Some years ago, in a swimming pool in Malta of all places, I was having a conversation with an attractive young woman who was very embarrassed about her weight and excess body hair. I had known her for barely a few minutes before she was telling me that she had PCOS (Poly Cystic Ovary Syndrome). It was as if she wanted to wear a T-Shirt explaining that what she saw as unsightly was not her fault – it was the fault of a horrible condition, which she longed to be able to overcome. When we chatted for longer, she discovered that I wrote about diet and healthy eating and she literally begged me to write about PCOS. She was so passionate, and convinced that diet was the secret to being able to manage this thing that she so loathed. I similarly have no doubt that diet plays a vital part in PCOS – just as it does in virtually every aspect of human health.
Since this chance meeting, I have had so many questions about Poly Cystic Ovaries, Poly Cystic Ovary Syndrome (PCOS) and weight that I thought it was time to devote some time to this. I first wrote this article for our on-line club in February 2012.
Let’s start with some definitions:
Poly cystic ovaries is literally the condition of having small cysts on the ovaries (usually no bigger than eight millimetres each). These cysts are egg-containing follicles that have not developed properly.
During each menstrual cycle, follicles grow on the ovaries and eggs develop within these follicles. One egg will develop faster than the others and be released into the fallopian tubes. This is known as ovulation. The remaining follicles naturally degenerate.
With poly cystic ovaries, the ovaries are larger than normal and the underdeveloped follicles appear in clusters. Poly cystic ovaries per se are not too problematic. However, they all too often occur in parallel with a hormone imbalance and this is when other conditions appear alongside the poly cystic ovaries and this is when we get…
Poly Cystic Ovary Syndrome (PCOS) is the name for a wider group of conditions – including poly cystic ovaries – but also irregular periods, painful periods, unwelcome hair growth, acne, fatigue, weight gain etc – all really unpleasant symptoms. Someone can have poly cystic ovaries without more widespread symptoms, but this is rare. Usually the questions are – how many of the additional symptoms does someone have and how bad are they? Some of the conditions associated with PCOS are serious, for example Non-Alcoholic Fatty Liver Disease (NAFLD), sleep apnoea (abnormal breathing patterns during sleep), immune system deficiencies, increased incidence of diabetes and heart disease and so on. (Please note that the word “associated” does not mean causation – please always take care with this).
Mood disorders are commonly reported with PCOS – hardly surprising given the hormonal imbalances going on and the stress of anything from facial hair to acne to weight gain – all things that impair our sense of well being. The hormonal imbalances that can accompany PCOS include:
– androgens (androgens is the collective name for steroidal hormones – testosterone, often called the male hormone, being one of the most well known and the one of interest to us with PCOS);
– cortisol (often called the stress/adrenalin hormone);
– insulin (which we know as the fattening hormone);
– thyroid hormones (which are known to impact energy, appetite and weight); and the
– female gender hormones – oestrogen, progesterone, FSH (follicle stimulating hormone) and LH (luteinizing hormone). These gender hormones are the ones changing in absolute and relative levels throughout the normal menstrual cycle and hence mood and mind swings are very understandable with PCOS. I have always found this picture to be a really useful diagram of what is happening to all the different hormones during a typical menstrual cycle.
Incidence & causes
The incidence of PCOS is estimated to be approximately 10% – so that’s one in ten women of reproductive age. The symptoms often appear soon after puberty and, therefore, women have often been aware of and lived with this condition for years, if not decades. Many women are unaware that they have the condition and put early signs down to teenage acne and longer term weight gain down to getting older. PCOS is generally recognised to be the most common hormonal disorder in women of reproductive age.
The causes of PCOS are not agreed upon. There does seem to be a genetic element – a mother having PCOS will be more likely to have a daughter with PCOS. The genetic aspect we can do little about in terms of managing our likelihood of being pre-disposed to PCOS, but we absolutely can do things to manage the symptoms – all of this will be covered later in this article. Beyond the genetic element, other associations (please note associations – not causation – we really don’t know a clear cause) have been observed with one or more of the following:
1) Factors that impact hormone levels;
3) Insulin resistance or hyperinsulinism (high blood levels of insulin).
Let us look at each of these in turn:
Factors that impact hormone levels
These fall into two further categories – endogenous and exogenous factors that impact hormone levels. By endogenous we mean things happening within the body and by exogenous we mean things happening outside the body.
