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Could Red Wine Prolong the Effects of Testosterone?

Could Red Wine Prolong the Effects of Testosterone?

Written by Hershil Parekh, RPh – Women’s International Pharmacy

red wine may help testosterone functionDoes that glass of red wine you enjoy with dinner affect your testosterone levels? A study published in the Nutrition Journal suggests that it may help prolong testosterone’s effects by slowing down how fast the body metabolizes it.

Testosterone is broken down in the liver by a process known as glucuronide conjugation. The enzyme involved in this process is called UGT2B17, and belongs to the UDP-glucuronosyltransferase (UGT) enzyme family. Certain medications—such as non-steroidal anti-inflammatory drugs (NSAIDS) which include ibuprofen and naproxen—and flavonoids (catechins in certain teas) have been shown to inhibit UGT2B17 when used with testosterone, thus increasing the availability of testosterone in the body.

A British study evaluated the inhibitory nature of the common phenolic components found in wine on the activity of the UGT2B17 enzyme. In a laboratory setting, Carl Jenkinson, et al. measured initial testosterone levels and then added evaporated red wine at concentrations varying from 2-8%. The study’s aim was to determine the extent to which wine inhibited the UGT2B17 enzyme in the body.

One and two hours after the addition of the red wine, Jenkinson, et al. analyzed the remaining testosterone to determine if there was any increase in testosterone concentration. The results from this portion of the testing showed glucuronidation through the UGT2B17 enzyme was reduced to 10-70% of normal activity levels. The highest level of reduction was seen after measuring testosterone levels two hours after adding 8% red wine.

The main phenolic components of red wine were found to be gallic acid, chlorogenic acid, caffeic acid, and quercetin. The reduction of glucuronidation of testosterone by the UGT2B17 enzyme was statistically significant for quercetin and caffeic acid, which reduced glucuronidation activity by 28.01% and 78.9%, respectively.

Even though these results were statistically significant, it is difficult to know if they are clinically significant because we do not know to what extent testosterone concentrations were altered. The results are promising, showing that testosterone metabolism was reduced by a wide margin from what is normally seen. Perhaps one day practitioners may recommend a glass of wine with a patient’s testosterone supplement, or (more likely) a quercetin supplement, which could lead to better testosterone availability for patients.

Jenkinson C, Petroczi A, Naughton DP. Red wine and component flavonoids inhibit UGT2B17 in vitro. Nutr J 2012; 11:67. doi: 10.1186/1475-2891-11-67.

Could Red Wine Prolong the Effects of Testosterone?2018-12-21T14:42:07-05:00

Sarcopenia: Age-Related Muscle Loss

Sarcopenia: Age-Related Muscle Loss

Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

woman lifting weightsSarcopenia, the muscle loss related to aging, may start slowly in your thirties and continue progressing with growing rapidity into your seventies. It is not identified with definite biomarkers as medical practitioners prefer to use today. Sarcopenia tends to get an “I know it when I see it” sort of diagnosis.

Although this difficulty in diagnosing sarcopenia is understandable considering the mental picture of the frailty associated with aging, loss of muscle mass is a major health issue.

  • With a loss of muscle comes a loss of strength
  • It is more difficult to get around, climb stairs, or walk long distances
  • It leads to falls and serious injuries including broken bones
  • When injuries occur, it takes longer to heal
  • Surgeries may be less successful and infections take hold more readily

Unless measures are taken to stop it, sarcopenia may lead to prolonged hospitalizations, nursing homes, and possibly even death.

Anabolism and Catabolism

Our bodies are in the constant process of remodeling. We build and rebuild molecules, break down old cells and tissues to make way for the new, and dispose of or reuse the molecules. When we are young the rate at which we rebuild (anabolism) exceeds the rate at which we break down (catabolism). There are multiple factors that trigger more catabolism than anabolism as we age, including:

  • Changes in neurochemistry
  • Hormone imbalances
  • Production of inflammatory cytokine (cells produced by the immune system that act on other cells)
  • Inadequate nutrition
  • Environmental hazards
  • Declining physical activity

Satellite Cells

Muscle is composed of many different cell types. Muscle stem cells are called satellite cells. Satellite cells are located on the outside membrane of the muscle cells and next to the blood vessels. These cells are not active unless there is some stimulus from injury to the muscle or from the environment carried in the blood stream. When activated, these satellite cells become new muscle cells.

Estradiol and Testosterone

Sarcopenia develops with the decline of sex hormones. Research in the last decade reveals that the satellite cells have receptors for–and respond to—estrogens (such as estradiol) and androgens (such as testosterone). Studies support that estradiol has beneficial effects on muscle strength.

Most muscle cell types have receptors for testosterone, but testosterone receptors predominate in satellite cells. Administration of testosterone increases the number of satellite cells, and also directly inhibits inflammatory cytokines. Higher testosterone levels contribute to increased strength and mass; since women generally have less testosterone than men, this might explain why women tend to develop sarcopenia at twice the rate as men. 

DHEA and Human Growth Hormone

Adrenal DHEA, another androgen, also declines with age, and may affect muscle strength via a number of mechanisms.  DHEA is converted to estrogens and testosterone in the body, which may have a direct effect on receptors. Also, DHEA increases sensitivity to insulin, another anabolic hormone, which may also increase levels of IGF-1 (the active metabolite of growth hormone). Increased IGF-1 may indicate increased levels of growth hormone. Growth hormone has been shown to increase muscle mass in many studies.

The Triad of Frailty

In their article Frailty and the Older Man, Drs. Jeremy Walston and Linda Fried proposed looking at the concept of frailty in the elderly as a triad:

  1. With aging the hypothalamic responses to stress change, cortisol levels increase, and the signals to produce sex hormones and growth hormone decline
  2. The immune system is affected, producing fewer antibodies and more inflammatory cytokines
  3. Both of these effects contribute to sarcopenia

All three systems are interdependent: the endocrine system, the immune system, and the muscular system participate together in a spiral of decline.


Maintaining the health of the body requires collaboration between various factors. Our awareness of these factors gives us the tools to optimize our aging with strong bodies. Such factors include:

  • Eating well and ensuring our digestive systems work
  • Bolstering our metabolic processes with vitamins and minerals
  • Avoiding environmental challenges to our biochemistry

In addition to these factors, our health is profoundly affected by hormones. Sarcopenia illustrates how hormone deficiencies hinder us from achieving optimal health. Fortunately, our ability to supplement the hormones that decline as we age may help stave off the effects of sarcopenia and other age-related conditions.

