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Hormones, Hysterectomy and the Hippocampus

Published on April 5, 2013

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hormones, hysterectomy and the hippocampus

New research, conducted on rodents, suggests that pre-menopausal hysterectomy with ovariectomy induces changes in the hippocampus (memory center of brain) making it hypersensitive to ischemic stressors (reduced blood flow). In contrast, ischemic stressors did not cause hippocampal damage in non-ovariectomized female rats or even gonadectomized male rats

The hippocampus, located in the temporal lobe of the brain, is responsible for working memory formation, storage and retrieval. Researchers have long known that damage to cells in the hippocampus cause significant problems in short-term, long-term and working memory, ranging from mild cognitive decline to complete impairment. Certain cells in the hippocampus are particularly sensitive to the amyloid protein buildup associated with Alzheimer’s disease.

In the current study, removal of the ovaries and the associated long-term estradiol deprivation made the hippocampus hypersensitive to ischemic stressors and induced a myriad of events leading to significant hippocampal CA3 cell damage and cell death. The long term estradiol deprivation also led to increased amyloid production and associated neurodegeneration. As one might expect, damage and disruption to the hippocampus, the brain’s memory center, was associated with the animal’s ability to learn, remember and function.

What was particularly interesting, female animals who retained their ovaries and were exposed to the same ischemic stressor demonstrated neither the brain damage nor the decline in cognitive function. Similarly, male animals whose gonads were removed, suffered no notable brain damage or cognitive decline either. It was only the female animals whose ovaries were removed and whose systems were deprived of estradiol for a long period of time.

When estradiol was added back to the ovariectomized female animals shortly after the surgery, the female animals were able to weather the ischemic stressor and hippocampal damage was reduced significantly. However, when the estradiol was added back after an extended period of deprivation, it had no effect on the hippocampal damage or subsequent decline in memory.

Estradiol is important for cognitive function.

It is important to note, that animal researchers use 17B-estradiol, the same form of estradiol produced in the ovaries. In contrast, researchers who study human memory, often supplement with synthetic estrogens (Premarin, Prempro etc.), which is molecularly different than what is produced in our bodies. Indeed, the synthetic estrogen is actually about 20 different estrogenic compounds synthesized from pregnant horse urine. With synthetic hormone replacement therapy (HRT), recently renamed menopausal hormone therapy (MHT), the difference in molecular structure, as well as the long chain of metabolites that MHT produces, lead to an increase in the number of illnesses and may or may not be protective against the diminished estradiol induced hippocampal damage or the associated cognitive decline.

Of BPA and Endocrine Disruptors: New Research, Same Flaws

by Chandler Marrs, PhD

Published on April 3, 2013

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Bisphenol A or BPA is the ubiquitous estrogenic compound used to create plastics. It leaches into our food stuffs and because of its hormone-like qualities elicits a myriad of health issues in adults but especially in children and most especially when exposed in utero or during key developmental phases.

As we cover the expanding research base on BPA, it becomes increasingly clear that traditional methods of toxicology do not work for understanding endocrine disruptors – the man-made chemicals that alter our hormone pathways . A case in point, the latest research on BPA.

Exposure in Adults

A report published online in June of 2011 and presented at a prominent toxicology conference in February 2013, measured BPA exposure levels over a 24-hour period in adults fed a high BPA diet (lots of canned food and water from plastic bottles). The report showed that the concentration of BPA measured from blood was below the level of detection in most of the study participants, even though urine concentrations were extremely high and indicated exposure levels above the 95th percentile of the US population.

From urine tests, researchers were able to detect an average 84% – 97% of the dosed BPA and its metabolite, BPA glucuronide – indicating a high rate of clearance from the body. The ranges varied widely by time of day (morning tests showed significantly less clearance) and gender of participant (women did not process the hormone as well as men).

The researchers argue that their failure to detect BPA in blood, combined with the high concentration in the urine meant that risk was minimal. Their reasoning, even though BPA exposure was high, most of the BPA was cleared from the body rapidly and efficiently; no harm, no foul.

Medical and science marketers latched on to this and soon every major and minor media outlet was reporting that risks were minimal. Here are just a few headlines.

