Monthly Archives: November 2016

Avoiding HRT increases Mortality in Women

This important study reaffirms what I have been saying for a long time. Oestrogen is a women’s friend. The scare campaign about oestrogen has been based on a false premise, as a result of which many millions of women have suffered unnecessarily and many have died as a result. (see very thorough study below). Also check my blog of the 8th Sept which is very pertinent to this discussion.

The Mortality Toll of Estrogen Avoidance: An Analysis of Excess Deaths Among Hysterectomized Women Aged 50 to 59 Years

Am J Public Health. 2013 September; 103(9): 1583–1588.
Published online 2013 September. doi:  10.2105/AJPH.2013.301295
PMCID: PMC3780684

The Mortality Toll of Estrogen Avoidance: An Analysis of Excess Deaths Among Hysterectomized Women Aged 50 to 59 Years

At the time of the study, Philip M. Sarrel was with the Departments of Obstetrics and Gynecology and Psychiatry, Yale University School of Medicine, New Haven, CT. David L. Katz was with the Prevention Research Center, Yale University School of Public Health, Griffin Hospital, Derby, CT; and with the Department of Medicine, Yale University School of Medicine. Valentine Y. Njike was with the Prevention Research Center, Yale University School of Public Health. Valentina Vinante was with the Departemento di Sanita Pubblica, Universita di Firenze, Florence, Italy.
corresponding authorCorresponding author.
Correspondence should be sent to Philip M. Sarrel, MD, Emeritus Professor, Yale-Griffin Prevention Research Center, 130 Division St., Derby, CT 06418 (e-mail: ude.elay@lerras.pilihp). Reprints can be ordered at by clicking the “Reprints” link.
Peer Reviewed


P. M. Sarrel directed the literature search and assessment, and wrote the primary draft of the article. P. M. Sarrel and V. Y. Njike acquired the data. V. Y. Njike analyzed the data and developed the data tables. V. Vinante conducted the literature search. D. L. Katz developed the MTEA formula, reviewed and edited drafts of the article. All authors participated in data interpretation and critical article review.

Accepted February 18, 2013.


Objectives. We examined the effect of estrogen avoidance on mortality rates among hysterectomized women aged 50 to 59 years.

Methods. We derived a formula to relate the excess mortality among hysterectomized women aged 50 to 59 years assigned to placebo in the Women’s Health Initiative randomized controlled trial to the entire population of comparable women in the United States, incorporating the decline in estrogen use observed between 2002 and 2011.

Results. Over a 10-year span, starting in 2002, a minimum of 18 601 and as many as 91 610 postmenopausal women died prematurely because of the avoidance of estrogen therapy (ET).

Conclusions. ET in younger postmenopausal women is associated with a decisive reduction in all-cause mortality, but estrogen use in this population is low and continuing to fall. Our data indicate an associated annual mortality toll in the thousands of women aged 50 to 59 years. Informed discussion between these women and their health care providers about the effects of ET is a matter of considerable urgency.

In the 1990s, estrogen therapy (ET) became the standard of treatment of the almost 600 000 women a year in the United States undergoing hysterectomy. Clinical studies had indicated ET was effective for treatment of menopausal symptoms and appeared to be bone protective and cardioprotective. More than 90% of hysterectomized women in their 50s used ET, with a continuance rate averaging 4 to 5 years.1–3

In July 2002, the Women’s Health Initiative (WHI) published the results of the Estrogen Plus Progestin Trial and announced that the study was being terminated ahead of schedule because of adverse effects in the women receiving hormones compared with those receiving placebo.4 The media impact was immediate, widespread, and persistent.5 The study’s treatment drug (Prempro) was often referred to as “HT” (hormone therapy) or “estrogen.” As a consequence, the findings were generalized to all varieties of hormone replacement, including estrogen alone, in women without a uterus although only women with a uterus were randomized in this study. Prescriptions for postmenopausal hormone replacement declined precipitously. Within 18 months, half of the women in the United States using systemic HT stopped treatment.1–3 Included were almost 2 000 000 women who had no uterus who were using ET and not using the study drug.

Subsequently, the findings of the WHI Estrogen-Alone Trial (WHI-ET) for women without a uterus were published for the intervention phase (2004) and the postintervention long-term follow-up phase (2011).6,7 These findings showed mortality benefits for ET compared with placebo. Preliminary subgroup analysis of the intervention phase data (2004) indicated reduced total mortality in the women aged 50 to 59 years. However, it is only in the postintervention data (2011) that an absolute total mortality risk reduction of 13 per 10 000 women per year was reported for these women. The mortality decrease was almost entirely owing to a decrease in coronary heart disease (CHD) although reduced cancer mortality and other cause mortalities were also reported among the women who received ET.7

Despite the positive findings for ET, prescriptions for all forms of systemic HT have continued to decline.3,8–11 Currently, less than one third of hysterectomized women are using ET.12 The decline in ET prescription and usage seems to reflect a generalized avoidance of any forms of HT not supported by the WHI data. This raises the possibility that there has been and continues to be a considerable resultant mortality toll. We therefore undertook an analysis, on the basis of published data, to determine the likely toll of excess, premature death among hysterectomized women aged 50 to 59 years in the United States following the WHI publication in 2002.


The 2011 WHI publication indicated a 13 per 10 000 per year higher rate of mortality among hysterectomized women aged 50 to 59 years assigned to placebo than among those assigned to estrogen over a 10-year follow-up.7 We considered this figure a point estimate for the mortality burden associated with foregoing estrogen among members of this specific population.

To determine how this rate of excess mortality translated into an aggregate toll of premature death at the population level, we established the following formula to represent the mortality toll of estrogen avoidance (MTEA):

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  • t1–t10 = sum for years 1 through 10 (2002–2011),
  • CPF50–59 = size of population of women, aged 50 to 59 years, from US Census data (2002–2011),
  • PctHyst = percentage of women in CPF50–59 who have undergone hysterectomy (specific to year and age),
  • PctEsDec = absolute percentage decline in rate of estrogen use in group of interest, by year, following publication of WHI results, and
  • ExMoRate = excess mortality rate in group of interest as a result of estrogen avoidance.