A validated questionnaire called FRAIL can be used as a simple screen for sarcopenia. Three or more “Yes” answers are considered “frail,” signalling the possibility of sarcopenia.

  1. F. Fatigue: Did you feel tired all or most of the time in the last 4 weeks?
  2. R. Resistance: Is it difficult to walk up 10 steps without resting?
  3. A. Ambulation: Is it difficult to walk several hundred yards?
  4. I. Illnesses: Do you have more than four illnesses?
  5. L. Loss of weight: Have you lost 5% of your normal weight in the last year?
  • La Colla A, et al. 17 Beta Estradiol and testosterone in sarcopenia: Role of satellite cells. Aging ResRev. 2015 Nov:24(Pt B): 166-177. doi: 10.1016/j.arr.2015.07.011. Epub 2015 Aug 3.
  • Health Sciences Institute. This hidden disease will land you in a nursing home. February 2016 (20) 6.
  • Walston J, Fried L. Frailty and the Older Man. Med Clin North Am. 1999 Sept;83(5):1173-1193.
  • Balagopal P, Proctor D, Nair KS. Sarcopenia and Hormonal Changes. Endocr. (1997) 7:57-60. https://doi.org/10.1007/BF02778064.
  • Morley JE, Malmstrom TK. Frailty, Sarcopenia, and Hormones. Endocrinol Metabl Clin N Am. (2013)42:391-405. https://doi.org/10.1016/j.ecl.2013.02.006.
  • Morley JE, Malstrom TK, Miller DK. A simple frailty questionnaire (FRAIL) predicts outcomes in middle aged African Americans. J Nutr Health Aging. 2012 Jul;16(7):601-8.

© 2018 Women’s International Pharmacy

Edited by Michelle Violi, PharmD; Women’s International Pharmacy

For any questions about this article, please e-mail

Carol Petersen at carol@womensinternational.com

Sarcopenia: Age-Related Muscle Loss2019-02-13T09:53:55-05:00

DHEA and Healing Skin Wounds

DHEA and Healing Skin Wounds

Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

DHEA may improve skin's ability to healDehydroepiandrosterone (DHEA) is produced primarily by the adrenal glands and is the most abundant of all the steroidal hormones. The quantity of DHEA in the body drops significantly during the aging process. This is so predictable that DHEA levels could be regarded as an aging biomarker.

One of the problems of aging is that it impairs the rate of wound healing in the skin. Many people begin to notice that cuts take longer to heal as they age. Ulcerations may develop which become chronic.

In the UK, Stuart J. Mills and colleagues at Manchester University investigated the role of DHEA in aging skin. This group had already demonstrated that estrogens have a positive effect on skin healing whether used directly on the wound or throughout the body. They wondered if DHEA would have a similar effect, since it is an immediate precursor of both estrogen and testosterone. Understanding that DHEA has many positive effects on the immune system, the researchers also wanted to establish whether DHEA would work directly, or whether it had to be converted into estrogen or testosterone to be effective in healing skin wounds.

First, they compared two groups of human subjects. Those suffering from ulcerations or other signs of slow wound healing were compared with healthy individuals with normal healing. The researchers were able to demonstrate that those with slow skin healing had significantly lower DHEA levels in their blood than the healthy group.

Next, they procured estrogen-deficient mice. Unlike humans, mice do not produce DHEA but they do have the necessary enzymes in their skin to convert DHEA to estrogen or testosterone. After producing superficial wounds, the researchers gave these mice DHEA throughout their bodies. This did not produce any noticeable effect on healing. However, a marked increase in healing did occur when DHEA was applied directly to the damaged skin area.

Finally, in order to determine whether DHEA was working directly or whether the metabolites of estrogen or testosterone were the key to improved healing, the researchers used substances that blocked the conversion enzymes for estrogen and testosterone. Healing and inflammation relief did not occur when estrogen production was blocked. With only testosterone blocked, however, the benefits of the DHEA treatments remained. Mills et al. concluded that DHEA could be effective for targeted treatment of damaged skin, and that the effectiveness depended on the conversion to estrogen and its local action on estrogen receptors.

  • Mills SJ, et al. The Sex Steroid Precursor DHEA Accelerates Cutaneous Wound Healing Via the Estrogen Receptors. J Invest Dermatol. 125: 1053-1062 2005.

© 2018 Women’s International Pharmacy

Edited by Michelle Violi, PharmD; Women’s International Pharmacy

For any questions about this article, please e-mail

Carol Petersen at carol@womensinternational.com

DHEA and Healing Skin Wounds2018-11-05T13:27:54-05:00

Book Review – The End of Alzheimer’s

Book Review – The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline by Dale E. Bredesen, MD

Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

older couple taking a walkAlzheimer’s disease is a grim disease that causes both the mind and body to deteriorate. In 1906, Dr. Aloysius Alzheimer identified plaques in the brain autopsy of a patient who had suffered from dementia, and in doing so he discovered what is generally thought to cause the symptoms of the disease that bears his name. These plaques, made from a protein called amyloid-beta, are thought to interfere with the functioning of our brains.

Since Dr. Alzheimer’s discovery over a century ago, the focus has not been in pinpointing the cause of Alzheimer’s disease, but rather in finding an effective treatment for the related symptoms. Theoretically, if we can find a drug that will stop the formation or contribute to the removal of plaques in the brain, we will be able to prevent or reverse the development of the symptoms associated with Alzheimer’s disease. We have been using this line of thinking to develop drugs since the 1980s, without success.

Dr. Dale Bredesen has turned this thinking upside down. His book, The End of Alzheimer’s, poses the questions: What if the amyloid proteins are there to protect the brain rather than disrupt the brain? Is it only when plaque formation is excessive that it interferes with nervous tissue signaling?

A Leaky Roof

Dr. Bredesen uses the metaphor of a leaky roof for Alzheimer’s disease. The roof has approximately 36 “holes,” though a few more may yet be identified. These holes signify the number of contributors he and his team have identified as playing a role in the development of dementia and Alzheimer’s disease.

