Spring is coming! (to the southern hemisphere) so i’m excited to think about growing edibles in the garden once more. I’d really like to be successful at growing lettuce (and other leafy greens). It’s essential for making the healthiest salads and i’d like to stop buying the plastic bags of salad mix we currently rely on (whole heads of lettuce seem to be too much for our needs, and not as tasty as the mixes anyway). My previous half-hearted attempts have not been all that successful, unlike the extremely easy to grow tomatoes and herbs. One impressive hardy lettuce survived the winter frosts (we’ve had nights down to about minus 8 degrees Celsius).
Of course it was the red lettuce, which is a little bitter to eat on it’s own. Perhaps the perfect dressing would solve that? While i was pondering this someone else liked the flavour so much they ate the whole lot:
Luckily, it seems to be recovering already with new leaves appearing on those stripped stems.
Also, the broad beans are now flowering! Fresh broad beans are the best, I might have to install some sort of anti-possum security in case they try and get their hands on these too.
Oh, and i should mention that the broad beans were planted not just for their lovely beans. When we moved here last year we were really pleased that there were already multiple little vegie garden beds set up. The soil in these beds clearly hadn’t been tended though, it was compacted and nutrient poor. I’m digging in compost whenever i can, but the broad beans will also add an injection of nitrogen. This should help for an even more productive tomato crop over summer. Perhaps this year i’ll make my own passata??
Before starting this blog I thought long and hard about the responsibility of science communication. This blog was started as a way for me to consolidate my growing understanding of a health issue of mine*. If gathering sources of evidence to help me learn and make choices also helps someone else with this rare condition (POI affects about 1% of women of my age, fewer women at younger ages) then that’s great. But I’ll always need to stress that none of this is advice. I am in no way an authority on ovarian health, female fertility, human reproduction or even human biology. After my initial medical appointments I had to look up ‘luteal phase’, ‘dominant follicle’ etc etc (Wikipedia is fantastic for these ‘revision’ type questions, where you know there is a textbook answer).
That leads to my next point; accepting knowledge from an authority is not the only way to learn. This is what a research degree (such as a masters or a PhD) teaches you; how to assimilate and analyse information to come to new and interesting conclusions. I’ve been lucky enough to complete my PhD and gain some additional research experience after that, and I’m sure my research skills have improved greatly along the way. But certain aspects remain difficult. That sounds like a negative point but it also highlights something quite positive. I believe that anyone can research, anyone can delve deeply into a subject that they are motivated to learn about. No promises that it won’t leave you feeling mentally fatigued, or that you will be rewarded with answers/conclusions. If done properly I can guarantee that you will be left with more questions than you started with. Each time I research a new topic area there is a huge learning curve purely because of lots of new material. I would hazard a guess that the mountains of information are predominantly what dissuade people from research in the first place. I advise students to get their head around the language of a subject area first, build a glossary if you will, and half your learning curve will be conquered.
Not only do I believe that people are generally capable of research, I also wish that more people were interested in doing so. Oh boy, this topic could really get me ranting and it’s a hugely complex area that deserves more than a flippant blog post… Suffice to say, I think that more people being interested in science, learning about science, discussing science and contributing to science is a wonderful idea. So I was a little disappointed to see this on social media:
Context: there is a battle going on between ‘science advocates’ and ‘pseudoscience’. The battleground is social media. I 100% understand where Biology Babe is coming from. Certain businesses thrive off sounding sort of scientific in order to sell stuff (cosmetics, ‘eco’ products, food, news). People (including science advocates) ask for claims to be supported by evidence. Then things get a little murky. There are, indeed, some dicks out there.
What disappointed me was the thought that someone would be dissuaded from even dipping their toe into the vast resources available. Some people misuse scientific references in order to sell a product, others may simultaneously misunderstand a scientific reference (or two) while having an emotional reaction to a subject and subsequently miscommunicate science. I see both of these things as fairly inevitable. People will always want to sell you something (even if just an idea) and we are ALL emotional beings (yes! Scientists too!). The real issue lies in the next step. The next step should be carefully considered discussion and I personally would like to see more people getting involved.
The main trick of course is scepticism, but not just scepticism applied to what you are reading, but also scepticism applied to your own understanding. You have to be prepared for continual learning and readjustment of old ideas. You have to be aware of your own biases, how your hopes and worldview might affect your convictions. And you have to be prepared for questions. It’s all really mature stuff.