When a single best estimate was available in the peer-reviewed literature or government data for any given entry in the formula for the entire span of 10 years or the entire population of women across the age range, we used that. If more precise estimates specific to year or age were available, we entered these and we then aggregated the calculations across years and age groups. Because of a distinctly differential rate of hysterectomy for women in the lower than the upper half of the age range of interest, we conducted separate calculations for these 2 populations and aggregated the results. To enhance the accuracy of our calculation, we applied the relevant rates to portions of the specified range and generated an estimate for the entire age range by determining the weighted average.

We calculated the mortality toll estimates on the basis of population estimates from census data, age variability for hysterectomy prevalence reported in the peer-reviewed literature, and different rates of ET use before 2002 affected by whether the women had their ovaries removed (oophorectomy). We applied the WHI absolute mortality estimate for women aged 50 to 59 years (13/10 000/year) in all the calculations, along with the extremes of the 95% confidence interval (CI) around this point estimate.

We derived the annual populations of women aged 50 to 59 years from 2002 to 2011 US Census estimates.13,14 We derived the hysterectomy prevalence rates, with and without oophorectomy, from 1997 to 2005 National Hospital Discharge Survey data.15,16 For women aged 50 to 59 years the rates ranged from 33% to 40%. The rates are consistent with an average of almost 600 000 hysterectomies per year among women of all ages in the United States. The average age for hysterectomy is 46.1 years.15,16

An estimated 54% of women have their ovaries removed at the time of hysterectomy.16 Before 2002, the ET use rate for women posthysterectomy without ovaries was 90% and with ovaries was 53%.17 Therefore, we calculated the mortality associated with a decline in ET use separately for women with and those without ovaries.

Compared with 2001, use of oral estrogen only in women aged 50 to 59 years declined almost 60% by 2004, reached a 71% relative decline by 2006, and remained at that level through 2009.3 Since then there has been further decline in ET use, with 2010 and 2011 showing a 79% decline for these particular women.10,11 We used these figures to generate a year-by-year absolute percentage decline in the use of estrogen beginning with a baseline rate in 2002.

We entered best estimates for each component of the formula to generate a single aggregate estimate for the total excess in premature mortality attributable to estrogen avoidance in the population of interest. We made a particular effort to choose well-validated and conservative entries.

We identified the range of reasonable estimates around the best point estimate when possible for purposes of sensitivity analysis, that is, determining the sensitivity of the calculated estimate to variation in a given entry. For each entry in the MTEA formula, we attempted to identify well-validated figures representing reasonable low- and high-end values.

We calculated the 95% CI around the excess death rate as a result of estrogen aversion using the sample size from the WHI study to generate high- and low-end estimates for the excess mortality in the placebo group relative to the estrogen group.

The range of values we produced in the sensitivity analysis is reflected in the data tables, which indicate how we altered our assumptions, which led to specific estimates of MTEA. There were ranges of relevant values for the rate of hysterectomy, the rate of estrogen use, and the exact mortality excess as derived from the WHI-ET study. Our sensitivity analysis involved entering values at the extremes of the range for each of these parameters and calculating an MTEA estimate accordingly. We analyzed the data using SAS, version 9.1 (SAS Institute, Cary, NC).


Table 1 displays the estimated mortality toll of estrogen avoidance among all women aged 50 to 59 years assuming the rate of estrogen use at baseline and decline in estrogen use over time were common to women both with and without oophorectomy at the time of hysterectomy (Figure 1). Applying the lower estimate for hysterectomy rate in the population,16 the best point estimate for excess mortality over 10 years is 49 128 excess deaths, and the extreme low estimate is 22 677 excess deaths. Applying a higher estimated rate of hysterectomy in the population,16 the best point estimate for excess mortality over 10 years is 59 549 excess deaths, and the extreme high estimate is 91 610.


Mortality Estimates for All Women Aged 50–59 Years Using 2 Different Rates of Hysterectomy: United States, 2002–2011


Mortality toll of estrogen avoidance estimates flowchart.

Tables 2 and and33 show the differential mortality toll of estrogen avoidance for women with retained ovaries and ovaries removed, respectively. Estimates for the entire population thus require summing the totals from Tables 2 and and33 under similar assumptions. Applying the lower estimate for hysterectomy rate3 to both populations, the best point estimate for total excess mortality is 13 462 + 26 830, or 40 292. The low-end estimate is 6216 + 12 385, or 18 601 excess deaths. Applying the higher estimate for hysterectomy rate3 to both populations, the best point estimate for excess mortality is 16 316 + 32 519, or 48 835. The high-end point estimate is 25 098 + 50 027, or 75 125.


Mortality Estimates of Hysterectomized Women Aged 50–59 Years With Retained Ovaries Using 2 Different Rates of Hysterectomy: United States, 2002–2011


Mortality Estimates of Hysterectomized Women Aged 50–59 Years With Ovaries Removed Using 2 Different Rates of Hysterectomy: United States, 2002–2011

Thus, across a reasonable range of all assumptions, the excess mortality was between 18 601 and 91 610. Using the best available point estimate values with year-by-year adjustment and adjustment for differential rates of estrogen use among women with and without retained ovaries at hysterectomy, the range was 40 292 to 48 835.


Our analysis suggests that between 2002 and 2011 a minimum of 18 601 and as many as 91 610 excess deaths occurred among hysterectomized women aged 50 to 59 years following the publication of the original WHI findings because of the resulting aversion to hormone replacement therapy of all kinds that ensued among doctors and patients alike. The actual toll of excess mortality is likely to be between 40 292 and 48 835.