No Ill Effects Found in Human BPA Exposure, says the Wall Street Journal

Majestically Scientific Federal Study on BPA has Stunning Findings: So Why is the Media Ignoring it? – says Forbes

No toxic effects from controversial food packet, says expert – the Guardian

Ahh, where to begin?

Flaws in the Research

Conflicts of interest. Always look for industry sponsorship of for research, see my previous post on evaluating endocrine research for details. The relationship between the investigators in the present study and industry are muddled, but they do exist. For more information, click here.

Below the level of detection. When researchers report that their tests are unable to detect a visible pathology or measure a particular compound that any reasonable person would expect to be present, the test is likely at fault. Below the level of detection, means just that. It does not mean the compound was not present or that it was not exerting effects, only that the tests were not sensitive enough to measure the compound. This was case here and I suspect as testing methods improve, we’ll see higher detection levels in blood.

High clearance is not the same as never exposed. In this study, not all of the hormone was recovered in the urine, only an average of 84% – 97%. That sounds like a lot. With hormones, however, small amounts do great damage. Why? Because steroid hormones are stored in fat (and other tissues). They accumulate over time and metabolize into a myriad of different hormones (metabolites), some more potent than the parent compound. After the initial exposure and certainly after repeated exposures, our bodies become little (or big) hormone factories, storing and creating more and more hormones and hormone metabolites.

Metabolites matter. Hormones are shape shifters. Every time they meet an enzyme, the interaction between the enzyme and the hormone creates a new, similar, but differently shaped hormone. Hormones are never ‘one and done’ metabolizers. Even though a large percentage of the original hormone and its primary clearance metabolite were measured from urine in the present study, one cannot assume that there were not still other metabolites circulating within the body and wreaking havoc.

BPA has metabolites. This is critical and often ignored in toxicology research. BPA is a hormone like substance and as such, it metabolizes into many different forms. BPA has metabolites that are more potent than BPA itself. New research shows that BPA metabolizes into a compound called 4-methyl-2,4-bis(4-hydroxyphenl)pent-1-ene or MBP for short. MBP is 1000-fold stronger than BPA in its estrogenic effects. MBP binds strongly to both types of estrogen receptors (ERa and ERb) and may change the activity of the cell, displacing native or endogenous estradiol. So within that 3%-16% range of BPA not cleared, comes a compound 1000 times stronger than the BPA itself. As the research progresses, who knows how many other active and potent metabolites from BPA or MBP we’ll see. With hormones, nothing is simple or straightforward.

What this Means

Avoid medical marketing, it’s usually incorrect. Learn how to evaluate endocrine disruptor research. Once you get the hang of it, you’ll be able to dismiss faulty research at a glance. More importantly, learn about hormone systems and environmental hormone disrupting chemicals. Otherwise, our children will bear the brunt of our ignorance.

A good review article: Bisphenol A and the Great Divide: A Review of Controversies in the Field of Endocrine Disruption.

The Soy Connection

by Jordan Davidson

Published on December 31, 2012

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As a firm believer in natural and holistic health, I believe that the food you eat can have a direct impact on your health. For those dealing with reproductive and or endocrine disorders simple dietary changes may help prevent or relieve a number of troublesome symptoms. For women across the board, especially those with estrogen sensitive diseases (e.g. endometriosis) minimizing soy in one’s diet can provide a lot of relief.

But, isn’t soy good for you? That’s not an easy question to answer. In moderation soy can provide a lot of benefits to one’s diet. However, soy should not be a staple in your day to day meal planning. To better answer the question we need to break it down.

Phytoestrogens

Soy is filled with phytoestrogens also known as “dietary estrogens,” which mimic the hormone estrogen that is naturally produced by the human body. Research has shown that phytoestrogens are beneficial for women going through menopause, since menopause is marked by a reduction in estrogen levels. Some menopausal women say that eating soy products helps relieve some symptoms of menopause such as hot flashes. Research has shown that phytoestrogens help maintain cholesterol levels and bone density in post-menopausal women. In addition phytoestrogens also help protect against a number of different cancers, such as prostate and breast cancer, cardiovascular disease and help with cognitive functioning.

However, soy being filled with phytoestrogens, can also be bad for you. Estrogens are female sex hormones – estradiol is the most common. Estradiol promotes the growth of female sex characteristics. Soy is also high in phytic acid which if consumed in high quantities can affect the absorption of other minerals. That is why third world countries that survive on grain and legume based diets have high rates of mineral deficiencies.

