November 18th, 2008
By Dr. Nancy Dunne and Bill Slater
PCOS Review
Nov. 2008
We can hardly stress enough how important vitamin D is for you. Some of you may be wondering why there is so much vitamin D in our d-pinitol formula.
In the full article on our site, we list a number of previous newsletter articles that review the benefits of vitamin D for ovarian health and reducing insulin resistance.
We then go on to review some new research data about vitamin D. Several studies indicate a correlation between low levels of vitamin D and an increased incidence of breast cancer. One study suggested that intake of 2,000 IU of vitamin D could increase vitamin D levels in your body enough to reduce the incidence of breast cancer by 50%. Fifty percent is a very big drop in risk!
The other interesting study showed large doses of vitamin D for one year were useful for depression in people who were overweight.
In summary, there are multiple health benefits from making sure your vitamin D levels are optimal. You may need to take a significant amount of supplemental vitamin D to reach an optimal level. This is why there is so much vitamin D in the d-pinitol product.
Read the full article here:
www.ovarian-cysts-pcos.com/news69.html
To purchase D-pinitol (U.S. Only):
www.ovarian-cysts-pcos.com/store/pinitol
November 7th, 2008
Science Daily
Nov. 6, 2008
A two-year study conducted by researchers at George Mason University, INOVA Fairfax Hospital and the National Cancer Institute may open the door to new therapies for combating chronic diseases associated with obesity, a condition that affected more than 33 percent of American adults in 2005-06 according to the Centers for Disease Control and Prevention.
While analyzing samples taken from morbidly obese patients undergoing weight loss surgery, the researchers discovered that substantial quantities of melanin—a pigment that gives the skin, the hair and the iris of the eye their natural color—were being produced in the study participants’ fat tissue.
Ancha Baranova, assistant professor in George Mason University’s Department of Molecular and Microbiology and the paper’s lead author, explains that melanin production has never before been identified in fat tissue. She believes that the antioxidant, which has been shown to have anti-inflammatory properties, could be the body’s natural defense against obesity-related conditions such as type 2 diabetes, coronary heart disease, fatty liver disease, polycystic ovary syndrome and some cancers.
“Stockpiling extra calories is difficult even for specialized fat cells; having too much lipid molecules takes its toll on the fat cells, producing oxidative stress,” says Baranova. “It’s not unthinkable that these cells would adapt and produce melanin as a form of self-protection. As a side benefit, melanin may suppress inflammatory properties of the extra pounds of the fat.”
Baranova notes that a larger study is needed in order to confirm the role that the body’s production of this compound plays in fat tissue. However, the discovery suggests that melanin-based therapies may one day be used to reduce the incidence of chronic diseases among the morbidly obese.
“This opens an entirely new avenue for medical interventions because the process of biosynthesis of melanin is relatively easy to meddle with,” says Baranova. “We hope that this study will spur the development of preventive medications aimed at curtailing devastating metabolic complications in obese and overweight populations.”
The paper was co-authored by Manpreet Randhawa, Tom Huff and Vikas Chandhoke of George Mason University; Julio C. Valencia and Vincent J. Hearing of the National Cancer Institute; and Zobair Younossi of INOVA Fairfax Hospital. The study was funded by the Thomas F. Jeffress and Kate Miller Jeffress Memorial Trust and by the Intramural Research Program of the National Cancer Institute at the U.S. National Institutes of Health.
The findings appear in the current Web edition of the FASEB (Federation of American Societies for Experimental Biology) Journal and will be published in the March 2009 print edition.
Journal reference:
1. Randhawa et al. Evidence for the ectopic synthesis of melanin in human adipose tissue. The FASEB Journal, 2008; DOI: 10.1096/fj.08-116327
Adapted from materials provided by George Mason University.
http://www.sciencedaily.com/releases/2008/11/081106164818.htm
October 30th, 2008
Sathyapalan T, Kilpatrick ES, Coady AM, Atkin SL
Department of Diabetes and Endocrinology, University of Hull, Hull, UK; Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, UK; Department of Obstetric Ultrasound, Hull & East Yorkshire Women’s & Children’s Hospital, Hull, UK.
Source J Clin Endocrinol Metab 2008 Oct 21.
Abstract Context: Polycystic ovary syndrome (PCOS) is associated with increased risk of cardiovascular morbidity whereas statins are proven to reduce cardiovascular mortality and morbidity through lipid lowering and perhaps through their pleotrophic effects. Statins can also reduce testosterone in vitro by inhibiting ovarian theca-interstitial cell proliferation, steroidogenesis and reducing inflammation in vivo.
Objective: To assess the effect of atorvastatin on inflammatory markers, insulin resistance and biochemical hyperandrogenemia in patients with PCOS.
Design: Randomised, double blind placebo controlled study.
Setting: Tertiary care setting in United Kingdom.
Patients: Forty medication naïve patients with PCOS and biochemical hyperandrogenaemia.
Methods: Patients were randomised to either atorvastatin 20mg daily or placebo.
Main outcome measures: The primary end point of the study was a change in the inflammatory marker hsCRP. The secondary end points were a change in insulin resistance and total testosterone.