These numbers translate the WHI statistic for excess mortality in hysterectomized women aged 50 to 59 years who received placebo versus estrogen into an actual number of deaths. We believe that a mortality toll will better communicate the meaning and significance of the WHI-ET findings to women, health care providers (HCPs), and the media. The reported reduction in mortality for women aged 50 to 59 years in the WHI-ET reports was exactly the same (HR = 0.73) in 2004 and 2011.6,7 Neither the 2004 nor the 2011 WHI-ET reports reversed the decline in use of ET. The 2011 report of the 10.7 years of follow-up of ET-treated women, which included the absolute risk reduction in mortality rate of 13 per 10 000 per year in the hysterectomized women aged 50 to 59 years, was barely noticed. Decline in ET use has continued since its publication. Currently, it appears that only about one third of women having a hysterectomy with removal of their ovaries, regardless of age, are using ET.12 Before 2002, 90% of these women used systemic hormone replacement.17,18

Estrogen Therapy and Mortality

ET reduces total mortality primarily through reducing CHD-related deaths. Since 1959 there have been many reports showing increased risk of CHD mortality after early surgical menopause and especially after oophorectomy.19–21 Essentially, estradiol inhibits the development of atherosclerosis and helps maintain normal arterial blood flow.22,23

A 1998 meta-analysis of 25 observational studies reported a 30% lower risk of CHD in ET users.24 The California Teachers Study, in which 97% of the oophorectomized women used HT (almost entirely ET), shows an all-cause mortality reduction similar to the WHI-ET results.25

The WHI-ET and the California Teachers Study results indicate that the decrease in CHD events and all-cause mortality are limited to hysterectomized women younger than 60 years or within 10 years of menopause. A meta-analysis of 23 trials found that HT significantly reduced CHD events in these women.26 In fact, for CHD, the WHI-ET findings among women aged 50 to 59 years are in line with the reduced risks reported in the observational studies and support a “timing hypothesis” for ET cardioprotection when ET is started close to the time of menopause.27,28 The current thinking is that by age 60 years, pathological changes in vascular endothelial cells compromise the ability of estrogen to inhibit atherosclerosis and promote blood flow.27,28

Although prevention of cardiovascular mortality is by far the major benefit from ET in younger women, the WHI-ET and the California Teachers Study also show a reduction in cancer deaths. In 2012, the WHI-ET investigators reported a 63% reduction in mortality because of invasive breast cancer in the almost 12 years of follow-up in the postintervention study of ET users versus placebo users.29

Lack of Impact of the WHI–Estrogen-Alone Trial Findings

Continuing decline in ET prescriptions through 2011 attests to the WHI-ET data’s lack of impact.3,10,11 Numerous reasons for this can be suggested. Knowing the history of HT in the United States helps in understanding why there has been a strong reaction against the use of ET. In the 1960s, enthusiasm about using estrogen for menopause symptoms led to widespread use. In 1975 it was reported that unopposed estrogen in women with a uterus increased the risk of endometrial cancer. These findings led to fear of using estrogen. However, in the 1970s and 1980s, research on the addition of a progestin to ET showed that endometrial hyperplasia and carcinoma could be all but eliminated. At the same time, other research indicated that estrogen had bone-protective and cardioprotective effects. Confidence was restored, and once again there was widespread use of HT.

When the first WHI report came out in 2002 its findings about the health risks of postmenopausal HT were startling and frightening.5 Almost no one emphasized or even seemed to recognize the fact that the worst findings might not apply to hormones other than Prempro or might not apply to all age groups. Deciding not to use HT appeared to be the most appropriate and rational choice for almost all women. Aversion to all forms of HT became almost automatic, and the idea that there might actually be positive health outcomes of ET use was often dismissed.

There are other influences on women’s decisions about ET that are important but are beyond the scope of this study. These include HCPs paying little attention to WHI-ET reports; failure to differentiate between the findings of the 2 different WHI studies; mistrust of pharmaceutical companies and their products; peer group pressure to avoid estrogen; nonhormonal alternative therapies for hot flashes, prevention of osteoporosis, and sleep disturbance; the use of bioidentical hormones not approved by the US Food and Drug Administration; and pendulum swings in medical recommendations, which have created general skepticism about medical treatments.

Presenting Complex Biomedical Findings to the Public

Research findings are often nuanced and need to be reported accordingly in both the peer-reviewed literature and the popular press.30 It is the responsibility of biomedical researchers to report findings in a way that the media and the general public can clearly understand. With most medical interventions, as with hormone replacement, the findings and implications are not merely about what is done. They are also informed by how the intervention is delivered, exactly what preparation is used, under what particular circumstances, and in just what population. When findings pertain to specific preparations or populations, this should be stated explicitly and emphatically. Special effort should be made to explain the study nuances to HCPs. It is also the responsibility of the media and HCPs to convey this information so that it is clearly understood. Distortion of details can prove to be nothing less than lethal.

The WHI findings need to be presented so that the very important differences between the 2 treatment modalities are emphasized and the benefits for hysterectomized women aged 50 to 59 years are appreciated. This effort has clearly been inadequate to date.5,31


The growing practice of performing hysterectomy outside hospitals using a laparoscopic transvaginal approach has decreased the number of hospital-based procedures. The prevalence estimate, therefore, may be less than the actual number of hysterectomized women aged 50 to 59 years.15 If so, our mortality estimates are all biased downward.

We used the decline in use of oral ET for our estimates. We did not include data for use of transdermal estradiol, nonsystemic estrogens, and bioidentical preparations, although millions of postmenopausal women currently use 1 or more of these preparations.

We did not include transdermal ET use in the WHI studies. The use of transdermal estradiol in the United States has declined since 2002. Transdermal estradiol has been reported to be more effective than are oral estrogens in preventing cardiovascular events, so decline in its use could contribute further to the mortality toll.

Vaginal estrogen use did show a substantial increase between 2001 and 2009.3 The effects of vaginal estrogen are thought to be local and nonsystemic. However, a recent report shows an unexpected finding of a reduced rate for myocardial infarction in women using vaginal estrogen. Whether vaginal estrogen has an effect on mortality needs further study.

There has also been an increase in the use of bioidentical hormone preparations since 2002, but we are not aware of mortality data for these compounds.