The size of the holes—that is, the probability of developing Alzheimer’s disease–depends on the impact of genetics and the environment. Because each hole is a different size (depending on genetics and other factors) for each person, not every single hole needs to be patched; however, if you only patch one hole in the roof, you will still have a leaky roof. Our pharmaceutical model only has touched on one pathway—trying to stop the formation of plaques—and overlooked other possible causes, which is why our attempts at treating Alzheimer’s disease have failed.

What Causes Amyloid Production?

Among the 36 “holes” that contribute to developing Alzheimer’s disease, there are three major categories. These categories contain conditions that can be grouped together. The three major categories are inflammation, deficiencies in hormones or nutrients, and exposure to stress or environmental toxins. All of these conditions force the body to defend the brain by producing amyloid plaques, thus leading to Alzheimer’s disease.

Inflammation is the first category that may increase amyloid production. While inflammation is often related to infection, it may be caused by other things such as food or food sensitivities. Dr. Bredesen uses the example of ingesting trans-fats or sugar, substances that are known to be inflammatory.

The second category includes hormones and nutrient deficiencies and imbalances that interfere with neuronal repair in the brain. For example, vitamin D deficiency may be a critical trigger for amyloid production. See below for a more detailed description of this category.

The third category includes exposure to significant stress, poisoning with heavy metals and mold toxins, or other environmental or chemical exposures. Even the stress of menopause may instigate the disease. Because this category tends to present psychological symptoms (such as depression), which mask the symptoms of Alzheimer’s disease, these contributors can be easily missed.

Alzheimer’s Disease By the Numbers

The Alzheimer’s Association has gathered these statistics about this increasingly-prevalent disease:

  • An estimated one in ten of people over the age of 65 is affected.
  • Two-thirds of those diagnosed are women.
  • It is the sixth leading cause of death in the United States.
  • Life expectancy after diagnosis is 4 to 8 years.
  • The cost of care for Alzheimer’s disease and other dementias in the United States is estimated at $277 billion for 2018 alone.
  • One-third of seniors die with Alzheimer’s disease or another form of dementia.
  • 7 million Americans are living with dementia as of 2018.
  • In the United States, every 65 seconds a patient is diagnosed with Alzheimer’s disease.

Hormones Are a Key

As mentioned above, some of Dr. Bredesen’s findings show that the key to preventing or recovering from Alzheimer’s disease may be restoring depleted hormone levels. Of the 36 and more contributors identified, several involve hormonal imbalance. Dr. Bredesen states, “Reaching optimal hormone levels is one of the most effective and most critical parts of ReCODE (reversing cognitive decline protocol).” Based on his observations, Dr. Bredesen recommends optimizing:

  • Insulin secretion and signaling
  • Estradiol
  • Progesterone
  • The ratio of progesterone to estradiol
  • Free T3 (the active thyroid hormone liothyronine)
  • Free T4 (the thyroid hormone thyroxine which is the precursor to T3)
  • Thyroid stimulating hormone (TSH), made by the pituitary gland to stimulate the thyroid gland to produce T3 and T4
  • Pregnenolone
  • Testosterone
  • Cortisol
  • Dehydroepiandrosterone (DHEA)

Dr. Bredesen takes great care to explain the development of his ideas and the work in his laboratory. With decades of research behind him, he presents a theory addressing everything we do know about Alzheimer’s disease, and as a researcher and physician, he has been able to practically apply this theory to successfully treat patients.

Connection with Insulin

Another contributor to inflammation—and by extension, developing Alzheimer’s disease—is insulin resistance. Insulin resistance, metabolic syndrome, and diabetes all involve abnormally high levels of insulin. Some even call Alzheimer’s disease “Type 3 diabetes” because of the problems high insulin levels cause the brain. Dr. Bredesen explains that the enzyme, insulin degrading enzyme (IDE), helps us break down excessive insulin. This same enzyme can break down amyloid. If we follow a lifestyle and eating program that constantly elevates insulin, IDE may not be available in amounts needed to break down and help stop amyloid overproduction.

Sex, Adrenal, and Thyroid Hormones

A common factor of aging is the depletion of adrenal hormones (although cortisol is sometimes high), sex hormones, and thyroid hormones. The loss of hormones parallels an increased risk of Alzheimer’s disease as we age.

For each of the markers that Dr. Bredesen has identified, he also describes how to test or evaluate hormone levels, and presents what he believes are the optimal parameters. Replenishing these depleted hormones may help patients prevent or recover from Alzheimer’s disease. To restore proper hormone function, bioidentical rather than synthetic hormone replacement must be used, as bioidentical hormones are equivalent in structure to the hormones our own bodies make.

Diagnosing Alzheimer's Disease

Alzheimer’s disease used to be diagnosed only after the patient had died. An autopsy would reveal the presence of amyloid plaques, explaining the decline in the patient’s health and eventual death. Now we have testing that can identify the presence of plaques during the patient’s own lifetime. These include scans of the retina, brain scans, and checking the cerebral spinal fluid. A genetic test for Apolipoprotein (APO)E also shows potential to predict susceptibility to this disease.

Mending the Holes in the Roof

Alzheimer’s disease does not follow the “one disease, one treatment” model our current medical system relies upon. Each patient should be evaluated for their individual needs. Successfully treating Alzheimer’s must involve a personalized, complex therapy program, but the reward—giving patients the ability to reclaim their brains and their lives—makes the effort more than worthwhile. The End of Alzheimer’s presents an opportunity to forestall and correct the onslaught of this devastating disease. Thanks to his groundbreaking work, dedication to making this information available, and training practitioners to use his guidelines, Dr. Bredesen demonstrates that patients with Alzheimer’s disease do have treatment options.

© 2018 Women’s International Pharmacy

Edited by Michelle Violi, PharmD; Women’s International Pharmacy

For any questions about this article, please e-mail

Carol Petersen at carol@womensinternational.com

Book Review – The End of Alzheimer’s2019-08-09T11:06:49-05:00

Virility Drugs for Erectile Dysfunction…What about Sex Hormones?

Virility Drugs for Erectile Dysfunction…What about Sex Hormones?

Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

Virility drugs such as Viagra, Cialis and Levitra work by inhibiting the breakdown of cyclic guanosine monophosphate (cGMP), a molecule which enables the penis to fill with blood and become erect for intercourse. However, these treatments are not always a “magic bullet.” They may not work for many men who try them and they may not enable the same quality of erections men experience in their teenage years.  Also, they do not increase sexual desire and using these drugs does not address any of the underlying medical conditions that may be the cause of erectile dysfunction (ED).