Too Much Dietary Estrogen

Increased estrogen consumption can be particularly detrimental to a number of people (i.e. babies, children, men, women sensitive to estrogens). Studies have shown that giving babies/infants soy formula is the estrogenic equivalent to giving them daily birth control pills. Obviously, such small children shouldn’t be on any form of contraception. It has also been suggested that this increased ingestion of estrogen can lead to estrogen sensitivities, earlier onset of puberty and reproductive diseases/disorders such as endometriosis. For older children increased amounts of estrogen also cause pubertal issues. Large quantities of estrogen can delay puberty for boys and lower the age of menarche (first menstruation) for girls. The average age of menarche decreases every year and a lot of researchers and medical professionals hypothesize that is has to do with the environment, toxins and the estrogen that comes from outside sources. Early puberty can also lead to short stature in women.

Estrogen in abundance is also bad for grown men. Men produce both testosterone and estrogen, with testosterone being the predominant hormone by far, and responsible for masculine features. Too much estrogen in males can offset their testosterone to estrogen balance, causing hormonal deficiencies. Lastly, estrogen is bad for women who are sensitive to estrogen, such as women with endometriosis. The endometrium that builds up in endometriosis responds to estrogen. The more estrogen you give your body the more the endometrium can build up, which leads to additional inflammation and bleeding.

Not all Soy Products are Created Equal

If you are still confused as to how soy can be both ‘good’ and ‘bad’ for you consider this: soy products come from a soy bean – however, if you take a good look at your soy-patties or chips made with soy you won’t see mashed up green beans. The invisible soy you eat come from processing the beans. ‘Asian’ soy which is usually quoted as being “good” soy is fermented soy. The process of fermenting soy can reduce a lot of the detrimental qualities of soy, but not entirely. Unfermented soy contains antinutrients such as tripsin inhibitors which can produce serious gastric distress, reduced protein digestion and create chronic deficiencies in amino acid uptake. When soy is processed and manufactured it isn’t always fermented. There are two popular forms of processed soy:

Soy Lechitin: Soy lecithin is basically a waste product of refining soybean oil. In small amounts it isn’t harmful, but if you look at food labels it is found in a large amount of products. Putting soy products in everyday foods provides a lot of nutritional benefits (lower fat, lower calories, higher protein) while being cost effective to the manufacturers. Unfortunately when you process soy it also increases the levels of estrogens and goitrogenics. Goitrogenics decrease the productivity of the thyroid and are bad for those with thyroid disease. Although ironically enough lecithin by itself (not soy lechitin just plain old lechitin) is good for you, it is a natural product high in choline.

Soy Protein Isolate: Soy Protein Isolate is the key ingredient in most imitation meat and dairy products. It is also found in other manufactured goods and protein powders. To make soy protein isolate, the soy beans must first be mixed with an alkaline solution to remove fiber, then rinsed and separated using an acid wash and, lastly, neutralized in an alkaline solution. The resulting products are finally dried at high temperatures to produce a high-protein powder. A similar process is used to make textured vegetable protein which is a high-temperature, high-pressure extrusion processing of soy protein isolate. With natural almost always being better for you, a process like this is by no means healthy. It doesn’t sound good for you and it isn’t. This process can also increase the amount of trypsin inhibitors.

So… Is soy good for you? Studies show that a glass of red wine at dinner is good for you. But we all know that washing dinner down with a bottle of red wine every night would not be good for us. Approach soy in the same way; some soy products several times per week, especially if it is fermented, organic soy (think tofu cubes and not ‘fake pepperoni’) will provide more benefits than detriments. In general be smart about what you put in your body, be an educated consumer and read your labels. Just because it has soy doesn’t make it good. But, that doesn’t mean you need to take all soy products out of your life.

Controversy, GMO Research & Women’s Health

by Chandler Marrs, PhD

Published on October 8, 2012

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If you’ve been on the internet at all over the last several weeks, you’ve likely come across these pictures- the white rats with grotesquely large mammary tumors warning of the dangers of GMO foods. A controversial and not yet even officially published study out of France on the Long term toxicity of Roundup herbicide and a Roundup-tolerant genetically modified maize is responsible.