Alternatively, more often than not we won’t want a thing to do with any of the ‘source material’ (the actual scientific data) and instead are looking for more easily digestible material to learn from. In a future post (soon! maybe tomorrow!) I’ll post some of the best resources that I know of for learning about biological stuff.
*Balanced by discussion of something I find uplifting, sustainability
After my last appointment with the doc in June a little voice in my head starting getting louder and louder: “well, DO you feel menopausal?”. Symptom monitoring became a bit of a problem. One night I even woke and freaked out a tiny little bit when I discovered I was sweating and that was why I had woken. It turns out there were just too many blankets on the bed, my husband was also sweaty. The doc would like to see me on HRT, I know that is the current medical advice and that she has a duty of care. I’m just not a fan of the idea because 1. What if it prevents me from ovulating? (even though that is not happening) 2. I will lose touch with what my body is doing, I won’t actually know if I am still ‘menstrual’ 3. I’m just a bit stubborn and don’t like taking pills 4. I’m scientifically curious, and want to see the data that justifies the prescription
Some of the available information on POF/POI is quite depressing, equating the whole thing with menopause, with concurrent risks of everything from osteoporosis to heart disease to mental confusion. The thing that troubles me is that I know that some of these pathologies are difficult to pin on menopause as opposed to aging in general. The one risk that is stressed for POI ‘sufferers’ is osteoporosis, but I’d still like to see conclusive data that that risk alone is enough to justify me taking HRT for more than a decade.
In the meantime, this review was published earlier this year and i finally got around to reading it properly. It looks at AMH as a marker of ovarian reserve and what that might tell us about cardio-metabolic health (i.e. are POI or PCOS or both (!) associated with heart disease and the like). The authors seem almost disappointed that there is no conclusive relationship between AMH and heart health but for me it was good news, of course.
I think it’s worthwhile that they consider opposing ideas re: any connection between cardiovascular risk and ovarian function. That is, that a lack of oestrogen from the ovaries leads to poor cardiovascular health or that poor vascular health leads to a loss of ovarian function. Alternatively, the idea that POI is a sign of advanced aging in general is also considered. They do cite an interesting study looking into telomerase in granulosa cells (those that surround follicles) of women with ‘diminished’ or normal ovarian reserve. However, I’m not sure that reduced telomerase activity in a particular cell type can tell you much about the whole body? (I suspect there is published evidence to help answer this question, but I’ll save that for another day).
Oh and I’m doing fine with symptom monitoring now. If I feel sluggish, lacking in energy, sensitive to discomfort and slightly emotionally unbalanced it’s generally because I have forgotten to exercise for a few days (blame it on the rain).
A new article out this week caught my eye after writing about menstrual cycles last week – Zhang et al. This is a ‘short communication’ type article, so not a study itself but a report on a new technique. The new technique is based on the ‘wave theory’ of follicle recruitment, leading to ovulation (and indirectly, menstruation). I had read about this recently (sorry, I can’t remember where!) as I try to learn more about the biology of ovulation.
Data that supports multiple waves of growing follicles has been available since at least 2003. In Baerwald et al. 2003, normally menstruating women were found to have 2-3 waves of growing follicles occurring in between two ovulatory events (as opposed to one burst of growth and then a rest or a more continuous process). Perhaps surprisingly, some women were found to have follicles that grew to a preovulatory size (>15mm) even though they were in the luteal phase of their menstrual cycle (i.e. after ovulation for that menstrual cycle). The authors note the potential for utilising this information in assisted reproduction.
Ten years later, the results of a large study showing that viable eggs can be harvested in the luteal phase is published by Kuang et al.