The WHI cohort of hysterectomized women aged 60 to 69 years showed no significant mortality difference between estrogen use versus placebo. For this reason, we did not do a calculation for this age group. For women aged 70 to 79 years in the WHI study, there is an increased absolute death rate of 19 per 10 000,7 and this age group has shown a 78% decrease use in ET since 2002.3 As a result, some reduction in mortality could be calculated because of not using estrogen. However, compared with the younger women, the overall population in this age group is much smaller and the percentage of hysterectomized women living into their 70s is less. Also, the use of ET before 2002 was much lower in these women.2

We did not include women younger than 50 years, as there were no comparable WHI data for this age group. Nevertheless, hysterectomy occurs most often before aged 50 years (the average age is 46.1 years).16 Mortality is increased in younger women who have a hysterectomy and oophorectomy who do not use ET. Therefore, it is likely that nonuse of ET in women younger than aged 50 years has an additional mortality toll. For example, in the California Teachers Study, women aged 36 to 59 years show a 46% reduction in mortality among current ET users.18 This exclusion biases our estimates downward.

We do not address the issue of estrogen plus progestogen therapy for women with a uterus except to recognize that the treatment is different from ET as are the mortality results

Health Check: is it normal not to want sex?


Health Check: is it normal not to want sex?

May 30, 2016 1.12pm AEST

Many people aren’t interested in having sex or don’t feel sexual attraction to other people, loosely termed as asexuality.

Few of these say will say, “I’m asexual” in the same way that someone else might say, “I’m gay”. More might identify this way, though, if they felt they wouldn’t be judged.

Are these people odd? Is it normal not to have sex or not to be interested in having it?

Sex in Australia

In the Sex in Australia national survey, our interviewers spoke to more than 20,000 people between 16 and 69. Around 6% of all respondents had never had penis-in-vagina intercourse (some of whom were same-sex-attracted) and nearly half of those had never had any kind of sexual experience with another person. But about two-thirds of virgins were under 20 and would probably go on to have intercourse.

Less than 1% – around 70 people – said they’d never felt sexually attracted to anyone, but this number is probably higher in the real population.

Some people who suspect they might be confronted with questions about their sexuality and feel uncomfortable answering them might refuse to take part in such surveys. Even in the best random-sample population surveys, on any topic, one in every three or four eligible people refuses to participate.

We know the people who refuse sex surveys are not the same as those who take part. Refusers are likely to be less sexually liberal in their attitudes and also younger.

Thus many sexually inactive people, especially virgins, are probably missing from sexual behaviour surveys. For a start, in Sex in Australia, 99% of people over 30 say they have had intercourse. This is surprisingly high when you think about lifelong singles, including some disabled people, nuns and priests.

What others think

In the 19th century, lots of people had never had intercourse. Many in domestic service, armed forces, the church and so on never married and this was thought quite normal. Sex outside marriage, masturbation and sex with same-sex partners were all much more stigmatised than now (though sex work was far more common).

But these days, failure to achieve partnered status is often seen as a problem. So one issue for people not interested in sex is created by everyone else’s idea that they should be and that there’s something wrong with them.

These days, failure to achieve partnered status can be seen as a problem. from

Even among people in male–female regular sexual relationships, the Sex in Australia survey showed about one person in six had not had sex in the past four weeks. Asked: “During the last year, has there been a period of one month or more when you lacked interest in having sex?”, about a quarter of all men and half of all women said yes. This is much the same in Britain and the United States.

But, somehow, the question itself sets up the expectation that not feeling like having sex is a failing or problem, especially as it’s followed by other questions about things that really sound like problems, such as painful intercourse and trouble keeping an erection.

Feeling up-for-it is also quite subjective and relates to personal circumstances; sometimes it’s relative. Some people feel they lack interest because they don’t want sex as often as their partner, even if they would miss it if they had to go entirely without.

Sexual variation

People who don’t feel the need for sex are rarely or never aroused. They can go for days, weeks, months or even years without sex, whereas others are irritable, distracted and unhappy after even a few days of sexual abstinence; “biting the walls”, a colleague of mine once called it.

And some people are interested when there’s someone around to have sex with, but with no partner there as a prompt, they don’t miss sex.

Sexual interest comes and goes over time. It can disappear at times of illness and stress (even though some people use sex as a kind of stress-reliever). Most parents of young children know the sensation of being far more keen on sleep than on sex.

For many, sexual interest wanes in later life, though it may flower again in a new relationship. The social institution of monogamous marriage means that people might at times feel they should supply the sexual “needs” of their partner and it can become a duty to have sex, and want it.

Even people who identify as asexual are not all the same. Some are not interested in having sex with other people, but still have a libido, feel sexual arousal and still masturbate.

Some of those people may have personality traits that would put them on the autism spectrum, such as generally lacking interest in other people. Others are simply not aware of any internal sexual drive, although they may still have close, even romantic, relationships.

Sex was once something that was either done in the marriage bed, whether as a pleasure or a duty, or not done at all except by libertines and reprobates. The idea that everyone should have and enjoy sex, and continue doing so through old age, is recent. It seems a pity to replace a set of prohibitions on sex with a prohibition on not having it.

Five reasons to put the kettle on and have a cup of tea.

Health Check: five reasons to put the kettle on and have a cup of tea

August 24, 2015 3.52pm AEST

Around the world, tea is the most common drink after water.

Disclosure statement

Clare Collins is affiliated with the Priority Research Centre in Physical Activity and Nutrition, the University of Newcastle, NSW and has received funding from a range of research grants including NHMRC, ARC, Hunter Medical Research Institute, Meat and Livestock Australia. She has consulted to SHINE Australia and Novo Nordisk.

Growing up, tea drinking was reserved for my grandmother’s visits. Making it followed a strict and fascinating ritual. Take scalding hot water. Warm the tea pot. Add one spoon of tea leaves for each person and one for the pot. Cover with a tea cosy. Turn the pot three times to the left, three to the right, then three to the left. Leave to brew. Warm the cups; milk in first, pour through a tea strainer.

Two-thirds of over-70s are tea drinkers. Louise Lj/FLickr, CC BY-NC

My grandmother could taste any attempt you made to shortcut the process. Once Grandma approved the tea, pressure eased and conversation flowed.