In this 2 year study (compared to the 90-120 days for most previous protocols) researchers purportedly demonstrated the ill-effects of glyphosate (active ingredient in Roundup herbicide) and its adjuvants (putatively inactive ingredients that enhance the absorption, distribution or metabolism of the active ingredient), but also inadvertently, and despite the rampant criticism of the study, may have identified a mechanism of action for the growth of these tumors; a disruption of the estrogen pathway perhaps linked to primary kidney and liver damage. Moreover, and again perhaps inadvertently, the research points to a possible player in the development of fibroid type tumors.

How GMO Research is Conducted

There is great debate over the safety of herbicide rendered or engineered, genetically modified organisms (GMO) within the food and water supply. Studies on the side of industry, suggest no major ill-effects, while those on the side of environmentalist indicate differently. Research design likely contributes to the disparate findings. Much research to date has been short-term (90-120 days) and/or has limited the analysis to testing or manipulating only the active ingredient in the herbicide (glyphosate) and not the variety adjuvants found in the total herbicide formulation and that would be dispersed into the natural environment (food, water) post herbicide use.

The current study sought to remedy some of those short-comings and approximate what humans might be exposed to with current regulatory standards in place and in an ‘natural environment’ where exposure rates and types would necessarily vary. (Whether lab rats can approximate human physiology or the lab can be considered a ‘natural environment’ are debates for another day).

The Seralini GMO Study

Using healthy male and female Sprague-Dawley rats, the researchers evaluated the long-term (two years), across a life-span effects, of eating Roundup treated foods (maize) and water with Roundup residue at levels below the currently parts per billion standard and consistent with what humans might be exposed to in the current environment. Control rats were fed non-GMO diets and the test rats were fed varying levels of GM maize (11%, 22% and 33% of the total diet) and water with Roundup – well below the approved levels found in the environment.

Tumors, Toxicity, Death and the GM Diet

Compared to control rats fed a non-GM diet, those fed the GM-maize and Roundup water, died five times sooner and developed huge tumors, often greater than 25% of their body weight and requiring euthanasia to reduce suffering. There were distinct differences between the male and female treated animals. The females died more quickly and developed primarily mammary tumors, followed by a lower percentage of pituitary tumors and kidney and liver toxicity. While the males, demonstrated more severe kidney and liver disease along with skin tumors. The females were more susceptible to the Roundup in the water and both groups were equally susceptible to both the lower and higher percentage (11% and 33%) exposure to GM food, suggesting a threshold effect for disease initiation rather than a cumulative or additive effect.

Endocrine Disruption

The endocrine effects were also telling and pointed to sex-dependent differences in the tumor and disease expression. The ratio of testosterone to estradiol was disrupted in both males and females. Males in the highest Roundup treatment group (33% of total feed maize), demonstrated double the levels of circulating estradiol (see Evolution or Extinction of Men for details on male endocrine disruption) when compared to the control group. Whereas the exposed females showed increased testosterone levels.

Potential Fibroid Connection

The explosive growth of tumors in the female treated rats is notable both because of the large size and location of the tumors (mammary and pituitary) but more so perhaps because of the nature and physiology of the tumors themselves. In all but two cases, the tumors were non-cancerous, non-infective or non-metastatic. The tumors were benign adenomas and fibroadenomas, those commonly found in human women as they age (also common in this strain of lab rat as it ages). Fibroadenomas are comprised of fibrous and glandular tissue located in the breast. Fibroids are similar in tissue composition, but are found in the uterus. In the present study, fibroadenomas were found in the mammary tissue and adenomas in the pituitary gland. There was no mention of uterine fibroids or adenomas in other female reproductive regions. Similarly, although, the authors make no such claim regarding the expression of fibroid type tumors, relative to hormone changes and concurrent liver dysfunction (where the enzymes and proteins involved in the hormone regulation reside), I surmise that perhaps there is a connection there as well. It is conceivable that the combined insult of aging and environmental toxins on liver function alters hormone pathways sufficiently to promote this type of tumor growth.