This was a feasibility study, which may explain the restrictions placed on the patient cohort, these were not poor responders, they were ovulating women. 93% of the patients produced eggs that led to high quality embryos that could be frozen (fresh transfers are not possible with this protocol). The main results stressed by the authors are successful pregnancies. However, I wonder if any of these were natural conceptions? Since embryo transfer was performed during some natural cycles this seems at least possible? Similarly, and slightly worrying was the rate of ectopic pregnancies at 3.2% (cf. a rate 1.2% seen after frozen embryo transfer in a large study)
Another study published by the same team, is somewhat more impressive in that oocytes were retrieved from poor responders twice within a cycle. Statistically more oocytes were retrieved from the second stimulation, although there was no difference in number of metaphase II oocytes retrieved. Therefore, even though a higher dose of gonadotropin was used for the second stimulation a larger number of useful oocytes were not obtained. This study had similar limitations to the one noted above in that they are both single-arm studies (no control group) and there may be natural conception that is not accounted for. Some of the women studied were not poor responders due to an actual poor response to a previous stimulation attempt but must have been recruited on another basis (actually 31.6% of the patients). All of the patients had a basal FSH reading under 13*.
Concerns over effectiveness notwithstanding, the idea that more oocytes can be retrieved seems promising. Further support for the idea of double/dual stimulation and more explanation can be found in Moffat et al. 2014.
*On a personal note, my FSH is a good deal higher than this at around 40, and double zero is still zero (how many eggs i would expect to be retrieved). So while a double stimulation is not something i’m going to try myself, i’m happy to practice my science reporting skills in case this is useful information for anyone else. Disclaimer: none of this is medical advice, i am not an expert in assisted reproduction techniques or even human biology.
I had an appointment booked with the infertility specialist this week, but I cancelled it. I had additional blood tests done in June (estradiol, FSH, AMH, maybe a few others) so the point of this appointment was to discuss those results and for me to get advice in regard to HRT (hormone replacement therapy). I’m still reluctant to go on HRT. A good reason for that is that I have not been feeling ‘menopausal’. So I don’t need pills to manage symptoms because there doesn’t appear to be any. Taking pills as a preventative to ward off osteoporosis, heart problems and mental deterioration is a whole other consideration, and one that I’ll save for a future blog post.
So, no pills because nothing is wrong, .. or is it?
At my last appointment the first question was whether I had been having hot flushes/night sweats. No. The next question then was, had I had any menstrual periods? Yes! I was happy to report that while my menstruation had been a bit haphazard over the last 6 months or so, my last menstrual period was a satisfyingly normal 27 days. It was light, but took the standard 4-5 days and occurred along with strong cramps. I joked that it was just like the periods I had when I was a teenager so that is how I knew it was really menstruation (as opposed to spotting). The doc agreed that it was a real period.
But that was 2 months ago now and I haven’t bled since. Crap, so that 27 day period was not a sign that my exercise and low-stress lifestyle were paying off, I am still ‘irregular’. But I actually always have been, as far as I can recall. It’s hard to say, because I was on the pill so often. Thinking about this, I wondered what the variability is, between women and within individuals and how do we know what a pathological state looks like?
I should mention why this is all so interesting to me. I look forward to a menstrual period because it is an indication of ovarian activity. You can have an anovulatory period (menstruation but no ovulation) but the only time that you can have the opposite (ovulation but no menstruation) is pregnancy. So I end up taking a lot of pregnancy tests. A negative pregnancy test used to put me in a bad mood for an entire day but these days it hardly bothers me at all. Each day past the 28 day mark though, has the potential to make me wonder if my last period was my LAST period. There’s also the annoying, constant, nagging thoughts of ‘should I be doing something about this? Is there something I should not be doing??’
Having some sort of explanation always helps me turn off those annoying intrusive thoughts. For this reason, it was excellent to find Treloar et al. 1967. This is an old paper that contains evidence for an average menstrual cycle/interval being 26-30 days long. This is what we are all taught in school. What these authors appreciated, and reiterated many times throughout this 50 page article (scientists were more verbose back in the day) is that a 28 day cycle might be expected as an average figure, across populations and throughout the most fertile years of womanhood, but by no means should any woman expect any particular menstrual period to be 28 days long.
In fact, only one almost perfectly regular woman was found. This woman’s periods were 28 days long for 2 years, all except for one interval which was 27 days. It surprised me to find that this woman ended up having a hysterectomy! (see Treloar pg. 109) Although this may have had very little to do with whether her ovaries were performing wonderfully or otherwise.
My cycles are certainly unusual. Figure 3 in Treloar (pg. 88) shows a beautiful figure constructed from the statistical frequency of menstrual period length/interval against age. I’ve read from plenty of other sources that menstruation becomes more irregular as menopause approaches. I don’t remember being told that the same thing happens in reverse at the other end (menstruation is often irregular in the years following menarche). Any interval over 3 months is quite rare though, at any age.