The hormone system in the body is also called the endocrine system. In Appendix 1, I’ve attached an extract from Chapter 3 of my book The Obesity Epidemic: What caused it? How can we stop it? to give you a summary of the human hormone system. I’ve focused on the main hormone issues related to PCOS here below:
The Rotterdam Consensus workshop (2003) on PCOS defined the condition as “PCOS is a syndrome of ovarian dysfunction along with the cardinal features hyperandrogenism and poly cystic ovary morphology” (Ref 1). (Hyperandrogenism means excessive production of male hormones). The workshop proposed that diagnosis of PCOS can be made on the basis of two out of three of the following:
– Oligoovulation (infrequent, irregular ovulation) – or anovulation (absence of ovulation);
– Clinical or biochemical signs of hyperandrogenism (e.g. facial hair);
– Polycystic ovaries on ultrasound or direct inspection.
The third point brings in the influence of the ovaries as part of the endocrine (hormone) system. PCOS is also characterised by excess production of oestrogens and fertility problems (this is often the route through which PCOS is diagnosed). So we have an enormously complex, multi faceted, medical condition, integrally linked with at least three parts of the endocrine system (See Appendix 1 – the pituitary gland, the adrenal glands and the ovaries).
Again, sadly we don’t know why any of these circumstances occur. However, given the delicate balance that the body is continually trying to achieve, with all parts of the hormone system, I’m actually more surprised that anyone manages to achieve balance in our modern world of medication, chemicals and fake foods, not that 10% of women ‘fail’ to!
A woman of reproductive age could produce more testosterone because of a genetic disposition to do this or, for example, because of stress driving cortisol driving testosterone or for many other reasons. Whatever the root cause, the outcome will be excessive production of male hormones – Hyperandrogenism and one of the Rotterdam workshop defined criteria is in place. She only then needs her ovaries and female hormone production to be out of balance and another characteristic will be met. The Pill, modern chemicals and modern ‘foods’ will all be possible factors in triggering an imbalance, which brings us on to these external issues…
These can be many and varied and can include the disturbing level of environmental hormones that surround us in modern life. They can range from chemical pollution, which can affect any aspect of our hormone system, to the troubling levels of female hormones, which have been found in the water supply for more than a couple of decades. Regarding the latter, it does not appear that the progesterone and oestrogen in The Pill, taken by millions of women, can be completely removed from the water supply and traces remain affecting not just female fertility, but male fertility also.
I remember seeing a Horizon programme in the 1990s about the ‘desexualisation’ of alligators in Florida. Alligators are particularly interesting to study, as they represent a kind of ‘eco-barometer’. They live in and around water and hence any contamination of our environment affects them early on. Plus they are at the top of the water side of the food chain and, as a result, they amplify any impact of changes in our water. Younger alligators eat insects and small fish; more mature alligators eat fish and small animals in or by the water side – frogs and snakes etc. Fully grown alligators will eat a human if they get the chance! They would certainly drag a deer into the water to drown it if one were grazing close enough. Here is an interesting, short article on some of the observed changes in gender characteristics of alligators.
For those of you who have read Margaret Atwood’s “The Handmaid’s Tale” (or seen the movie), you will be aware that this 1985 work called ‘speculative fiction’ forecast a time when fertility would be so rare that women who could still bear children would be considered properties of the state so that the population could continue. Given that the global population broke through the seven billion figure in late 2011, this apocalyptic scenario doesn’t seem to be upon us yet. However, the British Fertility Society estimates that “at some time in their reproductive lives at least a quarter of couples experience a period of infertility (inability to conceive) lasting over 1 year” (Ref 2). Furthermore that “Some of these couples continue to be unable to conceive, leading to at least 1 in 6 couples seeing an infertility specialist at a hospital” (Ref 3). This does indicate that fertility levels are by no means secure and healthy. At least five friends we know needed fertility treatment to have their child(ren) and this was something that was unheard of just a generation ago.
Here’s where association is particularly important to note, as opposed to causation. We can observe that obese people are more likely to have PCOS, but PCOS sufferers are also more likely to be obese (as one of the symptoms is a tendency to gain weight). Hence don’t assume obesity causes PCOS any more than the other way round.