The linchpin in the series of reactions needed for healthy erections is cGMP. The enzyme PDE5 acts to break down cGMP. Virility drugs block the PDE5 enzyme which prolongs cGMP activity in the penis allowing it to fill with blood and become erect. Although these drugs can restore erectile function by slowing the enzymatic breakdown of cGMP, hormones, such as estrogens, progesterone, androgens (e.g., DHEA, testosterone and dihydrotestosterone (DHT)), insulin, and growth hormone can actually increase cGMP production by modulating nitric oxide (NO) production.

NO is an extremely important signaling molecule generated in the body and lasting just a few seconds before it is broken down. It is a potent smooth muscle relaxant and mediates the transformation of guanosine triphosphate (GTP) into cGMP. Hormones are important modulators of NO production and stimulate the production of NO and cGMP. By contrast, glucocorticoids (for instance, cortisol) and prolactin can reduce the bioavailability of NO, possibly reducing the amount of available cGMP as well.

Documentation submitted for a US Patent by Steven Ferguson reveals interesting observations and data about ED. The patent application centers on a clinical trial of 20 men with ED, ranging in age from 21 to 88 years old.

When measuring their hormone status, Ferguson found that these men were low in testosterone, low in progesterone, and normal to high in estradiol. All had some health issue(s) such as hypertension, diabetes, heart disorders, prostatic hyperplasia, renal insufficiency, depression, high cholesterol, chronic obstructive pulmonary disease (COPD), or cerebral palsy. Many of these health issues or the drug treatments for them are known as risk factors for the development of ED. Ferguson’s treatment was to supply progesterone and testosterone together in topical creams which were applied to non-hairy skin areas daily.

Ferguson’s group was reflective of the general health status of men who experience erectile dysfunction. In one to three months, the majority of men treated with his progesterone with testosterone cream were able to achieve full erections. These results were stunning in that no attempt was made to address any underlying disease states.

Although virility drugs are widely used, they do not address the underlying cause of ED. Diminished hormone production with aging or from other causes may be the root of the problem. Ferguson’s successes illustrate just how important hormone balance can be in reversing ED.

  • Duckles S, Miller V. Hormonal Modulation of endothelial NO production. Pflugers Arch. 2010 May; 459(6): 841–851
  • Ferguson SW. Progesterone/testosterone cream for erectile dysfunction. Google Patents. https://www.google.com/patents/US20070167418. September 7, 2004. Accessed July 2018.
  • Huang SA, Lie J. Phosphodiesterase-5 (PDE5) Inhibitors In the Management of Erectile Dysfunction. P T. 2013 Jul; 38(7): 407, 414-419. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3776492/. Accessed July 2018.

© 2018 Women’s International Pharmacy

Edited by Michelle Violi, PharmD; Women’s International Pharmacy

For any questions about this article, please e-mail

Carol Petersen at carol@womensinternational.com

Virility Drugs for Erectile Dysfunction…What about Sex Hormones?2018-09-11T14:42:30-05:00



Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

gears with rustThe world abounds with substances that affect hormone balance. It is widely accepted that that there are many organic substances that affect hormone activity in the body. For example, soy has estrogen-like qualities and ginseng acts as an adrenal adaptogen. We can use these organic substances in ways that are beneficial to the body. On the other hand, organic substances like phthalates, PCBs and BPA mimic estrogens in a negative way. They create a burden of too much estrogen activity in the body.

Researchers are now turning to inorganic sources of hormone disruption. In 2006, Dr. Philippa Darbre published a paper that identified many metals that have an effect on estrogen receptors. These effects include: altering gene expression, estrogenic activity, and displacing estrogens from estrogen receptors. Metals that have been identified to exert an influence on estrogen receptors include aluminum, antimony, arsenite, barium, cadmium, chromium, cobalt, copper, lead, mercury, nickel, selenite, tin, and vanadate. These metals are referred to as metalloestrogens. The paper also identified metalloestrogen activity at progesterone, testosterone and glucocorticoid (hydrocortisone-like) receptors. For example, cadmium has been shown to produce testosterone activity, displace testosterone from testosterone receptors and affect gene changes. Dr. Darbre concludes that all steroid hormone receptors may be affected.

Some metalloestrogens are essential minerals. Cobalt, chromium, copper, and nickel are all needed in trace amounts for normal human body function. When the amounts of these minerals exceed the amount needed by the body, they begin to interfere with the hormone receptors.

Other metalloestrogens, such as cadmium, aluminum, and lead, are not needed by the body in any amount. Cadmium is problematic because the human body doesn’t have an enzyme system to eliminate it once we are exposed. Making matters worse, the kidneys reabsorb cadmium rather than eliminate it. The amount of cadmium in our bodies continues to increase as we age. Common sources of cadmium, outside of industrial uses, include cigarette smoke and certain foods due to cadmium pollution in our environment. Cadmium may be a trigger for endometriosis. Several studies point to an association between the presence of cadmium in the body and endometrial tissue proliferation. One especially interesting study found melatonin was able to block the estrogenic effect of cadmium in endometrial tissue.

Lead acts as a metalloestrogen by occupying hormone receptors. Unsurprisingly, lead contributes to a number of health conditions. The Environmental Protection Agency (EPA) recognizes lead can cause a number of problems for women. After menopause, increased levels of lead in the body increase one’s risk for hypertension, atherosclerosis, reduced kidney function, and decreased cognitive functioning with symptoms similar to dementia. Osteoporosis, another condition common in menopause, can cause lead to be released into the body as bone breaks down. Those of us who have been exposed to lead paints and leaded gasoline have higher levels of lead in our bones, causing higher levels of lead in our bodies as lead is released from our bones. (For more information, read our article Lead Toxicity and Disease.)

As research expands and we dig deeper into hormone balance issues, more information emerges to help us solve the riddle of hormone imbalance. The effects of metalloestrogens are not always considered by busy practitioners. Furthermore, many are not trained to help reduce the body’s load of metalloestrogens. Three medical groups that focus on reducing metalloestrogens in the body are the International College of Integrated Medicine (www.icimed.com), the American College for Advancement in Medicine (www.acam.org), and the American Association of Naturopathic Physicians (www.naturopathic.org).