Controversy and Criticism

As this study was released both pro- and anti-GMO factions got their pants in a bunch. On the anti-GMO side, this study represented proof-positive that GMO foods were bad. The results of this study, and in particular, the pictures of the tumor-ridden rats went viral on the internet. On the pro-GMO side, the criticism was as swift as it was vitriolic, with claims ranging from poor methodology, to outright scientific fraud. I suspect the truth lay somewhere in between.

My Take

Releasing to press first. This merited all sorts of criticism, most of which has no bearing on the actual study but does suggest a less than forthright approach to media relations. However, given the politics surrounding this topic, one can understand this PR approach.

Sprague-Dawley rats are prone to tumors. Yes, they are and as they age, tumors become more frequent. But here we have a little pot and kettle action going on. Sprague-Dawley and other outbred strains of rats and mice, all have predilections for certain diseases and tumors, but are nevertheless what is used in all industry supported (even the studies supporting the safety of GMO) and academic research. The choice of lab rat/mice is important, but even within specific strains there is huge variability. Nullifying the study because the researchers used the same strain of lab rats that other researchers also use, is a weak criticism at best and more than a little disingenuous. Perhaps a better criticism would be the use of lab rats in general to extrapolate human physiology.

Sprague-Dawley rats are prone to tumors as they age. Well guys, so are women. By the time a woman reaches age 50, upwards of 70% of women have fibroid type tumors. And frankly, aging, whether in animals or humans, increases disease expression. Our bodies just don’t work as well when we are older. Simply measuring the effects of a toxin for a short period of time in youthful animals does not, in any way, mirror the real life of the animal or a human, where effects are cumulative over time and sometimes even multiplicative and synergistic.

The study was too long and the control rats were dying too. Life is longer than adolescence. If one wants to evaluate how a treatment or toxin affects an organism over time and as it ages, one has to evaluate across that life span. This study compared tumor progression, disease and death rates between the non-GM controls and the GM fed groups, across the rodent’s life span, which is about 2+/- years. As the rodents aged, both groups developed tumors and some died, but there were more tumors and earlier deaths in the experimental group.

Failure to observe or measure is not synonymous with non-existence. Neglecting to measure a particular toxin or analyte, a specific symptom or disease process, or failing to evaluate long term effects does not mean that the toxin, analyte, symptom or disease process in question did not happen or does not exist. It simply means that you chose not to measure it. So claiming that a 3-month study in youthful rodents nullifies results from a longer study, regardless of any other methodological issues with either study, is an utterly false, and more than a little dishonest argument.

The dose response-curve was not linear. Damn it, how dare our complex physiology not conform to the simplicity of linear statistics. A common dose-response reaction is highly linear, where a small dose elicits a similarly small response and a larger dose increase the response size. This is not case when dealing with endocrine disruptors. Hormone systems are complex and highly non-linear. Hormone reactions occur at extremely low doses and often interact synergistically with other factors and respond differently over time and with cumulative exposures. This was the case in the current study.

In spite of the flaws with this study and contrary to the criticism, the Seralini study represents one of the only, if not the only, long term evaluation of the effects of Roundup and GM feeding on health. Long term studies, even in rodents, are not common place. They should be.

The next long term study (and there should be many more) should include different strains of rodent, measure additional hormones and steroidogenic proteins altered with liver disease and if they want to be really ingenious, look at the estrogen, androgen and progesterone receptor densities in the tumors.

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Vaginal Atrophy – The Great Wall of the Vagina

by Elena Perez

Published on August 27, 2012

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Does it hurt when you have sex? What about when you pee? Maybe just riding a bike is uncomfortable. This pain or discomfort may be attributed to vaginal atrophy.

Vaginal atrophy, or atrophic vaginitis, is a medical condition that refers to the thinning, drying and inflammation of the vaginal walls. This change in the vagina is due to a loss of endogenous estrogens and may account for discomfort and pain that women feel during everyday activities, such as sex, urination, or exercise.

This condition causes the vaginal walls to become fragile, and good bacteria in the vagina are often replaced by harmful bacteria and fungi. Since the vaginal wall is more susceptible to small tears, the possibility for infection increases.

Endogenous Estrogens

Our bodies naturally make a variety of estrogens. The most common endogenous estrogen is estradiol, which is produced in a woman’s ovaries. The remaining endogenous estrogens include estriol, which is produced by the placenta during pregnancy; and estrone, which is made by the ovaries and the adipose tissue – which is just a nice term for body fat.