In Australia 38% of the general population and 67% of those aged over 70 are tea drinkers. Our median intake is two cups a day, about 400mls.

By world standards we rank 55 for tea consumption, compared to the United States at 69, New Zealand 45 and the United Kingdom, number five. Turkey takes out the number one spot, consuming more than ten times the per capita intake of Australians.

1. Tea and survival

Around the world, tea is the most common drink after water. Popularity increased in the 1800s because the practise of boiling water to make the tea meant water-borne pathogens like cholera and typhoid would be killed, making it safer to drink.

Tea comes from the leaves and buds of the plant Camellia sinensis. Black tea, green tea, white tea, and oolong varieties all come from the same plant, but are processed into dried leaves differently.

Science has muscled in on our tea drinking habits and started to unravel what makes us love our “cuppa”. There is a large group of bioactive components in tea called polyphenols, which include catechins and tannins. Concentrations of these compounds vary depending on how you make the tea, including the amount of tea leaves per cup, water temperature and brewing time.

Catechins have anti-oxidant properties and are most abundant in green tea. Tannins, which inhibit non-haem iron absorption in the gut, are most abundant in black tea. So if you have iron deficiency, avoid drinking tea with meals. But if you have the excessive iron storage condition haemochromatosis, drinking tea with meals will help reduce iron absorption.

2. Tea and your brain

Components of tea that can boost brain activity include caffeine, catechins and the amino acid, L-theanine.

In a systematic review of the effects of tea on mood and cognitive function, the combination of L-theanine and caffeine was shown to increase alertness and attention-switching accuracy up to two hours after consumption. The researchers also found small enhancements in accuracy of visual and auditory attention.

Catechins and the amino acid, L-theanine, can boost brain power. ned the head/Flickr, CC BY-NC-ND

Preliminary evidence also suggests catechins may have a calming effect during the second hour post-cuppa. The authors called for further research using a greater dosage range of catechin and L-theanine to help separate any effects due to caffeine intake.

At this stage however, there is no clear evidence that drinking tea will protect people from developing dementia.

3. Tea and weight loss

There has been a lot of interest in whether tea, particularly green tea, can increase energy expenditure and help with weight loss.

Two Dutch meta-analyses have examined the evidence in studies comparing catechin-plus-caffeine mixtures versus caffeine-only supplements on energy expenditure and fat oxidation (breaking down fat). They found that compared to placebo and caffeine-only groups, people who had catechin-plus-caffeine mixtures were more likely to break down fat.

They also evaluated whether green tea could improve body weight regulation. Their meta-analysis found the group consuming catechins from green tea had a 1.3 kilogram greater weight loss and were more likely to maintain this loss; although there were some differences based on ethnicity and usual caffeine intake.

4. Tea and diabetes

Last year, a pooled analysis of 12 cohort studies compared tea drinking with risk of type 2 diabetes. Researchers found that among those who drank three to four or more cups per day there was a 16% lower risk of developing type 2 diabetes, compared to those who usually drank just one or no cups of tea.

But when they drilled down into the studies, the lower risk was only found in women and those of Asian ethnicity. We need to keep in mind that associations found in cohort studies do not prove causation.

In a meta-analysis of ten randomised controlled trials that lasted eight weeks or more, totalling 608 adults with type 2 diabetes, researchers found mixed results for the impact of drinking tea, or consuming various tea extracts, on blood markers of diabetes control.

While there were improvements in fasting blood insulin and waist circumference, there was no impact on other markers, including fasting blood glucose, LDL (bad) or HDL (good) cholesterol, body mass index or blood pressure.

Both green tea and black tea can significantly reduce blood pressure. Selma Broeder/Flickr, CC BY

Researchers are now focusing more closely on the phenolic components in tea to try and develop compounds that could be used to prevent or manage type 2 diabetes.

5. Tea and heart disease

A Cochrane review evaluated 11 randomised controlled trials that ran for at least three months and were aimed at preventing heart disease in healthy adults or those at high risk of heart disease.

Pooled results showed that both green tea and black tea significantly reduced blood pressure, with black tea lowering LDL-cholesterol and green tea lowering total cholesterol. The small number of studies to date though means these results need to be interpreted with caution, but they do look promising.

Meanwhile, for a host of other reasons it seems that my grandmother was right: a good brew does more than than just warm you up (or cool you down). So put the kettle on, get out your best tea cups, create your own tea making ritual, gather the clan and relax with a cuppa.

Omega 3 reduces breast cancer risk.

I have been recommending fish oil for the prevention of arthritis, heart disease and memory loss to my patients for many years. Here is another benefit from fish oil (Omega 3)

Modulation of Breast Cancer Risk Biomarkers by High Dose Omega-3 Fatty Acids: Phase II Pilot Study in Post-menopausal Women

Carol J. Fabian 1 , *, Bruce F. Kimler 2, Teresa A. Phillips 3, Jennifer L. Nydegger 3, Amy L. Kreutzjans 3, Susan E. Carlson 4, Brandon H. Hidaka 4, Trina Metheny 5, Carola M. Zalles 6, Gordon B. Mills 7, Kandy R. Powers 3, Debra K. Sullivan 8, Brian K. Petroff 9, Whitney L. Hensing 10, Brooke L. Fridley 11, and Stephen D. Hursting 12



Associational studies suggest higher intakes/blood levels of the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) relative to the omega-6 arachidonic acid (AA) are associated with reduced breast cancer risk.