Dr. Nuha Haboubi, a chemical pathologist, has been instrumental in reviewing the contribution of PCOS to the obesity epidemic. Speaking at the Wales National Obesity Forum conference in May 2010 she noted that PCOS affects approximately 10% of women and that in some countries one fifth of PCOS sufferers are obese and in other countries it is as high as three quarters. Haboubi presented evidence that 69% of PCOS sufferers in the USA are obese. This concurred with a UK 2009 health sciences research audit where dietitians were surveyed to request information about how many of their patients with PCOS were obese. The result was that 24% of PCOS sufferers remained lean while 76% were found to be obese.
It is uniformly noted that the fat storage, in PCOS patients, is more commonly observed around the abdominal area. Excess production of androgens is noted with PCOS sufferers (as we noted in the previous section) and obese women produce more androgens. So we have a vicious circle of raised androgen production and PCOS and obesity and I have made no assertions about causation thus far. If, however, you are a calorie theorist, you will believe that putting too many calories in (or not expending enough calories) is the cause of obesity and this in turn (somehow) causes PCOS and the pituitary master gland is telling the adrenal cortex to produce too many androgens, all because the woman ate too much. This is one of many reasons why weight is not about calories!
This, for me, is the most positive part of this article, as it starts to illustrate something that we can do to mitigate the symptoms of PCOS as far as possible…
In much literature on PCOS, the debate is not just that insulin resistance and PCOS are connected, but that insulin resistance causes PCOS. This raises a key question – how might insulin resistance cause PCOS? I’ll try to illustrate the possible step by step process:
1) Insulin resistance describes the situation where cell walls have become de-sensitised to insulin. So, when glucose tries to get into cells where it is needed for energy, insulin is supposed to assist this process, but where insulin resistance occurs, the process doesn’t work properly. The cell then doesn’t get the glucose it needs, the body over produces insulin thinking that more is needed – hence weight is gained with insulin being the fattening hormone.
2) When glucose doesn’t get into the cells, it is left in the blood stream, causing raised levels of blood glucose. This is toxic to the body, so it has to find another way to get glucose out of the blood stream, so it is converted to glycogen (stored glucose) and stored in the liver/muscles of the body. Within 24 hours, the liver will convert the glucose/glycogen to fat and the person gains weight – and we understand that weight itself makes someone more disposed to having PCOS.
3) The second route by which insulin resistance can ’cause’ PCOS is that excess insulin (when the body over produces insulin not realising that the insulin resistance is preventing the insulin already released from being used properly) stimulates ovaries to produce large amounts of testosterone (the male hormone). This alone may prevent the ovaries from releasing an egg each month. Hence the irregular periods and difficulty conceiving that go with PCOS. High levels of insulin also increase the conversion of androgens (male hormones) to oestrogens (female hormones). This upsets the delicate balance between these two hormone levels and this can also impact weight, and prevent normal egg ovulation development, leading to cysts.
The best way to manage PCOS
If you are genetically pre-disposed to PCOS, there’s nothing you can do about that, but you can manage the condition in just the same way as anyone else who develops it. The key to managing PCOS lies in the three main causal/associated factors that we have looked at above: 1) endogenous and exogenous hormonal factors; 2) obesity and 3) insulin resistance. Like a lovely jigsaw puzzle, these are all going to come together and be helped by a basic principle of valuing real food. We need to stop eating modern fake food and start eating traditional real food: meat, eggs and dairy products from pasture living animals; fish; vegetables and salads; nuts and seeds; and fruits in season. I truly believe that the answer to any modern condition is to return to eating real food as far as is practical – what we ate before we had such massive incidence of obesity, diabetes and PCOS.
On the subject of hormones – minimise things that could imbalance your system as much as you can. Is there any alternative to taking The Pill? How best can you manage your stress/cortisol levels? How far can you limit your chemical and modern pollution exposure – particularly to things known to impair hormone functioning, such as plastics? (Here’s a 56 page document called “Endocrine-Disrupting Chemicals”!)
The second two aspects – obesity and insulin resistance – are complete partners in crime. The most likely cause of both is our high modern carbohydrate diet. We therefore need to manage our carbohydrate intake carefully to avoid/overcome obesity and to simultaneously avoid/overcome insulin resistance.
The Harcombe Diet® is therefore perfect to help optimally with PCOS – real food, with optimal nourishment for optimal health and managed carb intake to deal with weight and to reduce the demand upon the body for insulin.
The NHS advice, no surprise, is the Eatbadly plate! The NHS calls it the “eatwell plate”, of course, but it is anything but.