What truly amazed me in this article was Figure 14 on pg. 110. This figure charts the menstrual periods for one of the most irregular women in the study. The intervals in between menstruation were often very long (the longest being 30 weeks!), with her menstruation only becoming somewhat regular after the age of 40. I have to wonder if this woman would be diagnosed as POF/POI these days? What is necessary for a diagnosis is an interval of 4-6 months*, low antral follicle count and either high FSH/low AMH. All of these things co-occur, and plenty of doctors still claim that these are all signs of impending menopause**. If this particular individual had been tested for serum FSH/AMH at the age of 22, after not menstruating for 6 months, would she have been told that she had ovarian failure and that she would never have her own biological child? Instead, this woman went on to have three children. Intriguingly, these pregnancies are seen to occur directly after long periods (10, 18 or 27 weeks). This is enough to satisfy me that abnormally long periods, as an individual factor, are not sufficient to give up all hope of ovarian function (which I knew anyway, but so so nice to have confirmatory data).
Of course I have to stress this caveat: this woman had all of her pregnancies before the age of 34.
Nevertheless it was quite rewarding to ponder biological variability in relation to my not-so-monthly bleed***. Research scientists in the field of biology have to tackle variability as a challenging aspect of their data, but it’s nice to be reminded that the most probable state is not the only viable one.
Treloar et al. 1967 is a great article, this is further evidenced by the 995 times it has been cited. I’ll continue to dig through these and other more recent studies to learn more about ovulation etc.
*I actually don’t yet fit this diagnostic criterion because my longest interval has been 15 weeks. There are no strict diagnostic criteria anyhow, though.
Bulk buying of foodstuffs satisfies a bunch of my sustainability desires:
reduced amount of packaging
less shopping trips
forces me to make stuff from scratch
No 1. was my initial motivation. Landfill is just waste, so i started cutting down on non-recyclable waste a while ago. Now our little household of two only produces one small grocery bag of rubbish per week.
Ideally our local health food store (where i get my dried beans) would have a dispensing system, but I think getting their 3kg bags is still better than many cans of beans, even if those cans are recyclable. I make my own refried beans now 🙂
Oil and rice are no-brainers, i’ve been buying these in bulk always. I’ve yet to find the best supplier of olive oil in Canberra though, let alone other European delicacies. There are a few small deli’s that have a good range but they overcharge. I have been known to drive a tin of olive oil back from Melbourne (a 7 hr drive).
This was my first bulk purchase of flour though:
It was daunting as i’ve never been a baker (pizza dough doesn’t seem to count). Luckily, i came across this great instructional:
I did make a rookie mistake though and ruined a favourite kitchen item while embarrassingly forgetting some simple physics. The instructions mention using a cast iron pan and ice cubes to create steam (for an excellent crust). I didn’t have any cast iron or ice cubes so thought i’d try a ceramic dish and water, not a smart move.*
I’ve also been buying vegetables ‘in bulk’. Not really though, as that doesn’t make sense with perishable items. I just decided i didn’t want to buy plastic-wrapped vegetables anymore. This means buying the whole pumpkin/squash, cabbage etc instead of a wedge. This means you have to cook more, and also forces me to try new recipes (to avoid boredom). It turns out you CAN eat red cabbage all week without getting bored. Sometimes you might have to resort to giving away food/inviting friends around to help you eat it all. This is also not a problem.** Oh, and stocking up the freezer with home-made handy meals (this is why i didn’t have ice-cubes! you also have to remember to eat the frozen meals).
*I’ve since used a metal cake tin with ice-cubes, that seems to work ok, as long as you pre-heat the oven enough (but not for 50 min!). I also didn’t use any plastic wrap, it’s completely unnecessary. I just covered my bowl with a tea towel and left it next to a sunny window to prove.
** Also, in case anyone is wondering, I personally have no problem with cutting my own wedge/section off a hard vegetable such as pumpkin or cabbage and putting the rest back in the fridge, uncovered. The cut edge may look ‘icky’ after a day or so but that is a result of it drying out. This is not a problem, in fact i think it’s a better protective layer than plastic wrap when you consider water availability and bacterial growth.