We performed a pilot study of high dose EPA + DHA in post-menopausal women to assess feasibility prior to initiating a phase IIB prevention trial. Postmenopausal women with cytologic evidence of hyperplasia in their baseline random periareolar fine needle aspiration (RPFNA) took 1820 mg EPA +1530 mg DHA ethyl esters daily for 6 months. Blood and breast tissue was sampled at baseline and study conclusion for exploratory biomarker assessment, with p values uncorrected for multiple comparisons. Feasibility was pre-defined as 50% uptake, 80% completion and 70% compliance. Trial uptake by 35 study entrants from 54 eligible women was 65%, with 97% completion and 97% compliance. Favorable modulation was suggested for serum adiponectin (p=0.0027), TNF-alpha (p=0.016), HOMA 2B measure of pancreatic beta cell function (p=0.0048) and bioavailable estradiol (p=0.039). Benign breast tissue Ki-67 (p=0.036), macrophage chemoattractant protein-1 (p=0.033), cytomorphology index score (p=0.014), and percent mammographic density (p=0.036) were decreased with favorable effects in a proteomics array for several proteins associated with mitogen signaling and cell cycle arrest; but no obvious overall effect on proteins downstream of mTOR. Although favorable risk biomarker modulation will need to be confirmed in a placebo-controlled trial, we have demonstrated feasibility for development of high dose EPA and DHA ethyl esters for primary prevention of breast cancer.

Received October 2, 2014.
Revision received July 23, 2015.
Accepted August 3, 2015.

Copyright © 2015, American Association for Cancer Research

What is pain and what is happening when we feel it?

Explainer: what is pain and what is happening when we feel it?

November 19, 2015 6.11am AEDT

Disclosure statement

Lorimer Moseley consults to Pfizer, NOIgroup Australasia and worker’s compensation boards in Australia, Europe and North America. He receives Fellowship and Project Funding from the National Health & Medical Research Council of Australia. He receives royalties for several books related to pain and rehabilitation and receives speaker’s fees for lectures in Australia and abroad.


University of South Australia provides funding as a member of The Conversation AU.


If someone has a pain in his hand […] one does not comfort the hand, but the sufferer. – Philosopher Ludwig Wittgenstein, 1953

What is pain? It might seem like an easy question. The answer, however, depends on who you ask.

Some say pain is a warning signal that something is damaged, but what about pain-free major trauma? Some say pain is the body’s way of telling you something is wrong, but what about phantom limb pain, where the painful body part is not even there?

Pain scientists are reasonably agreed that pain is an unpleasant feeling in our body that makes us want to stop and change our behaviour. We no longer think of pain as a measure of tissue damage – it doesn’t actually work that way even in highly controlled experiments. We now think of pain as a complex and highly sophisticated protective mechanism.

How does pain work?

Our body contains specialised nerves that detect potentially dangerous changes in temperature, chemical balance or pressure. These “danger detectors” (or “nociceptors”) send alerts to the brain, but they cannot send pain to the brain because all pain is made by the brain.

When you’re injured, the brain makes an educated guess which part of the body is in danger and produces the pain there.

Pain is not actually coming from the wrist you broke, or the ankle you sprained. Pain is the result of the brain evaluating information, including danger data from the danger detection system, cognitive data such as expectations, previous exposure, cultural and social norms and beliefs, and other sensory data such as what you see, hear and otherwise sense.

The brain produces pain. Where in the body the brain produces the pain is a “best guess scenario”, based on all the incoming data and stored information. Usually the brain gets it right, but sometimes it doesn’t. An example is referred pain in your leg when it is your back that might need the protecting.

It is pain that tells us not to do things – for example, not to lift with an injured hand, or not to walk with an injured foot. It is pain, too, that tells us to do things – see a physio, visit a GP, sit still and rest.

We now know that pain can be “turned on” or “turned up” by anything that provides the brain with credible evidence that the body is in danger and needs protecting.

All in your head?

So is pain all about the brain and not at all about the body? No, these “danger detectors” are distributed across almost all of our body tissues and act as the eyes of the brain.

When there is a sudden change in tissue environment – for example, it heats up, gets acidic (cyclists, imagine the lactic acid burn at the end of a sprint), is squashed, squeezed, pulled or pinched – these danger detectors are our first line of defence.

They alert the brain and mobilise inflammatory mechanisms that increase blood flow and cause the release of healing molecules from nearby tissue, thus triggering the repair process.

Local anaesthetic renders these danger detectors useless, so danger messages are not triggered. As such, we can be pain-free despite major tissue trauma, such as being cut into for an operation.

Just because pain comes from the brain, it doesn’t mean it’s all in your head. from

Inflammation, on the other hand, renders these danger detectors more sensitive, so they respond to situations that are not actually dangerous. For example, when you move an inflamed joint, it hurts a long way before the tissues of the joint are actually stressed.

Danger messages travel to the brain and are highly processed along the way, with the brain itself taking part in the processing. The danger transmission neurones that run up the spinal cord to the brain are under real-time control from the brain, increasing and decreasing their sensitivity according to what the brain suggests would be helpful.

So, if the brain’s evaluation of all available information leads it to conclude that things are truly dangerous, then the danger transmission system becomes more sensitive (called descending facilitation). If the brain concludes things are not truly dangerous, then the danger transmission system becomes less sensitive (called descending inhibition).

Danger evaluation in the brain is mindbogglingly complex. Many brain regions are involved, some more commonly that others, but the exact mix of brain regions varies between individuals and, in fact, between moments within individuals.

To understand how pain emerges into consciousness requires us to understand how consciousness itself emerges, and that is proving to be very tricky.

To understand how pain works in real-life people with real-life pain, we can apply a reasonably easy principle: any credible evidence that the body is in danger and protective behaviour would be helpful will increase the likelihood and intensity of pain. Any credible evidence that the body is safe will decrease the likelihood and intensity of pain. It is as simple and as difficult as that.


To reduce pain, we need to reduce credible evidence of danger and increase credible evidence of safety. Danger detectors can be turned off by local anaesthetic, and we can also stimulate the body’s own danger-reduction pathways and mechanisms. This can be done by anything that is associated with safety – most obviously accurate understanding of how pain really works, exercise, active coping strategies, safe people and places.

A very effective way to reduce pain is to make something else seem more important to the brain – this is called distraction. Only being unconscious or dead provide greater pain relief than distraction.

In chronic pain the sensitivity of the hardware (the biological structures) increases so the relationship between pain and the true need for protection becomes distorted: we become over-protected by pain.