  • Darbre PD. Metalloestrogens: An Emerging Class of Inorganic Xenoestrogens With Potential to Add to the Oestrogenic Burden of the Human Breast. J Appl Toxicol. 2006 May-Jun;26(3):191-7. DOI:10.1002/jat.1135.
  • U.S. Environmental Protection Agency Aging and Sustainability List Serve
  • Silva N, et al.  Metalloestrogen cadmium stimulates proliferation of stromal cells derived from the eutopic endometrium of women with endometriosis.Taiwan J Obstet Gynecol. 2013 Dec;52(4):540-5.
  • Jackson LW, Zullo MD, Goldberg JM. The association between heavy metals, endometriosis and uterine myomas among premenopausal women: National Health and Nutrition Examination Survey 1999 – 2002. Hum Reprod. 2008 Mar;23(3):679-87. DOI: 10.1093/humrep/dem394. Epub 2008 Jan 12.
  • Chemical of the Day. Metalloestrogens. https://chemicaloftheday.squarespace.com/most-controversial/2014/9/4/metalloestrogens.html. September 2014. Accessed August 2018.
  • Martínez-Campa C, et al. Melatonin inhibits both ER alpha activation and breast cancer cell proliferation induced by a metalloestrogen, cadmium. J Pineal Res. 2006 May;40(4):291-6.

Premature Balding in Men

Premature Balding in Men

A Symptom of Metabolic Syndrome and Benign Prostatic Hyperplasia

Written by Women’s International Pharmacy Staff

premature balding in menAccording to Statistic Brain, 35 million men in the US experience hair loss, 40% of which have hair loss by the age of 35.(i) The same hormonal imbalances that contribute to early onset balding may also cause more serious conditions. Because of its strong association with hormone imbalances, prostate enlargement, and metabolic syndrome, premature hair loss could be indicator for men of deeper health concerns.

A Male Version of PCOS?

Polycystic Ovary Syndrome (PCOS) is a hormonal disorder common among women of reproductive age. At the Progressive Medical Education meeting in Irvine, CA in August 2017,(ii) Dr. Matthew Cavaiola presented a hypothesis published by Kurzrock et al.(iii) He stated because the primary defect underlying PCOS may not be a defect in the ovaries themselves, it is possible that this condition can also occur in men.

Symptoms of PCOS in women include:

  • High androgen hormones (like DHEA and testosterone) in the blood
  • Obesity focused on the waistline
  • High insulin levels
  • Development of diabetes
  • Infertility

Dr. Cavaiola stated that young men can suffer from similar symptoms:

  • Insulin resistance
  • Obesity
  • Increased risk for diabetes and cardiovascular disease
  • Early onset of male pattern baldness
  • Excessive body hair
  • High levels of testosterone and dihydrotestosterone (DHT, the active form of testosterone)

In addition to the symptoms listed above, sex hormone binding globulin (SHBG) levels may be low which further increases the amount of available testosterone and DHT in the body. Dr. Cavaiola also pointed out that when SHBG levels are low, insulin levels are abnormally high. Persistently high levels of insulin may lead to metabolic syndrome, prediabetes, and diabetes.

Prostate Enlargement and Insulin Resistance

Benign Prostatic Hyperplasia

Benign prostatic hyperplasia (BPH) is the enlargement of the prostate gland and is a common condition as men age. Common signs and symptoms of BPH include a frequent or urgent need to urinate, increased frequency of urination at night (nocturia), difficulty starting urination, a weak urine stream or a stream that stops and starts, dribbling at the end of urination and an inability to completely empty the bladder. There appears to be a strong correlation with early onset balding and BPH, as men with BPH tend to have more inherited baldness and an increased severity of baldness. Some studies also point to an increased risk of prostate cancer.(iv, v)

Insulin Resistance

Insulin is a hormone made by the pancreas. It allows cells in the body to use glucose (sugar) for energy. Insulin resistance (also called metabolic syndrome or prediabetes) is a condition where cells throughout the body don’t recognize insulin as they should. This causes the cells to have trouble absorbing glucose, which causes a buildup of sugar in the blood. It also causes the body to produce more insulin leading to high insulin levels in the body. These high levels of insulin may be a major contributor to BPH and early onset balding as postulated by Ajit Vikram et al.(vi)

Insulin resistance may also be associated with, high blood pressure, high triglycerides and acanthosis nigricans (dark patches of skin usually on the back of the neck, groin, and armpits).

Treatment Options

Addressing Baldness and Prostate Enlargement with Finasteride

Drug companies have come up with a possible solution for hair loss and prostate hyperplasia with a synthetic molecule, finasteride. Finasteride is the generic name for two prescription drugs: Propecia and Proscar. Propecia has been approved by the FDA to treat male pattern baldness at a dose of 1 mg per day. Proscar is the same drug in a 5 mg dose, and has been approved to treat BPH. Finasteride inhibits the 5 alpha reductase enzyme, which is the enzyme responsible for converting testosterone into its more active form, (DHT). Studies suggest high levels of DHT may be responsible both for male pattern baldness and BPH.

Negative Side Effects of Finasteride

There are a number of negative side effects that have been associated with finasteride. The Post Finasteride Syndrome Foundation studies these persistent adverse effects,(vii) which include:

  • Loss of penis sensitivity
  • Decreased ejaculatory force and volume
  • Loss of libido and low penile temperature
  • Reduced feeling of pleasure or emotions
  • Lack of mental concentration
  • Loss of muscle tone/mass
  • Severe depression, suicidal ideation, and suicide
Why Not Progesterone?

Progesterone, a hormone that naturally occurs in the human body, also acts as a 5 alpha reductase inhibitor,(viii) as well as having a great number of other important functions in the body. The drug, finasteride, structurally resembles progesterone. The prostate has receptors for progesterone in addition to receptors for androgens (testosterone and derivatives) and estrogens. While many studies have explored the relationship of prostate enlargement and prostate cancer to androgen and estrogen receptors, little research exists for the relationship to progesterone.