“It starts with the egg”, Rebecca Fett, 2014, ISBN 978-0-9911269-0-3
This book review is actually just a chapter review. Chapter 2 of this book is titled “The dangers of BPA”. That in itself was enough to tell me that although this book is presented as a well-researched, evidence-based, non-biased view of the science of egg quality, it may be something less than those lofty ideals. So I skipped to the chapter on DHEA.
I read the chapter on DHEA in detail and checked most of the references therein (ignoring those regarding miscarriage and dosing). This was sufficient for me to not recommend this book to anyone else. Upon initial reading it does seem like the author has done a fair deal of research and analysis, but it is also easy to see that results are highly overstated: eg. “extraordinarily successful results from the use of DHEA” pg. 171. Not every fertility specialist will suggest you take DHEA for low ovarian reserve and that is because there are NO extraordinary results. Instead, there are quite a few studies with potentially interesting preliminary results but each of these studies has serious limitations and should therefore be taken with a grain of salt. Even an abundance of such studies does not constitute convincing evidence. For now i’m going to assume that anyone reading my blog is interested in an evidence-based view of the DHEA literature and has a basic understanding of how to assess clinical data including a basic understanding of statistics. It appears that Rebecca Fett does not. Either that, or there is wilful manipulation of information. This is illustrated by certain errors such as the following:
On pg. 156: “Because it [DHEA] is a precursor to estrogen and testosterone, when taken as a supplement it can increase the level of these hormones in the ovaries.” The citation given for this ‘fact’ is Wiser et al. 2010*. The findings in this article are: “The DHEA group demonstrated a non-significant improvement in estradiol levels on day of hCG (P[sic] = 0.09)”. This is hardly evidence that DHEA supplementation resulted in increased estradiol and therefore shouldn’t be used as a source for the quoted ‘fact’. Additionally, the article does not mention any testosterone measurements whatsoever.
The most interesting citation has to be an actual, prospective, placebo-controlled, randomized trial of DHEA (as proudly stated in the article title**). In this case, Fett has correctly cited this article to show their finding of more developing follicles in the DHEA treatment group as compared to the control group. Although, Fett states this finding occurred “after three to four months”. What the data actually shows is one statistically significant finding after 12 weeks of treatment, but the groups were no longer different at 16 weeks or 20 weeks (DHEA or placebo was taken for 16 weeks). This pattern of one significant finding amongst many weeks of no difference is not explained or accounted for. Wouldn’t you expect the effect to be cumulative? Fett implies as much throughout her chapter. Additionally, it can be seen that the size of the ‘effect’ or difference was very small, with the DHEA group showing 1-5 antral follicles and the control group showing 0-2. A sense of the natural variation can be seen with the placebo group, with results of between 0-4 antral follicles over the study period. As can be seen from Fig. 5 in the article, these results equated to 2 women having at least one follicle >10mm at week 12 compared to none of the women in the control group. No statistical analysis was carried out on these ‘percentage of women having at least one follicle >10mm’ comparisons.
This seems to be another small hint towards real evidence, helped by the study design but hindered by the size of the study. Luckily, the same authors have published a slightly larger study that looks eerily similar, just a few months after the initial study***. Unfortunately, this time no difference was found between antral follicle count at week 12. At least this time these authors suggest caution in interpreting their results due to the still small sample size. This second article was published after Fett’s book, although the conclusions had already been published in an abstract here: http://www.fertstert.org/article/S0015-0282(13)02300-5/pdf
Basically, at the time of publication of Fett’s book there was little in the way of quality data to support a recommendation of DHEA to women with low ovarian reserve/POI. Fett does admit as such, and mentions that this treatment is therefore criticised. At this point Fett raises an analogy to folate, but it is a very confused analogy.
“Thirty years after the initial discovery of folic acid’s benefits, we know that the early doubts about the value of folic acid in preventing birth defects probably caused many tragic outcomes that could have been avoided if medical advice had kept pace with research.”
This is an unfounded and backwards comment and once more seems to be either an inadequate understanding of the source material**** or a manipulation thereof. It’s true that a proper trial of folate was delayed 10 years but this was because the medical advice was to take folate supplements, even though the evidence was lacking. This is clearly the direct opposite of the current situation with DHEA. The ‘controversy’ mentioned in the articles cited by Fett had nothing at all to do with the ‘doubts about the value of folic acid’ but rather the opposite. Perhaps Fett has been confused over a more highly discussed controversy regarding folic acid/folate, which is the question of whether basic foodstuffs should be supplemented with this chemical so that all women are thereby ‘supplemented’ whether they are procreating or not.