Results: After 12 weeks of atorvastatin there was a significant reduction (mean+/-SEM) in total cholesterol (4.6+/-0.2 vs. 3.4+/-0.2 mmol/L,p<0.01), LDL cholesterol (2.9+/-0.2vs.1.8+/-0.2 mmol/L,p<0.01), triglycerides (1.34+/-0.08vs.1.08+/-0.13mmol/L,p<0.01), hsCRP (4.9+/-1.4vs.3.4+/-1.1mg/Lp=0.04), free androgen index (13.4+/-0.6vs.8.7+/-0.4 p<0.01), testosterone[4.1+/-0.2vs.2.9+/-0.1 nmol/Lp<0.01) and insulin resistance as measured by HOMA-IR(3.3+/-0.4vs.2.7+/-0.4). There was a significant increase in SHBG (31.1+/-1.0vs.35.3+/-1.2 nmol/L,p<0.01). There was a positive correlation between the reduction in HOMA-IR in the atorvastatin group with the reduction in triglycerides and the reduction of FAI. There was a significant deterioration of HOMA-IR in the placebo group (3.0+/-0.4vs.3.8+/-0.5).
Conclusions: This study suggests that atorvastatin is effective in reducing inflammation, biochemical hyperandrogenemia and metabolic parameters in patients with polycystic ovary syndrome after a 12 week period.
PubMed ID 18940877
January 7th, 2008
The following article on “Inflammation, Insulin Resistance and PCOS” by Dr. Sari Cohen was originally published in the PCOSA Newsletter “PCOSA Today”.
Scientists are investigating the role of inflammation in the pathogenesis of many conditions, including PCOS, diabetes, and heart disease. The question of whether or not inflammation is the underlying cause of PCOS remains unanswered. Also unclear is which aspect of PCOS specifically contributes to the increased risk of heart disease and type 2 diabetes: inflammation, insulin resistance, or other metabolic and hormonal disturbances? The research to date shows that insulin resistance, inflammation and the hormonal changes of PCOS are certainly related – but which came first remains a mystery.
PCOS has long been associated with insulin resistance, with many in the medical community believing that insulin resistance is the underlying cause of PCOS. Some evidence points to inflammation as causing insulin resistance. Researchers at University of California San Diego assert that inflammation induced by immune cells called macrophages leads to insulin resistance and type 2 diabetes. Their research on mice indicates that in the absence of inflammation, obesity alone does not cause insulin resistance. This means that, according to this study, some inflammatory mediators are necessary for the development of insulin resistance.
If this is true, one may extrapolate the data to indicate that women with PCOS do not develop insulin resistance unless inflammation is also involved. For this truly to be meaningful, we would have to prove that all women with PCOS exhibit signs of inflammation. This is easier said than done!
Research published in 2005 examining insulin resistance and inflammatory markers in obese and non-obese women with PCOS showed that all women with PCOS had elevated levels of inflammatory markers.
On the other hand, a study published in the European Journal of Endocrinology in 2004 concluded that PCOS was not necessarily correlated with inflammation after comparing levels of inflammatory markers CRP and IL-6 in women with PCOS to a control group. The authors write, “BMI was…the parameter most strongly related to IL-6 and CRP in PCOS… In PCOS, the type 2 diabetes risk may…be confined to those with obesity and/or metabolic alterations rather than affecting all women suffering from the syndrome.” In other words, lean women with PCOS may not be as likely to exhibit elevated inflammatory markers as their overweight counterparts with PCOS.
A similar trend was also noted in a 2003 study examining the effects of metformin therapy in lowering CRP levels in women with PCOS, where the researchers suggested that elevated CRP was related to obesity rather than PCOS itself.
Another article published in September 2007 in Gynecological Endocrinology concluded that obesity, rather than inflammatory markers, represented the greater factor in predicting whether or not women with PCOS would develop heart disease and/or type 2 diabetes.
Perhaps the contradictory results may be due to the fact that the community of women with PCOS is very diverse, not only ethnically but also phenotypically (that is, the physical manifestation of the disease). Furthermore, these studies have a relatively small number of participants, usually less than 100 people. Both of these factors may confound the attempt to simplify the issues of finding the one underlying cause of PCOS and even of the historical difficulty in establishing criteria for the definitive diagnosis of PCOS.
In conclusion, we clearly need more research with larger numbers of participants to determine the interrelationship between inflammation and insulin resistance in PCOS, and how these factors relate to hormonal imbalance and cardiovascular risk factors. This issue is important because it could dictate changes in treatment strategies for women with PCOS. Furthermore, more attention needs to be paid to the great ethnic diversity in this population with a future focus on examining trends among specific ethnic groups.
www.pcos.insulitelabs.com
(1) As reported in ScienceDaily (Nov 7, 2007)
(2) Yilmaz M. et al. Levels of lipoprotein and homocysteine in non-obese and obese patients with polycystic ovary syndrome. Gynecol Endocrinol. 2005 May;20(5):258-63. PMID: 16019370
(3) Mohlig M. et al. The polycystic ovary syndrome per se is not associated with increased chronic inflammation. Eur J Endocrinol. 2004 Apr;150(4):525-32. PMID: 15080783
(4) Morin-Papunen L. et al. Metformin reduces serum C-reactive protein levels in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2003 Oct;88(10):4649-54. PMID: 14557435
(5) Guzelmeric K. et al. Chronic inflammation and elevated homocysteine levels are associated with increased body mass index in women with polycystic ovary syndrome. Gynecol Endocrinol. 2007 Sep;23(9):505-10. PMID 17852421