This ‘role model for healthy eating’ is deemed to be perfect for everyone – no matter what health complaint they have. This NHS page on PCOS will recommend that you lose weight and the link telling you how to do this takes you here . Click on the eight tips for healthy eating and number one is “base your meals on starchy carbohydrates”. Quite incredible. The perfect recipe for weight gain and a sure way to guarantee that your body will be trying to release insulin every time you eat.
If you reject the government advice and look for help from books, there are limited resources available. I have a copy of a book by Colette Harris and Theresa Chung called PCOS Diet Book “How you can use the nutritional approach to deal with PCOS.” As you would expect, the book is not supportive of refined carbohydrates, but the advice still majors on carbohydrates. To the body, carbs are carbs. Refined ones are lower in nutrients than whole grain carbs, but the body still breaks down any carbohydrate into simple sugars. The authors’ top three diet tips are:
1) Drink more water (bit odd given that they have no idea how much you drink or need currently!)
2) Eat five portions of fruit and veg a day. To the body, fruit and vegetables are simply differing combinations of fructose and glucose.
3) Eat complex, low GI carbohydrates. Better than refined carbs, yes, but still glucose to the body.
You will be very unlikely to find any dietary advice in the public health or mainstream world that will buck the trend of telling people to base their meals on carbs. We can enjoy carbs on The Harcombe Diet® – but PCOS sufferers will need to manage their carb intake even more carefully than the average Harcombe follower because they simply cannot afford to allow insulin resistance to develop any more than it already has.
You will get good advice in the Paleo/real food world and from low carb communities generally. I recommend that you always follow The Harcombe Diet® number one principle of real food (never low carb fake food alternatives) and that you work out the carb intake that works for you.
If you get any of The Harcombe Diet® books, you’ll learn about what we call carb meals and fat meals. The simplest and safest option, for PCOS sufferers, will be to have as many fat meals as possible. However, you may be more active in your work or hobbies and you may find that you function better with one or even two carb meals a day. You would have to be in the situation where you were using up glucose pretty instantly as it was reaching your blood stream – or the insulin would get there first and start trying to get the glucose out of the blood stream. You may be only mildly insulin resistant and find you are able to cope with some carbohydrate and glucose response. However, I would strongly caution that the more you tax your pancreas and insulin response, the more sensitive it will get and the worse your insulin resistance and PCOS is likely to become.
I said to one woman who asked about PCOS – it’s incredibly unfair and cruel, but a PCOS sufferer needs to be even more careful and disciplined about carbohydrates than a non PCOS sufferer. It’s cruel and unfair because the PCOS sufferer already has so much to cope with – mood swings, period problems, facial hair, acne, increased risk of diabetes to name just a few. However – cruel and unfair though it undoubtedly is – those with PCOS simply must adhere to a real food/managed carb diet with commitment and diligence. You cannot afford to risk diabetes and heart disease as a result of your body becoming increasingly unable to remove glucose from the blood stream. This is literally life threatening.
I sincerely hope that this article has been of help to PCOS sufferers and to family members and friends of this nasty condition. I hope that some of you may resonate with some of the many symptoms mentioned in this article and realise that your weight problem, if accompanied by irregular periods and other conditions, may in fact be PCOS without you having realised this. I hope that all of you have found the hormone information interesting – weight is hugely about hormones at the end of the day.
Remember the three main factors associated with PCOS:
1) Factors that impact hormone levels;
3) Insulin resistance or hyperinsulinism (high blood levels of insulin).
The central theme running through all of these is insulin – the hormone that is released when we consume carbohydrates. Advising PCOS sufferers to base their meals on carbohydrates is malpractice in my opinion. If you have PCOS you need to ditch fake food, embrace real food – eat as well as your lifestyle and budget can support and manage your carbohydrate intake very, very carefully.
The Harcombe Diet® can help you with all of this – and tell you about three common medical conditions, which cause insatiable food craving. This in turn may help you to understand why you have found it so difficult to resist carbohydrates – especially refined ones. Whatever you do – hang on to the two key messages from this article: Eat real food and manage your carb intake.
I wish you all the very best in managing this distressing condition.
Very best wishes
Appendix 1 – Extract from Chapter 3 of The Obesity Epidemic
The endocrine (hormone) system
The endocrine system is made up of the endocrine glands that secrete hormones. The endocrine glands are:
3) Thyroid (and parathyroid);
4) Thymus (not strictly part of the endocrine system);
7) Ovaries in females; and
8) Testes in males.