Progesterone is produced in men by the testes and the adrenal glands. Men have progesterone levels similar to a woman’s progesterone levels during the follicular phase of the menstrual cycle. RuiQi Chen et al. present a case for inhibition of prostate enlargement—and possibly prostate cancer—using progesterone.(ix)


Some men may consult a practitioner when confronting hair loss and may be prescribed Propecia in an attempt to grow hair back, but why use a synthetic drug when rebalancing hormone levels with progesterone, a hormone natural to the body, may help? Hair loss may be the first sign of hormone imbalances that could lead to metabolic syndrome and prostate hyperplasia. Other potential risks may include high blood pressure, high cholesterol, obesity, diabetes, and heart disease. By proactively considering hormone balancing solutions, men may forestall the loss of their hair and prevent more drastic declines in their health.

  • (i) Statistic Brain. Hair Loss Statistics. https://www.statisticbrain.com/hair-loss-statistics/. August 2016.
  • (ii) Cavaiola M. Environmental Medicine: Focus on Men’s Health & Longevity. A presentation at the Progressive Medical Education Meeting. August 2017.
  • (iii) Kurzrock R, Cohen PR. Polycystic ovary syndrome in men: Stein-Leventhal syndrome revisited. Med Hypotheses. 2007;68(3):480-3. Epub 2006 Nov 28. (3)
  • (iv) Oh BR, et al. Association of benign prostatic hyperplasia with male pattern baldness. Urology. 1998 May;51(5):744-8.
  • (v) Papa NP, et al. Early onset baldness and the risk of aggressive prostate cancer: findings from a case-control study. Cancer Causes Control. 2018 Jan;29(1):93-102. doi: 10.1007/s10552-017-0981-0. Epub 2017 Nov 14.
  • (vi) Vikram A, et al. “Insulin-resistance and benign prostatic hyperplasia: The Connection” Eur J Pharmacol. 2010 Sep 1;641(2-3):75-81. doi: 10.1016/j.ejphar.2010.05.042. Epub 2010 Jun 9.
  • (vii) Post-Finasteride Syndrome Foundation. https://www.pfsfoundation.org. Last accessed: April 2018.
  • (viii) Ling YZ, et al. Synthesis and in vitro activity of some epimeric 20 alpha-hydroxy, 20-oxime and aziridine, pregnene derivatives as inhibitors of human 17 alpha-hydroxylase/C17,20-lyase and 5 alpha-reductase. Bioorg Med Chem 1998;6:1683-1693. https://www.ncbi.nlm.nih.gov/pubmed/9839000
  • (ix) Chen R, et al. Progesterone receptor in the prostate: A potential suppressor for benign prostatic hyperplasia and prostate cancer. J Steroid Biochem Mol Biol. 2017 Feb;166:91-96. doi: 10.1016/j.jsbmb.2016.04.008. Epub 2016 Apr 25.
  • Fung J. The Obesity Code: Unlocking the Secrets of Weight Loss. Greystone Books; Vancouver, BC, Canada: 2016.
Premature Balding in Men2018-07-17T16:31:21-05:00

Book Review – Estrogen’s Storm Season

Book Review – Estrogen’s Storm Season: Stories of Perimenopause by Dr. Jerilynn Prior

Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

stormDr. Jerilynn Prior is a Professor of Endocrinology and Metabolism at the University of British Columbia in Vancouver. She is also the Scientific Director of the Centre for Menstrual Cycle and Ovulation Research (CeMCOR).  Not only is Dr. Prior a dedicated scientist and medical writer, she has now turned to fiction to share her knowledge about women’s health. She knows from experience that it can take decades to disseminate information to those who would benefit the most. In Estrogen’s Storm Season she uses storytelling to carry her message by personifying the main challenges of perimenopause.

Perimenopause begins when the first symptoms appear and lasts until one year after the last menstrual cycle. In her book, Dr. Prior carefully documents the stages of perimenopause. Through fictional encounters with women going through perimenopause, she weaves useful information and helpful hints and concepts into her writing so that readers may be able to identify what is happening in their own lives. Here are the main symptoms she brings into focus:

  • Night sweats and hot flashes
  • Menorrhagia or heavy bleeding
  • Nausea
  • Infertility
  • Migraine headaches
  • Moodiness
  • Weight gain
  • Breast tenderness, pain, and swelling

While touching on these issues with broad strokes, she illustrates that life can be messy, as many other issues are entwined in her characters’ lives. Their concerns include high blood pressure, diabetes, heart disease, osteoporosis, and cancer. She also addresses the stress of work situations, relationships, financial concerns, and diet. Like real women, her characters discover that their discomforts and health concerns may be part of a bigger picture, and that solutions should be comprehensive, addressing health concerns and lifestyle modifications in addition to perimenopausal symptoms.

Many individuals may be unaware of an underlying theme of perimenopause, which Dr. Prior reveals in this book. Perimenopause has long been characterized as the time of life when women experience a decline in estrogen production. Dr. Prior claims this is not so; in fact, she has found in her studies that women experience the highest estrogen levels in their entire lifetime during perimenopause. In her opinion, too many women are prescribed estrogens (or birth control pills containing estrogens) when they are already suffering from too much estrogen. According to Dr. Prior, the hormone that is in decline is actually progesterone, which is needed to offset the effects of high estrogen levels. Dr. Prior has found success in progesterone treatments in tandem with employing a whole spectrum of life enhancements.

As her fictional characters come alive, Dr. Prior teaches women how to document their initial symptoms and their interventions with any subsequent symptom changes so that they can see for themselves what works and what doesn’t. These tools are available on the CeMCOR website, which overflows with practical information about the menstrual cycle as well as addressing questions and concerns a woman may have throughout her lifetime. Through Estrogen’s Storm Season, Dr. Prior’s guidance and understanding empowers women to take charge of their health.

Updates as of August 8, 2018:

The electronic version of the second edition of Estrogen’s Storm Season is available to download at the following additional sites:

Recent revisions to the print version of Estrogen Storm Season are posted to the Cemcor.ca site:

Additional Resources:

Book Review – Estrogen’s Storm Season2018-08-08T15:09:01-05:00

Vaginal Use of Estriol

Vaginal Use of Estriol

Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

Estriol is one of the three main estrogens made in a woman’s body. The other estrogens are estrone and estradiol. Estriol levels are highest in a woman’s body during pregnancy. Normal ranges for non-pregnant, non-menopausal and menopausal women are not usually noted, making it difficult to determine what would be considered “normal levels” in the body. Estriol may be used alone or in combination with the other estrogens in a number of different dosage forms, and has been shown in studies to have good activity in the vaginal area. In 1993, a landmark study published by Raul Raz et al. in the New England Journal of Medicine sparked great interest in using estriol vaginally, not only for improving the condition of the urinary tract, but vaginal tissue as well.[i]

In 2016, Salvatore Caruso et al. published a study in Menopause reaffirming the effectiveness of vaginally-used estriol.[ii] This study included monitoring the acidity of the vaginal tissue. Healthy vaginal tissue is in the slightly acidic range and favors the growth of friendly lactobacillus acidophilus bacteria. When this tissue becomes thinner and more alkaline as estrogen declines in menopause, the protection of the friendly bacteria declines, which may lead to infections by other less desirable organisms. Even the small amount of estriol used in this study, 50 microgram doses, caused an improvement in cell structure, acidity of the vaginal tissue, better urine control, and increases in sexual function and in quality of life. The study concluded that estriol should be a first choice in managing menopausal symptoms in the genital and urinary tracts in menopausal women.