In short, this book does not present a rigorous analysis of the available science and is written from the emotive standpoint of ‘those trying to conceive should try anything that may increase their chances’. I know that is a common standpoint in the infertility world but doctors are rightly wary of selling false hope, and I for one am grateful for that.
When i carried out a (quick) review of the literature on DHEA and fertility the other day i kept the focus of looking for data that might be useful to my own situation (very low ovarian function). In the process some other interesting information came up though. Perhaps this post will be intriguing to anyone who stumbles across my blog, although it comes with the caveat that i haven’t done much analysis into this subject. I don’t have to worry about miscarriage seeing as i’m not releasing eggs.
The most interesting article that turned up in my search of recent papers mentioning DHEA was not actually concerned with patients with diminished ovarian reserve. It was interesting because it is one of the few studies with DHEA and fertility that is from a double-blind, randomised, placebo-controlled trial*. Some findings of this study actually contradict earlier studies on DHEA and ovarian function, in that these women undergoing IVF did not produce more oocytes when given DHEA. Although, it must be remembered that this study involved women with normal ovarian reserve (high AMH level, high antral follicle count) and therefore is not directly comparable to studies of women with low ovarian reserve/function. Also, it is not known how DHEA (endogenous or otherwise) contributes to ovarian function. Without a mechanism of action to guide hypotheses, previous studies have investigated the use of DHEA to improve ovarian response in a quantitative manner, i.e. does DHEA treatment along with stimulation protocols result in more eggs to use in assisted reproduction?
This new study provides a suggestion that DHEA might not be useful to the issue of quantity, but rather quality. Women in the treatment group had a higher live birth rate (the one measure that the patients are really interested in!). This was not attributable to a higher pregnancy rate (similar in both groups) but seemed to be due to the miscarriage rate (none of the DHEA group pregnancies resulted in miscarriage, whereas 5 of the control group did). This is an interesting result due to the nature of the study. The patients enrolled in the study essentially had unexplained infertility, with age being the only indication of reduced ovarian function, and the randomisation of the patients appears to have been carried out without bias.
The authors (Tartagni et al.) speculate that their results are due to a difference in aneuploidy rates. They cite some earlier work from the Gleicher lab (at the Center for Human Reproduction, where the patent for using DHEA for DOR is held) to support this hypothesis. These earlier publications do not constitute strong evidence simply because they are case-control studies rather than randomised, prospective studies. Gleicher et al. 2010** for instance shows some difference in aneuploidy between women who had taken DHEA and controls who had not. However, I had some difficulty in understanding how the case reports were assigned to the two groups. The authors admit that the treatment group were those that were assessed as having lower ovarian reserve (surely this constitutes a confounding factor then?). Of note is a very odd error in that the authors at this point cite themselves (for AMH levels used to determine DOR), or at least appear to, in a citation that doesn’t exist:
“13. Barad DH, Weghofer A, Goyal A, Gleicher N: Age-specific anti-Müllerian hormone (AMH): Utility of AMH at various ages. Reprod Biomed Online .” This citation is clearly lacking some details (year?, journal volume?), additionally a search of the exact title as cited on google scholar or the journal website yields no such article.
A newer article from the Gleicher lab***, published after the Tartagni study confuses matters again. This analysis is a little different in that it is not concerned with DHEA supplementation really, but with endogenous androgens (DHEA and other hormones produced in the patients bodies themselves). Levels of androgens were expected to correlate with levels of aneuploidy in embryos from the women, but no such correlation was found. The authors claim there are previous reports of an association between aneuploidy and low androgen concentrations:
“Only two possible explanations come to mind: In the literature reported associations between LFOR and in-creased aneuploidy [4,5] and of increased aneuploidy with low androgen concentrations [7,8] are incorrect. While a possibility, we consider this a less likely explanation.”
7. Gleicher N, Weghofer A, Barad DH. Dehydroepiandrosterone (DHEA) reduces embryo aneuploidy: direct evidence from preimplantation genetic screening (PGS). Reprod Biol Endocrinol. 2010;8:140.