This is one significant reason there is no quick fix for nearly all persistent pains. Recovery requires a journey of patience, persistence, courage and good coaching. The best interventions focus on slowly training our body and brain to be less protective.

Feel-good exercise hormone irisin is real

The verdict is in: feel-good exercise hormone irisin is real

August 14, 2015 8.27am AEST

The hormone irisin is one of the things that makes exercise good for us. will ockenden/Flickr, CC BY

Working out, feeling good

Irisin received a lot of attention recently because of divisions in the scientific community about whether or not it actually existed.

Irisin’s discovery in 2012 was exciting because scientists had potentially found one reason why exercise keeps us healthy.

When irisin levels were increased in mice, their blood and metabolism improved. Results from human studies are still mixed as to what kinds of exercise raise irisin, but data suggest that high-intensity training protocols are particularly effective.

Professor Mark Febbraio, Head of the Cellular and Molecular Metabolism Laboratory and Head of the Diabetes and Metabolism Division at the Garvan Institute for Medical Research, said that the form of mass spectrometry used in the new study was far more accurate and reliable in measuring irisin.

“Using state-of-the-art technology, the researchers have proven beyond doubt that irisin is real. It settles the argument,“ said Professor Febbraio, who was not involved in the research.

Previous studies using commercially available kits called “ELISA” kits detected the presence of irisin, by recognising an antigen, in samples, which could produce inconsistent results with irisin, he said.

A pathway to benefits for other ailments

Febbraio said confirming the existence of irisin is a step towards potentially developing therapeutics that could benefit individuals with metabolic disease and obesity.

“There is a possibility they could make drugs that target the pathways that are activated by irisin” to produce similar affects of exercise on maintaining body weight, particularly for those who can’t exercise, he said.

However, he is sceptical about irisin being turned into a miracle injection, saying such a product would be “somewhat simplistic and fanciful”.

At this stage further studies are necessary to fully understand how the hormone works in humans, specifically how it relates to brown and beige fat tissue and energy use but it is an important breakthrough.

“It is basically another example that exercise can have multiple benefits to general health and wellbeing,” said Febbraio.

Dr Paul Lee, a research officer at the Garvan Institute who specialises in endocrinology, described the finding as “a remarkable step forward.”

“The study shows that irisin circulates in humans and it increases after exercise. What awaits exploration in future studies is the biological function of irisin in humans,” he said.

Do you really need a detox?

Do you really need a detox?

January 5, 2016 6.15am AEDT

Disclosure statement

Veronique Chachay does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond the academic appointment above.


University of Queensland provides funding as a member of The Conversation AU.


Early in the New Year is the traditional time for setting ambitious goals for better health, fitness and, often, a slimmer body. This resolve commonly reflects guilt stemming from the dissipation of the preceding festive season – and it often starts with a detox.

It’s unclear where the idea of an in-depth body cleanse or “the detox cure” comes from, but it’s worth noting that many traditional and complementary medicine practices describe cleansing and detoxification as a way to avoid illness, or engender wellness.

They’re based on the idea that “toxins” accumulate and the body needs regular purification. They cover everything from enemas and colonic irrigation, lemon juice detox or water fasts to exclusion of certain food groups, purging with herbs, large-dose nutrient supplementation and sweat lodges, among other things. And they’re generally a waste of money and effort.

Detoxing from what?

In medical terms, detoxification means removing poisons or the build-up of toxic substances, when large amounts have been consumed or have come into the body through inhalation or skin exposure. It’s only used when the amount or type of substance is such that our body’s natural detoxification systems are unable to clear it.

The body’s detoxification system uses the skin (via sweat and sebum), liver and gall bladder (bile), kidneys (urine), lungs, lymphatic system (lymph) and intestines (faeces) to get rid of toxins.

The toxins can be from both internal and external sources. Internal sources include the by-products from usual physiological processes and cells’ waste products. The process of breaking down food components to produce energy uses oxygen, for instance, and results in unstable molecules called free radicals. These molecules must be neutralised or converted to avoid build-up to toxic levels.

External sources of toxins can come from food and beverage-related compounds – molecules resulting from baking, deep-frying and char-grilling, as well as alcohol and additives in processed foods. Then there’s medication, tobacco smoke and exposure to environmental pollutants, among other things.

Toxic life

Many toxins from external sources (also known as xenobiotics) are fat-soluble and can accumulate in fatty tissue. Exposure to these has considerably increased with modern lifestyles because of industrial waste contaminating soil and water and, in turn, agriculture products and seafood.

Agriculture practices also use a variety of chemicals, resulting in residues in food products. And cosmetics, body care products, as well as plastic food and beverage packaging, all increase our exposure to a variety of chemicals.

These kinds of exposure are often used as the main rationale for commercial detox programs. In the absence of robust human data on acceptable non-harmful ranges for all the chemicals in our environment, the argument goes that any small amount may be toxic and should be removed. But our bodies are purging these chemicals all the time.

Not consuming unhealthy food will reduce the amount of detoxification your body needs to perform. Carlos/Flickr, CC BY-NC-ND

Anyway, no one-off detox regimen can “erase” the effects of weeks’ worth of excess and years of sluggish lifestyle habits. There’s no scientific basis or high-level evidence showing the benefits of commercial short-term detox programs.

Still, there’s good news too: your internal detoxification system, which includes numerous organs and enzymes coded for in your DNA, works around the clock to process toxins as needed.

Not consuming any alcohol, or masses of chocolate and fried food, for a few weeks may (depending on what you’re eating in their stead) reduce the amount of detoxification your body needs to perform. But real good happens over the long term. And anyway, all the alcohol you’ve drunk in the last few weeks has already been dealt with – principally by your liver – to avoid harmful effects.

Natural detoxification

Among its over 500 functions, the liver metabolises and detoxifies any dietary constituents (including caffeine or herbal teas and supplements) and any external toxins entering the body from a variety of exposure.

Detoxification is a three-step process. In the first two phases, fat-soluble compounds are converted to water-soluble compounds. And the third facilitates transport of the converted products out of the cells, then out of the body via the bile and faeces, or urine.

