, Wolk A. Fatty fish consumption and risk of prostate cancer. Lancet 2001; 357: 1764–6

Chavarro JE et al. A 22-y prospective study of fish intake in relation to prostate cancer incidence and mortality. Am J Clin Nutr 2008; 88: 1297–303.

Augustsson, K., et al., A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer Epidemiol Biomarkers Prev, 12(1): p. 64-7, 2003.

Szymanski KM, Wheeler DC, Mucci LA. Fish consumption and prostate cancer risk: a review and meta-analysis. Am J Clin Nutr. 2010 Nov;92(5):1223-33.

Leitzmann MF, Stampfer MJ, Michaud DS, et al. Dietary intake of n-3 and n-6 fatty acids and the risk of prostate cancer. Am J Clin Nutr. 2004 Jul;80(1):204-16.

Ritchie JM, Vial SL, Fuortes LJ, Robertson LW, Guo H, Reedy VE, Smith EM.Comparison of proposed frameworks for grouping polychlorinated biphenyl congener data applied to a case-control pilot study of prostate cancer. Environ Res. 2005 May;98(1):104-13.

Patient Testimonial - HormoneSynergy Detox Program

Loses 14 lbs. in 8 weeks, gains 3% lean body mass, all symptoms disappear

Meet HormoneSynergy's latest Rock Star. 8 weeks ago, Rod described himself as "an obese, tired, sick 51 year old."

After meeting with Dr Kathryn Retzler and then starting a HormoneSynergy Detox program he now describes himself this way: 

"I feel better than I have in ten years. I suffered from chronic heartburn, stomach problems, gout, joint pain and headaches. Since I started taking Dr. Retzler's recommended nutraceuticals and eliminating toxic foods, all of my aches and pains have gone away, I have lost 14 pounds in 8 weeks, gained 3% lean body mass and lost 3% fat. I am now eating healthier, working out, and I have more energy. Overall I just feel better."

We at HormoneSynergy congratulate Rod for his commitment to optimal health and continued success. Thanks for sharing your story, Rod! You are our latest Rock Star!

For additional information about our HormoneSynergy Transformation Health and Detox Program click:  HormoneSynergy Transformational Health and Detox

Hormone Imbalance Symptoms in Women and Men

Hormone Imbalance Symptoms in Women and Men 

Watch this short video from a recent HormoneSynergy Seminar in Portland Oregon.

What is HormoneSynergy?

HormoneSynergy refers to the interactive way that hormones influence each other, and emphasizes that vibrant health is the result of balanced hormones. Hormone balance requires adherence to the “Goldilocks principle” – not too much, not too little, just the right amount! This is why the standard of care “one-size-fits-all” approach to hormone replacement often leads to side effects. This is also why testing your hormones and working with an experienced physician who focuses on your individual needs and unique hormone blueprint is crucial.

In addition to providing bioidentical hormone options, HormoneSynergy focuses on the foundation of extraordinary health. By following the 8 Steps to Achieving HormoneSynergy you can slow the effects of aging, keep your mind sharp, maintain an attractive body, and continue to experience all the joys of life. You may also prevent diseases such as diabetes, heart disease, and obesity. Balanced hormones may also help you avoid arthritis, osteoporosis, Alzheimer’s disease and other forms of dementia, and some forms of cancer.  Bioidentical Hormones are best if supplementing.

Symptoms of Low Thyroid Hormone

Thyroid Hormone

The thyroid gland produces two hormones (T4 and T3) that control body development, growth, and metabolism. More than 90% of the hormones secreted by the thyroid is T4 (thyroxine); however, T4 is mostly inactive. To become active, T4 must be converted by the body into its active form, T3 (triiodothyronine). Regulation of thyroid hormone is controlled by the brain (via the hypothalamus and pituitary), the thyroid gland itself, and peripheral conversion of inactive T4 into active T3. Therefore, low thyroid (hypothyroid) symptoms can result from multiple causes:

• a problem in the brain
• a problem in the thyroid gland
• poor conversion of thyroid hormone from T4 into T3

Thyroid hormone is essential for contraction of your heart; low thyroid hormone (“hypothyroidism”) can cause heart enlargement, congestive heart failure, and low pulse rate. Hypothyroidism can also cause high LDL (“bad”) cholesterol, the type of cholesterol that can become oxidized, leading to plaques in the arteries or "atherosclerosis."Thyroid hormone is needed by every cell of your body. Without it, cells cannot function normally—this is why thyroid hormone deficiency can cause problems in nearly every body system. Thyroid hormone is the main hormone responsible for your metabolism and energy level. It’s also critical for normal immune function, as well as healthy skin, hair, and nails. 

Muscles require thyroid hormone for strength and function—in fact, insufficient production of thyroid hormone is commonly associated with muscle aching or weakness.

Lastly, thyroid hormone is vital for the health of your brain—it maintains a positive, stable mood and improves the speed of thinking. Without enough thyroid hormone, you can become depressed or anxious. This is in part due to T3 (active thyroid hormone) working between neurons to regulate the amount and activity of neurotransmitters (brain chemicals) such as serotonin and GABA.[i]^,[ii]

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[i] Kirkegaard C, Faber J. The role of thyroid hormones in depression. Eur J Endocrinol. 1998;138(1):1–9.

[ii] Dratman M, Gordon J. Thyroid hormones as neurotransmitters.  Thyroid.  1996;6(6):639–47. 

Watch Dr. Retzler discuss symptoms of Low Thyroid Hormone at a recent HormoneSynergy Seminar in Portland Oregon

Preventing Dementia and Alzheimer's - Brain Health

Preventing Dementia and Alzheimer's - Brain Health 

Optimal aging means more than just achieving peak physical health—it also means having a healthy brain. Much like physical health, brain health can be viewed along a continuum—from optimal function to mild cognitive impairment, to severe dementia or Alzheimer's. Brain or "cognitive function" includes your intelligence, memory, and creativity, and your ability to concentrate, communication, and interact with the world. Although you may notice some brain changes--memory lapses, decreased mental sharpness, slowed processing speed, poor attention span, or changes in mood--many forms of cognitive decline are too subtle to notice.

Mental decline does not have to be an inevitable part of aging. Early detection of cognitive decline is critical to reverse it, and to prevent further decline or dementia. Neurocognitive function testing establishes a baseline, and enables us to target treatments to your specific deficits. Follow up testing helps determine treatment success and guides future brain enhancement protocols.

HormoneSynergy offers inexpensive, thorough, computer-based neurocognitive function testing for patients and non-patients. This testing can be performed in our office or on your own home computer.

Watch Dr. Retzler's short video on Preventing Dementia and Alzheimer's below and let us know what you think!