Just as the central nervous system sends motion and sensory messages to control and co-ordinate the body, so the endocrine system has a similar job, but using hormones to communicate. The endocrine glands are ductless, which means that their secretions (hormones) are released directly into the bloodstream and travel to elsewhere in the body to target the organs upon which they act. Although there are eight major endocrine glands scattered throughout the body, they are still considered to be one system because they have similar functions, similar mechanisms of influence, and many important interrelationships.
Let us go through the functions of the endocrine system and draw attention to the roles that can clearly have an impact on weight:
1) The pineal functions as a gland, secreting the hormone melatonin during the hours of darkness, which regulates the pituitary gland and is associated with the biological clock. Melatonin is derived from serotonin, with which it works to regulate the sleep cycle. There have been some important studies on weight and sleep patterns and we know that shift work is conducive to weight gain. We also know that hours of sunlight per day and the mood aspect of serotonin play an important part in weight, but I do not intend to go further into the pineal gland, as there are bigger hormonal targets to catch.
2) The hypothalamus, which is part of the brain, links the nervous system to the endocrine system via the pituitary gland. The pituitary is thus known as the master gland and this part of the brain consists of two lobes called the anterior and the posterior. The anterior releases the following hormones: human growth hormone (HGH); thyroid stimulating hormone (TSH) (to release thyroxin); adreno cortico trophic hormone (ACTH), which stimulates the adrenal cortex to produce cortisol and androgens, amongst other corticosteroids; luteinizing hormone (LH), which brings about ovulation; follicle stimulating hormone (FSH) – another key hormone in the menstrual cycle; and the interstitial cell stimulating hormone (ICSH) to produce sperm. The main secretion from the posterior lobe is the anti-diuretic hormone (ADH).
Every one of the above can have a significant impact on size and weight. To share just a few examples:
– Too much (hyper) HGH can lead to the condition crudely known as gigantism and too little (hypo) HGH can lead to the condition equally crudely known as dwarfism.
– Cortisol is deemed to play a role in hormone related weight gain from literally stressing the body with intense exercise. This would benefit from further investigation, as we observe abdominal fat in a number of otherwise very fit people.
– Androgens play a crucial role in poly cystic ovary syndrome (PCOS), as we saw in the main part of the article.
– Finally, in this brief review of the pituitary gland, we have the known impact of hormones on weight even during the menstrual cycle, let alone from puberty to menopause. During a typical 28 day menstrual cycle, luteinizing hormone (LH) is fairly constant other than the significant rise a couple of days before ovulation and the rapid fall away at day 14. Follicle stimulating hormone (FSH) has a smaller peak also at the middle of the month and rises slightly at the end of the cycle to start the next cycle at one of its higher levels. Most women report small to considerable weight gain during days 21-28 of this cycle.
3) The thyroid gland secretes thyroxin, which is critical to metabolism and basal metabolic rate (BMR). We know that the thyroid gland is a clear and definite factor in weight. With no change in calories consumed, we could remove the thyroid gland in a thin person and make them fat. This is an extreme scenario, but an underactive thyroid, also known as hypo-thyroidism, will lead to a decrease in BMR, weight gain, lethargy and other unpleasant symptoms. Conversely, an overactive thyroid, hyper-thyroidism will lead to an increase in BMR, weight loss, hyper-activity and equally unwelcome symptoms. Indeed a blood test for thyroid functioning is one of the first tests done to investigate seemingly inexplicable weight loss or gain.
The parathyroid is primarily concerned with the growth of muscle and bone and the distribution of calcium and phosphate in the body and needs no further mention in this brief review of hormones and weight.
4) The thymus is strictly an immune system gland, but it is invariably included in reviews of the endocrine system. It activates the immune system and regulates lymphocytes (white blood cells associated with antibody production). It plays a critical role in transplant situations, but we need not devote more time to it here.
5) Adrenalin is the most common hormone secreted by the adrenal glands. This prepares the body for the fright, fight or flight mechanism and, in so doing, the action of the heart is increased, the rate and depth of breathing is increased, the metabolic rate is increased and muscular contraction improves – all excellent responses by the body, for the need to act. (For those interested in why such stress makes you want to go to the toilet, the blood supply to the bladder and intestines is reduced – as it is needed elsewhere – and the muscular walls in these regions relax.)