8. Gleicher N, Ryan E, Weghofer A, Blanco-Mejia S, Barad DH. Miscarriage rates after dehydroepiandrosterone (DHEA) supplementation in women with diminished ovarian reserve: a case control study. Reprod Biol Endocrinol. 2009;7:108.
Not only does this statement stand unjustified (no reason given for why they think it is ‘less likely’) but the references given in the case of the low androgen vs. aneuploidy are not adequate citations, even though they are their own work. That is, no association between androgen levels and aneuploidy is reported in these articles, no androgen levels are reported at all. The patients may well have been assumed to have low androgen levels, but this is hardly evidence of a ‘reported association’.
The alternative explanation given for no association is that there may have been bias in selecting the patients, in that they may form a strange group of ‘lean PCOS’ patients (with low androgens??). Then, in the fourth to last paragraph of the article, Gleicher et al. mention a possible threshold effect that doesn’t make sense to me at all. The idea seems to be that women with POI/DOR/LFOR (pick an acronym) have low androgen levels, and that this could lead to a higher miscarriage rate, although the women in this study had low androgen levels yet ovarian function was fine and miscarriage did not correlate with androgen level. Confusing? yes. And it’s my opinion that high quality data will be the only answer to ‘unfuddle’ this area. Tartagni et al. could very well be a start, and will hopefully be followed by more highly powered studies.
* Tartagni et al. 2015 http://www.biomedcentral.com/content/pdf/s12958-015-0014-3.pdf; DOI 10.1186/s12958-015-0014-3
I’ve been making a concerted effort to live more sustainably since i moved back to Australia in 2012. It’s been slow progress, with a new habit picked up every now and then, but i’m fine with that. If you try and change too many things at once, it’s easier to give it all up. At least that’s how it is with me.
Since i’ve not been working, my life is especially slower than ever. I had high anxiety last year, and becoming time-rich has been the best medicine for that. Especially because it means i can work on my sustainability goals in a relaxed manner, trying things out without the worry of ‘wasting my time’. Even if you could magically change all your habits overnight, you’d need extra time because most of the ‘sustainable actions’ that i do, replace modern conveniences. It’s a bargain that works for me personally, not only because i have the time but because i enjoy the activities and can see benefits that make up for the use of my time.
An example is homemade pizza dough. We used to get pizza delivered once a week, sometimes twice if we’d been working hard or were just worn out (and we both love pizza). I had made pizza dough before as a novel activity, but now it’s a regular occurrence. It’s a lot less spontaneous than delivered pizza, and requires energy from me, but it’s significantly cheaper, a good workout for the hands/arms, and is simply more delicious pizza.
I think i’ve said it before but it was never my dream to be a housewife. I do not particularly like baking and i’m not concerned with having the most pinterest worthy house. My science career didn’t pan out. I tried a more conventional, 9-5 type job but it drove me crazy. Most of the job seemed so pointless, but it was still stressful (time-pressures). I found myself working to earn money, so that i could buy things that i didn’t really want anyway. And a lot of that money went onto conveniences, oftentimes ones that saved us money but weren’t all that pleasurable. For example, buying lunch from a food court, spending $10-$15 for food that was ‘OK’, when i knew i could cook something healthier and oftentimes tastier for less than half that price.
Don’t get me wrong, i would still like to be employed and earning money (to pay off the mortgage faster, travel, and maybe even throw some at an IVF attempt). But at the moment i’m struggling to think of something worth pursuing that is more ‘helpful’ than me just running a nice, sustainable household.
I do still question my little experiments in sustainability. There are plenty of times where i wonder if what i’m attempting has any impact or merit.
Yesterday i had to go pick up my bucket full of vegie scraps. It was at my friend’s house, 20 min drive away, or 45 min bike ride away. So i rode. I’d almost reached the destination, and even got over the challenging hill when i started thinking “This is nuts, why i am putting in all this effort to pick up a small amount of waste?”. In my unfit state it was a bit of work, and not the nicest conditions (the sun was shining but my toes were still cold even in warm socks). But i remembered that some people commute this distance on a bike every day (!). And then i got there, and the little bucket was waiting for me, and it fit perfectly in my bike pannier, and i felt accomplished 🙂