Turns out, thin women are more susceptible to vaginal atrophy, which makes sense. Thinner women don’t have as much adipose tissue, so they don’t produce as much estrone. Women with more meat on their hips, however, have more fat tissue, which means they have another means of producing endogenous estrogens should they ever need backup.

Where Did the Endogenous Estrogen Go?

A woman’s endogenous estrogens can be impacted a number of ways. The simple joys of womanhood can affect hormone levels: Estradiol and especially estriol, decline dramatically following childbirth. Estradiol also declines while breastfeeding, and at menopause. In fact, the Harvard School of Medicine reported that within a few years of menopause, 50% of women have symptoms of vaginal atrophy.

Cesarean. Think you’re out of the woods because you haven’t had a child? Studies show that women who have never given birth vaginally are also more likely to have vaginal atrophy, according to Mayo Clinic. This means women who have only had cesarean sections are prone to vaginal atrophy, also.

Smoking. Don’t light up in frustration just yet: Women who are smokers are also prone to vaginal atrophy, which may be due to reduced blood circulation in the vaginal walls.

Cancer. Various cancer treatments can also decrease the production of endogenous estrogens. An oophorectomy, or the surgical removal of the ovaries, is performed to reduce the risk of ovarian cancer, and undoubtedly impacts the production of estradiol. Women undergoing pelvic radiation and chemotherapy can also experience lower endogenous estrogen levels.

Certain breast cancers are sensitive to endogenous estrogens, especially estrone, which encourage the growth of breast cancer tumors. In order to deter tumor growth, breast cancer patients may be given drugs that suppress endogenous estrogens. Sexuality, Reproduction and Menopause published a study that found 90% of breast cancer survivors report sexual problems and symptoms of vaginal atrophy.

Communicate Your Concerns

Although 50% of postmenopausal women and 90% of breast cancer survivors have symptoms of vaginal atrophy, Dr. Deborah Coady, who is the co-authored of Healing Painful Sex, said studies show only 10 to 20% of women discuss vaginal discomfort and pain with their doctors.

In the past, doctors linked vaginal dryness and dyspareunia, or painful intercourse, to emotional problems, discarding the possibility of a physical or hormonal change occurring. Now, however, more doctors are being educated on vaginal atrophy and are in a better position to discuss changes to the vaginal wall.

Oncosexology is developing to properly educate oncologists and patients alike, so they can prepare for the hormonal and vaginal changes that are likely to occur as a result of various cancer treatments.

If your doctor doesn’t bring it up first, though, don’t hesitate to speak up. Dr. Coady recommends talking about any vaginal discomfort, dryness, or pain right away. The longer the pain persists, the more likely it will result in nerve pain and dysfunction of the pelvic floor, so it’s best to diagnose the problem right away.

Treating Vaginal Atrophy

There are a slew of over-the-counter and prescriptions treatments available for women, such as vaginal moisturizers, lubricants, and low-dose vaginal estrogen. A list of these can be found on the Harvard School of Medicine website.

As for natural remedies, Dr. Coady found the application of natural oils, such as vitamin E, safflower, olive, or coconut oil effectively hydrates the vaginal wall when used three or four times a day for a month or two. A friend of mine uses coconut oil as a lubricant during intercourse, and says it works well.

As it turns out, the Harvard School of Medicine notes that sexual intercourse and/or masturbation is also good for your vaginal walls. This sexual activity stimulates blood flow to the vaginal walls, promotes vaginal elasticity, and, when aroused, increases lubrication. The Journal of the American Medical Association published a study that found women who are sexually active report less vaginal atrophy than those who are not, so feel free to get the blood flowing.

If you think you are suffering from vaginal atrophy, don’t suffer in silence. There are ways to improve this condition, and it starts by consulting your doctor and tending to your vaginal wall.

Male Breast Cancer: Know the Facts

by Amy Roost

Published on June 12, 2012

3014 views

Father’s Day is a day when we honor the men in our life. What better way to do so than to inform ourselves about potential health risks men face?

One rare, though oft ignored, due to its taboo nature, disease is male breast cancer. Men, like women, suffer from breast cancers that infiltrate the ductal tissue, lymph nodes and nipple. Also, like breast cancer in women, male breast cancer is marked by uncontrolled growth of the abnormal cells.