Noradrenalin is also released by the adrenal gland (also called adrenal medulla) and this has similar effects to adrenalin.
The adrenal cortex produces corticosteroids such as cortisol, cortisone, corticosterone and aldosterone. The first three of these are collectively known as glucocorticoids. The most interesting function amongst these, from a weight perspective, is the role of glucocorticoids on the utilisation of carbohydrate, fat and protein by the body. With the name derived from a combination of abbreviations of glucose, adrenal cortex and steroids, glucocorticoids play a key role in glucose metabolism and thus fat storage and utilisation. Aldosterone has a key role to play in the regulation of salt and water balance, which can impact weight to a more transitory extent.
6) The pancreas is the single most important part of the endocrine system for our review of hormones and weight. It is actually both exocrine (ducted) and endocrine (ductless). As an exocrine gland it secretes the following enzymes into the small intestine:
– Pancreatic amylase (which breaks down polysaccharides into simple sugars);
– Lipase (which breaks down triglycerides into fatty acids and glycerol);
– Protease (which breaks down protein into amino acids).
The weight gain resulting from insulin is so well known that, as far back as 1925, Wilhelm Falta began using insulin to treat underweight adults and anorexia (Ref 4). The weight loss at the onset of type 1 diabetes is equally long known and remarkable. The non diabetic person can produce the same fattening effect of administering insulin by eating carbohydrates frequently and causing the pancreas to release insulin. The impact of insulin on weight is irrefutable and substantial, as we will also see in the next section on medication.
7) Experiments with rats have shown that the removal of ovaries (and therefore the hormone oestrogen) can lead to excessive hunger and inactivity (and weight gain) (Ref 5). This can be observed in females following the removal of ovaries, as may happen with certain types of hysterectomy or treatment for ovarian cancer. The ovaries effectively cease to function with any hysterectomy or during the menopause, when the ovaries cease production of eggs and the levels of oestrogen fall measurably. The Wade and Gray study (referenced in this paragraph) of the gonad hormones (oestrogen, progesterone and testosterone) in 1978 noted four interesting things:
– “Estradiol (i.e. oestrogen) and testosterone decrease adiposity, while progesterone increases carcass fat content.” It is interesting to note that progesterone is the hormone that rises from day 14 of the menstrual cycle, coinciding with noticeable weight gain for many women. Additionally, the most common hormone taken by females, “The Pill”, typically contains 150 milligrams of progesterone and 30 milligrams of oestrogen for the combined pill and 350 milligrams of progesterone (usually norethisterone) for the progesterone only pill (POP). Women taking the pill commonly report weight gain.
– “These hormone-induced changes in body weight and composition are accompanied by changes in food intake and voluntary exercise, suggesting that the hormones induce behavioral changes which alter body weight and adiposity.
– “However, several lines of evidence indicate that these behavioral changes are neither necessary nor sufficient to produce the hormone-induced body weight shifts.
– “From this perspective, estradiol and progesterone-induced changes in food intake are viewed as consequences, rather than causes, of changes in fat metabolism.”
Taking the final three points together, the argument is that hormone changes do drive weight changes both directly, with a metabolic impact, and indirectly, with an effect on appetite and activity levels, and that the metabolic impact is likely the greater.
There are many examples of the impact of hormones on weight, which get completely disregarded if you are stuck in the narrow view that all that matters are calories consumed and calories expended in activity.
Ref 1: Rotterdam Consensus Workshop Group, “Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome”, Fertility & Sterility, (January 2004).
Ref 2: Gunnell D.J. and Ewings P. Infertility prevalence, needs assessment and purchasing. Journal of Public Health Medicine 1994; 16: 29-36.
Ref 3: Hull M.G.R., Glazener C.M.A., Kelly N.J. et. al . Population study of causes, treatment and outcome of infertility. BMJ 1985; 291: 1693-1697.
Ref 4: Wilhem Falta, Endocrine diseases including their diagnosis and treatment, (1923).
Ref 5: George N. Wade and Janet M. Gray, “Gonadal effects on food intake and adiposity: A metabolic hypothesis”, Physiology & Behavior, (March 1979).
Finn Molgaard Hansen, Nibal Fahmy and Jens Hoiriis Nielsen, “The influence of sexual hormones on lipogenesis and lipolysis in rat fat cells”, European Journal of Endocrinology, (1980).
These represent two examples. The evidence is so extensive that the term “ovariectomy-induced obesity” is widely used.