Also in 2016, Filippo Murina et al. studied the application of a 25 microgram dose of estriol (applied daily with a finger or cotton swab) to the vulvar vestibule. After the study period of 12 weeks over 80% of the participants experienced relief from pain on intercourse. The authors maintain that direct application of estriol to the vestibule, rather than applying it vaginally, is necessary for pain relief.[iii]

Estrogen Receptors

Although in reality, the process is much more complex, a simplified description of estrogen’s interaction with its receptors begins with an estrogen hormone binding to an estrogen receptor protein. When bound, the estrogen hormone-estrogen receptor complex is shuttled to the cell nucleus, where it gives specific DNA instructions and produces proteins to create an estrogen effect. This description is complicated by discoveries that there is more than one type of estrogen receptor (alpha and beta). The beta type tends to predominate in the mucosal areas, such as the vagina. The higher affinity of estriol to beta receptors over other estrogens such as estradiol predicts that estriol might be more effective in those tissues. (For more on this topic, see our article, How Hormones Interact With Receptor Sites.)

Labial Adhesions

Estrogens are sometimes used to treat labial adhesions in babies and young girls. Estriol may be the preferred choice because of its strong affinity to mucosal estrogen receptors. A study published in 2016 by Stefanie Bussen et al. demonstrated a favorable outcome in comparison to manual or surgical separation. A 1 milligram estriol dose was applied in this study nightly for four weeks at the fusion site. In most of the cases, further treatment was not needed.[iv]

Commercially Available Abroad

Estriol has been in use both as an oral and a topical estrogen supplement for many years in other countries. A product named Ovestrin, which contains a half milligram of estriol per dose, is government-approved for use in many countries.[v] The recommended dosing of estriol for the genital tract and urinary tract atrophy is one dose nightly for some weeks, then decreasing to a maintenance dose of twice weekly applications as symptoms improve. As the cells normalize and normal bacteria and acidity is re-established, issues such as infection, inflammation, pain on intercourse, dryness, itching, urinary complaints, and mild incontinence may resolve.

Estriol in the United States

Estriol has had a tumultuous time in the United States. Since there was no commercial product available, compounding pharmacists came to the rescue by preparing estriol containing creams or other dosage forms in varying strengths for individual use. The drug company Wyeth (the makers of Premarin and Prempro until purchased by Pfizer in 2009) sought to have the FDA ban its use in the United States, even while selling a commercial product containing estriol in Europe.[vi] To this date, there is no human drug product containing estriol in the United States which has been approved by the FDA. At this time, it is solely available through compounding pharmacies.

Ironically, there is an estriol product for animals approved by the FDA for use in spayed (the surgical removal of the ovaries and uterus) female dogs with estrogen-responsive urinary incontinence. Urinary incontinence is a common problem in spayed female dogs because the removal of the ovaries depletes hormones, including estrogens. This drug, Incurin, contains 1 mg of estriol in tablets.[vii]


The use of estriol vaginally is a clear illustration that our current medical system, based on government approvals and a one-size-fits-all model, leaves large therapy gaps. As of the time of this writing, no drug company in the United States has succeeded in bringing an estriol-containing product to market for human use. In the meantime, compounding pharmacists have made estriol available in a wide array of dosage forms and doses to address each woman’s individual needs.

  • [i] Raz R, et al. A controlled trial of intravaginal estriol in postmenopausal women with recurrent urinary tract infections. N Engl J Med. 1993 Sep 9;329(11):753-6.
  • [ii] Caruso S, et al. Quality of life and sexual function of naturally postmenopausal women on an ultralow-concentration estriol vaginal gel. 2016 Jan;23(1):47-54. doi: 10.1097/GME.0000000000000485.
  • [iii] Murina F, et al. Coital Pain in the elderly: could a low dose estriol gel thrill the vulva vestibule? Eur J Obstet Gynecol Reprod Bio 2016 Dec;207:121-124. doi: 10.1016/j.ejogrb.2016.10.016. Epub 2016 Nov 2.
  • [iv] Bussen, S et al, Comparison of Conservation and Surgical Therapy Concepts for Synechia of the Labia in Pre-Pubertal Girls. Geburtshilfe Frauenheilkd. 2016 Apr; 76(4): 390–395. doi:1055/s-0035-1558101.
  • [v] Ovestin cream (estriol). https://www.netdoctor.co.uk/medicines/a7950/ovestin-cream-estriol/. Accessed February 9, 2018.
  • [vi] Alliance for Natural Health USA. Access to Estriol. https://www.anh-usa.org/access-to-estriol-2/. Accessed February 9, 2018.
  • [vii] MSD Animal Health. Incurin product details. https://www.msd-animal-health.co.nz/Products/Incurin_/020_Product_Details.aspx. Last accessed: April 2018.

© 2018 Women’s International Pharmacy

Reviewed by Michelle Violi, PharmD; Women’s International Pharmacy

For any questions about this article, please e-mail

Carol Petersen at cpetersen@womensinternational.com

Vaginal Use of Estriol2018-12-14T12:08:39-05:00

Book Review – The LDN Book edited by Linda Elsegood

Book Review – The LDN Book, edited by Linda Elsegood

Written by Carol Petersen, RPh, CNP – Women’s International Pharmacy

Linda Elsegood’s personal success story tells how using low-dose naltrexone (LDN) to treat her multiple sclerosis restored her quality of life and gave her hope for the future. Now she is a woman on a mission to help others learn about LDN and to promote further research into how it may be used to treat a variety of diseases. In The LDN Book: How a Little-Known Generic Drug—Low Dose Naltrexone—Could Revolutionize Treatment for Autoimmune Diseases, Cancer, Autism, Depression, and More, Elsegood has compiled chapters written by practitioners who have become experts in the use of LDN.