Incidence

Male breast cancer makes up less than 1% of all breast cancers. Approximately 2,000 cases of male breast cancer are reported each year in the U.S. Roughly 400 men die each year from the disease. It occurs most often in older men between the ages of 60 and 70. The cause is not entirely known, but both environmental influences and genetic factors likely play a role and as with women, hormones influence the growth of certain cancers. An interesting note: although male breast cancer remains relatively rare, the incidence of male breast cancer has increased by 26% since 1975 according to data from the National Cancer Institutes Surveillance, Epidemiology and End Results (SEER) database.

Risk Factors

Men who have previously undergone radiation therapy to treat malignancies in the chest area (for example, Hodgkin’s lymphoma) have an increased risk for the development of breast cancer.

The majority of breast cancers in men are hormone receptor positive. Remember, men have the same compliment of steroid hormones as women. They differ only in the concentrations/levels. Women have higher estrogens and men higher androgens. As many as 77% of tumors are either estrogen receptor-positive, meaning that they grow in response to stimulation by endogenous estrogens such as estradiol and estrone or exogenous synthetic estrogens, or are progesterone receptor positive, tumors grow in response to endogenous progesterone or synthetic progestins/progestagens. There is also evidence linking metastatic prostate cancer to male breast cancer and the medications associated with the treatment of prostrate cancer. Additional conditions associated with an increased rate of breast cancer include: Klinefelter’s syndrome, cirrhosis of the liver and obesity.

Klinefelter’s syndrome is an inherited condition affecting about one in 1,000 men. Men with Klinefelter’s syndrome have inherited an extra female X chromosome, resulting in an abnormal sex chromosome makeup. Klinefelter’s patients produce high levels of estradiol and develop enlarged breasts. Men with Klinefelter’s have a 50 times greater risk for development of breast cancer than that of normal men.

Cirrhosis of the liver can result from alcohol abuse, viral hepatitis, or rare genetic conditions that result in accumulation of toxic substances within the liver. With cirrhosis, liver function is compromised and the levels of male and female hormones in the bloodstream are altered. Men with cirrhosis of the liver have higher blood levels of estradiol and estrone and have an increased risk of developing breast cancer.

Obesity. Men with a body mass index (BMI) greater than 30 have twice the breast cancer rate than men with BMIs <25.

Genetics. Men who have several female relatives with breast cancer also have an increased risk for development of breast cancer. About 15% of breast cancers in men are thought to be attributable to mutations in the breast cancer-associated BRCA-2 gene.

Finasteride, a drug used to treat baldness (Propecia) and benign prostatic hyperplasia (Proscar), may be associated with an increased risk for male breast cancer. Further studies are needed to clarify whether a causal relationship between the drug and the disease actually exists.

Symptoms of Male Breast Cancer

The most notable symptoms of male breast cancer include:

Lumps
Changes to the nipple (inversion) or breast skin
Pain or discharge of fluid from the nipple
Enlarged lymph nodes under the arms.

Of note, men with breast cancer experience bloody nipple discharge and inversion more commonly than women.

Treatment for male breast cancer is usually a mastectomy. Other treatments include radiation, chemotherapy and/or hormone therapy.

This Father’s Day, ask yourself if the man in your life may be at risk. If he is, have a conversation with him about what you’ve just learned. Who knows, you may save a life, and wouldn’t that be a great Father’s Day gift?

Stress, Learning and Estradiol

by Chandler Marrs, PhD

Published on November 29, 2011

2115 views

In many ways, we assume males and females are the same, even though we know each sex has distinct and obvious differences in physiology and behavior. In the case of the stress, although the basic physiological response is comparable, the chemical reactions that the stress response elicits in males versus females are quite dissimilar. The divergent reactions are mediated by the varying concentrations of reproductive hormones that each sex is exposed to. Far beyond just controlling sex differentiation and reproduction, sex hormones like progesterone, estradiol and testosterone modulate brain and body chemistry quite significantly. The differences in the circulating concentrations of these hormones may account for the unequal prevalence rates of many diseases such as of depression, auto-immune disease, or migraine. These diseases are far more common in women than men.