The internal production of toxins, such as free radicals, is kept under tight control by a sophisticated mechanism involving genes that code for antioxidant enzymes. Indeed, enzymes play a key role in detoxification and when there’s more to detoxify, the body produces more enzymes.

While the liver is the star of the show, most tissues in the body also participate in detoxification. But the differences between individual genetic profiles mean there can be large variation in responses to toxin exposure.

Vitamins and minerals in food are crucial for the optimal function of detoxification pathways and the function of enzymes. But this doesn’t mean you should consume large doses as that can also result in toxicity.

The crux of the story is that the human body is a comprehensive, self-mending, self-detoxing apparatus. It will perform its detoxification tasks regardless of whether you’re undertaking a rigid detox cure, or a gourmet food and wine tasting marathon. But providing the right ingredients for optimal function daily, rather than opting for a quick-fix detox, is the key.

Breast Cancer Treatment and D.C.I.S.: Readers React


A mammogram of a female breast shows a non-invasive cancerous tumor.CreditKings College School of Medicine/Science Source

An article Thursday on the results of a study indicating that aggressive surgical treatment of a possible precursor to breast cancer may be unnecessary prompted a wide range of responses from readers, among them anger, sadness and relief.

Many commenters said they — or their wives,mothers, daughters or other family members — had undergone either a lumpectomy or a mastectomy after receiving a diagnosis of ductal carcinoma in situ, or D.C.I.S., which involves abnormal cells confined to the milk ducts of the breast. The study’s lead author concluded that these procedures are not the best option for most women who have what is commonly called “Stage 0 cancer” because an analysis of 20 years of data showed the course of treatment made little difference in patients’ outcomes and that the chance of these patients dying from breast cancer was about the same as the general population.

“I think the best way to treat D.C.I.S. is to do nothing,” Dr. Steven A. Narod, the lead author of the study, which was published in JAMA Oncology, is quoted as saying in the Times article.

Readers whose surgery turned up more advanced cancers disagreed with Dr. Narod’s position. Many expressed relief about the choice they made.

“I will not be the statistic representing those who did not act,” said Aurace Rengifo of Miami Beach, Fla., who said she received a diagnosis of D.C.I.S. in 2006. “After my lumpectomy, it was detected that my cancer was not grade 0 but grade 1. I also had radiation therapy. I am, thank God, in remission and I would do it again in the same situation.”

Jennie Thompson of San Diego said that after she had a mastectomy, “analysis of the tissue post-surgery revealed many areas of cancer throughout the breast.” She concluded: “Losing a breast is nothing compared to living with fear the cancer will resurface.”

E. Rosner of Berkeley, Calif., said she sought a second opinion after a D.C.I.S. diagnosis and lumpectomy in 1998. “In my case, a lymph nodedissection (during a 2nd surgery) revealed 1 positive node and changed my diagnosis to invasive cancer, leading me to undertake chemo and radiation (both of which treatments I definitely would have avoided otherwise). No way of knowing this, but I suspect that had I moved forward with the false D.C.I.S. diagnosis, I’d be dead by now.”

Other readers were angry to learn they might have undergone possibly unnecessary procedures.

“Suspected this all along,” said SK of Concord, N.H. “Knowing it was probably unnecessary was the hardest part of treatment for me.”

“I had needle core biopsy, 2 lumpectomies, radiation and am going to soon undertake hormone therapy. I realize I do not have invasive cancer and am grateful,” said Cindy of Oregon. “But yes, I say, it was brutal.”

But even readers upset by the news differed on whether they would take the same course of action again.

“I railed against the idea of there being a ‘Stage 0’ cancer. It still infuriates me that I went through surgery (lumpectomy) and radiation treatment for what I believed at the time was possibly a ‘blip’ rather than a serious cancer,” said Judith of Asheville, N.C. “Waiting and watching is a good idea and what I wish I had done.”

Kathy Daly of Denver, Colo., said she was received a D.C.I.S. diagnosis in January 2014 and then one of melanoma in October 2014. “I then discovered that the incidences of melanoma for those having been treated for breast cancer are higher than the statistical norm. So, to read this article and realize that all or most of this could have been avoidable is very disconcerting. (And, as I type this, I am experiencing a whopper of aTamoxifen induced hot flash!),” she said. “At the same time, I cannot imagine doing nothing and just waiting.”

Some called the push to operate a money grab by doctors.

“I am angry as hell at this assembly line they stuck women on,” wroteNuschler from Cambridge, Mass. “Because it made people a LOT of money. That month in October of pink ribbons, pink N.F.L. uniforms and 10K runs raised a lot of cash. And surgeons and radiologists and med centers jumped in and grabbed as much cash as possible. Even second and third opinions said the same thing! And I’m an MD!”

Winker of Atlanta wrote: “Women do not overestimate their risk, they have been encouraged to overestimate the risk. Physicians make a lot of money by aggressively treating 97 percent of the D.C.I.S cases and it is a battle for every recommended treatment a woman tries to refuse. It is tragic, it is barbaric and as someone affected by this, it is beyond infuriating. ”

Get multiple opinions, urged many medical professionals who wrote.

“Would like to encourage women everywhere to get a second opinion on treatment from a ‘compassionate conservative’ and don’t forget about a second opinion on your pathology. Doctors are human after all and mistakes happen,” said Gemma of Austin, Tex., a pathologist.

Des of Worthington, Ohio, said, “As a physician involved in breast cancer treatment, I would agree with the general philosophy that many times less treatment is better. But treatment needs to be individualized to the patient and based on data and personal preference, not on anecdotal stories of treatment gone horribly wrong. My recommendation would be to seek care at a tertiary facility that specializes in breast cancer treatment to make the most informed decision about your care if you have access to such a place.”

The Use of High-Dose Estrogens for the Treatment of Breast Cancer

Most women have an erroneous view of the effect of oestrogen on breast tissue. For many years the standard treatment for breast cancer was high dose oestrogen.!!. Of course, we do not treat breast cancer with oestrogen routinely now, as there are better treatments available. However, we should not be as scared of oestrogen as at present.
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