Pharmacist Stephen Dickson provides a comprehensive history of the opium poppy and the subsequent creation of synthetic drug compounds called opiates, which are all active at the opioid receptor sites. Opioid receptors are meant to be activated by hormones produced in the body called endorphins and enkephalins, which can relieve pain and contribute to wellbeing. However, these receptors can also be stimulated by opiates. Naltrexone was originally developed to block these receptor sites in order to assist people addicted to opiates. The developers of naltrexone reasoned that when opioid receptors were blocked, there would be no need to use or abuse opiate drugs. While a logical theory, in actual practice they had little success.

However, in low doses, naltrexone acts to temporarily block opioid receptors. The body responds by producing increased amounts of endorphins and enkephalins. The opioid receptors also increase in sensitivity and number.

Multiple Sclerosis and Lupus

Dr. Deanna Windham begins with a thorough explanation of multiple sclerosis and lupus. While she recognizes that we do not currently have drugs that treat the complexity of these diseases, LDN has been shown in a number of studies to stabilize and stop their progression. The use of LDN is a pillar in Dr. Windham’s treatment plans, though she maintains that each patient must be treated individually for their toxic load, hormone imbalances, nutrient deficiencies, and sleep issues.

Inflammatory Bowel Diseases

Dr. Jill Smith was the first to publish a study on LDN and inflammatory bowel diseases. There are opioid receptors in the gut and on immune system cells. There are a number of different types of opioid receptors and naltrexone may target different opioid receptors depending on the dose.

Dr. Smith provides case studies of remissions of inflammatory bowel diseases, Crohn’s disease and ulcerative colitis with the use of LDN, both alone and with other commonly-used drugs. LDN blocks opioid receptors for about six hours, during which the body increases its endorphin and encephalin production. After about six hours, the LDN is removed from the opioid receptors by the body and the elevated endorphins and enkephalins can act at the receptor to block cell proliferation or reverse inflammation. LDN also sensitizes and increases the number of receptors. Remission may be confirmed with radiology showing healing of the intestinal tract.

Few of Dr. Smith’s patients have experienced side effects, however, one possible side effect is sleep disturbances, which can be alleviated by changing to a morning dose or using a lower strength.


Dr. Kent Holtorf, president of the National Academy of Hypothyroidism, explores LDN treatment with thyroid disorders. He explains how LDN can be used effectively in both Grave’s Disease (hyperthyroidism) and Hashimoto’s Disease (hypothyroidism). He believes LDN can potentially improve abnormal inflammation and immune dysfunction seen with thyroid disorders, and thus, improve the reduced tissue T3 (active thyroid hormone) levels inside the cells that these conditions can cause. Normal thyroid tests cannot predict the activity of thyroid inside the cell, and so this can go unidentified and untreated.

Chronic Fatigue and Fibromyalgia

Dr. Holtorf also addresses chronic fatigue and fibromyalgia.  He writes about phases of treatment with LDN:

  1. Stabilize the patient. This stage is where pain and sleep disturbances are addressed.
  2. Enhance mitochondrial energy production with nutrients.
  3. Balance hormones as these patients typically have deficiencies.
  4. Enhance the immune system function and treat the infectious components. LDN is often part of this stage of treatment.
  5. Address issues like heavy metals, leaky gut, mold toxicity, and coagulation problems.
  6. Maintain health and balance.

An integrative approach has shown success, with treatment plans adjusted to the individual needs of each patient.

Restless Leg Syndrome

Dr. Leonard Weinstock is a gastroenterologist and internist, with a special interest in restless legs syndrome (RLS) and has identified an association between RLS and small intestine bacterial overgrowth (SIBO) and other inflammatory conditions in the gut. He used LDN to treat patients with and without antibiotics for infection. In each case he found some positive results, and has used LDN for long-term remission.


Endorphins are very psychoactive, and account for the warm feelings of falling in love, coping with stress, and bringing joy and contentment. Dr. Mark Shukhman describes the symptoms of endorphin deficiency as including:

  • Discomfort with disturbances such as changes in sound, light, temperature, or touch
  • Immune system problems such as frequent infections, allergies, and autoimmune disease
  • Crying easily, and have difficulty with painful situations
  • Craving chocolate, wine, marijuana, and alcohol

LDN helps in these conditions by increasing the levels of endorphins. Many people who have turned to opiates describe that it is the first time that they have felt normal. Although his chapter focuses on depression, psychiatrist Dr. Shukhman has also used LDN in his practice for treatment of autism, post-traumatic stress disorder, multiple personality disorder, anxiety, obsessive compulsive disorder, psychosis, and even sexual dysfunctions.


Dr. Brian Udell has a special needs pediatric practice and has found a common theme with autism to be inflammation and gut disturbances. He cites Dr. Jacquelyn McCandless’ work with children using LDN as a cream, rather than tablets, because of its bitter taste. He has seen LDN increase speech and communication, decrease aggression, and improve social development. Beta endorphin levels can be measured to confirm LDN activity.


Dr. Angus Dalgleish, an oncology practitioner in the UK, writes that, while there is very little in the published literature, LDN seems to be universally useful across all tumor types. He writes of his personal experience treating patients with metastases, achieving stability and long–term, disease-free status. He finds that LDN affects more receptor sites than just the opioid receptors. Naltrexone in large doses actually promotes tumor growth in the laboratory, so the best effects occur when it is used in low doses and used intermittently rather than continuously. Its anti-inflammatory action can be helpful in cancer. Dr. Dalgleish reports that the use of LDN also increases the production of natural killer cells. Finally, LDN can produce positive effects on mood that help in combatting the disease. He writes that failure with LDN may be linked to low vitamin D levels.


The LDN Book is just a part of Linda Elsegood’s work. Under her direction, the LDN Research Trust has an incredible number of accomplishments, including organized conferences, LDN radio, and crowdfunded documentaries. This outreach has stimulated investigation into endocrine and immune system activity that was hardly known before. This book is a window into the large body of knowledge we have gained in the last ten years.

Book Review – The LDN Book edited by Linda Elsegood2018-02-26T12:09:00-05:00