Hormones also influence neurochemistry, and therefore, learning. In general, males and females learn quite differently from one another. Males tend to be better at spatial tasks while females tend to perform better at verbal tasks. Research suggests testosterone and estradiol may mediate those performance differences.

Estradiol affects learning under stress. When exposed to stressful conditions, male rodents learn certain classically conditioned tasks more rapidly than female rodents. However, when the female rodents’ ovaries are removed or estradiol is blocked by a drug like Tamoxifen, the difference between the two sexes is removed. That is, the female rodents acquire the conditioning as quickly and as effectively as the male rodents.

Even though, humans are far more complicated than rodents and the controlled stress and the scope of classical conditioning tasks in the lab are limited compared to the stress and learning that takes place in the real world, it is clear that sex matters, and thus by definition, sex hormones matter.

To read more about sex differences in neurochemistry:
The End of Sex as We Know It

Every Man Knows a Woman with Hormones

by Chandler Marrs, PhD

Published on September 14, 2011

2304 views

And we all have hormones. Those wonderfully mysterious chemicals circulating and cycling with the regularity and rapidity that makes one’s head spin, female hormones are at once the bane and the joy of man’s existence. Our hormones are what make us find you attractive, laugh at your jokes, date you, sleep with you and bear your children. Our hormones can also turn us into stark, raving lunatics at seemingly benign comments. Most men know and understand this, at least intuitively. You are prepared for the ‘wrath of raging hormones’ if not from direct experience with your mothers, sisters or girlfriends, then from the many locker room and sitcom epithets ever present in modern culture.

What most men (and many women) are not prepared for, and I’d venture don’t understand, is the very real chemistry changes behind the wrath. Much of this goes far beyond just mood changes, often eliciting a bevy of symptoms and disease processes that we’re only now beginning to understand.

In many ways, hormones are just like every other chemical circulating in our bodies, regulating this system or that, entirely responsible for certain functions, secondary and tertiary players in others. Men have the same hormones as women, just in different concentrations. And hormones cycle in men, but not so radically and regularly. What is different between ‘men’s hormones’ and ‘women’s hormones’ is not the hormones themselves, but the systems and structures on which they operate and the reproductive functions that ensue.

To state the obvious, women have ovaries and a uterus. Those structures, along with the brain form the foundation of a beautifully orchestrated and incredibly complex chemical feedback system that not only controls reproduction, but influences just about every aspect of our lives. Estradiol and progesterone concentrations increase several fold across an average cycle, preparing the uterus for a possible pregnancy. In the absence of pregnancy, hormone levels plummet and the lining of uterus, the endometrium sheds. The all-too-familiar mood changes and pain commence.

As a man viewing this process from the outside, it is difficult to appreciate the magnitude of hormone changes affecting the women in your life. When hormones act on the brain or in the body, they do so in much the same manner as many common drugs. In terms of chemistry, menstrual cycle hormone changes are very similar to a drug addiction/withdrawal pattern with increasing dosages of stimulants (like amphetamines) during the first two weeks, a combo pack of sedatives (like Valium or alcohol) plus a few stimulants during the second two weeks, followed by cold turkey withdrawal. Rinse and repeat, over and over again, approximately 450 times during the course of her lifetime. Pregnancy and postpartum follow the same pattern only the dosage of hormones, the duration of exposure and the magnitude of the withdrawal are increased exponentially. The veritable cocktail of hormones that make these functions possible is breathtaking.

What happens when one or more of these chemical messengers gets a little out of sync and the system become dysregulated, as is inevitable in any system that cycles so frequently? Or what happens when an illness or disease, maybe not caused by hormones, develops in the context of this ever fluctuating female chemistry? You get a bit of chaos (think butterflies, not randomness).

As a man, who has women in his life, you have two choices, ignore and avoid the chaos and hope there are no storms on the horizon, or embrace the chaos and find ways to anticipate and alleviate the pain. Many choose the former, including much of medical science. This is the avoidable ignorance, I wrote about last week. I’d like to think the men who love us, choose the latter. Certainly, the men who shared their wives’ and daughters’ stories recognize the need to investigate and develop better treatments for women. They may not understand fully the complexity of women’s hormones, but they understand the suffering, sense that symptoms are being ignored and want nothing more than to make it all better.

Hormones Matter

Where health, hormones, and a whole bunch of other stuff, make sense.

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