Menopause - Science topic

Hi Hana. Low load would likely be in the 30-50% of the RM range. The amount of time for body weight likely all depends. Probs after a few weeks of training(1-3 wks). The Training status definitely plays a role. The lifter with experience would likely need higher loads and more exercises. Hope that helps!

Dear, the following article might be of your interest

Sydora BC, Fast H, Campbell S, Yuksel N, Lewis JE, Ross S. Use of the Menopause-Specific Quality of Life (MENQOL) questionnaire in research and clinical practice: a comprehensive scoping review. Menopause. 2016 Sep 1;23(9):1038-51.

Regards

Dr Saba

When you hit menopause, your oestrogen levels begin to decline.

Radiotherapy is generally not used in treatment of endometriosis. Treatment of endometriosis is by medicines or surgery depending on patients symptoms and extent of endometriosis. radiotherapy is mainly used to treat malignant conditions.

You can not use kit method (manually) because there is just ELISA methods.

Hi Robert

I was trying to get more inputs/ideas on the question raised while providing a viewpoint at the same time.

Regards

Chandana

We are particularly interested in finding characteristics of females who consider themselves as healthy. Our study followes a biopsychosocial approach of health in pre, peri and postmenopausal women. We are therefore not addressing risk factors in psychological or somatic health.

Here's a recent comparative look at menopause in humans and non-human primates. There might be some references that could help you:

There might be relationship. It was found that some glucosyl/glucuronosyl transferases in the feeding females were upregulated in mountain pine beetle. Glutathion S Transferases are important detoxifying enzymes found in fat tissues. An NADPH-dependent nitroreductase has been reported in the soluble fraction of adult female house flies that changes parathion to aminoparathion. Nitrobenzene reductase activity has also been found in fat bodies of cockroaches. Also there are tons of literature on this thing. Before answering, I would like to know to which particular group of insecticide  and which particular group of insect (atleast order) you are talking about. I would suggest reading Robert et al. 2013 Plos One.

The cause of gender differences in puberty timing are not known althought there are some proofs of genetic loci correlated with these differences. Genetics,adiposity, Kiss peptin, leptin, BMI are correlated with puberty onset but they do not explain why girls start puberty earlier than boys.

On the other side, I do not understand why are you putting in morrir menarche/menopause with adrenarche/andropause. Beside the fact that andropause is not as certain and suddenly as menopause (there is a lower androgen production but not an inactivation of testicles function), adrenarche is not the equivalent of menarche since it is commun to girls and boys and correlated with adrenal function.

Hope that my answer will be helpful.

Best regards

Carmen Vulpoi

Excellent Dr, I'll look forward, thank you very much!

Regards,

Ana.

Very impressive, and detailed information. I believe your comments will help much understanding especially the influence of early menopause and its proper care and management. Many thanks Dr Astrit  for your so nice comments.

Thank you very much!

As I have already indicated, any study looking into the efficacy of existing or novel therapeutics for AD in women versus men has to consider duration of estrogen replacement in female subjects.  Both animal models and human studies suggest that estrogen replacement is protective if used for a sufficient period of time.  Therefore, if female subjects are not stratified by their duration of HRT use this could potentially confound your data. 

A 56 year-old woman (menopause since 2007) applied to our clinic. She received hormone replacement therapy and suffered from severe hot flashes and night sweats.

History of HRT: At first she received Divigel 1,0 (estradiol 1,0), but has gained weight (+6kg) and stopped  the treatment. Then she started to receive Femoston 1/5  (estradiol 1,0, didrogesteron 5 mg), but effect was not sufficient.

We relived the symptoms by combination: Femoston 1/5 and Melatonin3 mg.

How is hertongue and pulse?

Hey

Generally it takes 12 months but it  greatly influcenced by genetic variation

Dear Grandhi,

the bold answer is that there is no treatment for dementia whatever the category of patients. Ache inhibitors have some short-term effect in patients with Lewy body disease but fail to show any efficacy otherwise. Other therapeutic strategies like cognitive training have not shocn yet convincing proofs of efficacy. We have so far only small measures like lowering vascular profile (hypertension, diabetes) in order to reduce the vascular part of dementia and suggesting to patients to do regular physical exercise and maintain social activities.

best

Christophe

diabetes alter  lipid metabolism and adverse effect of lipotropic factor  biochemical  efficiency  . plasma protein  and  lipoprotein  value  imbalance ,  increases  VLDL  very much   it also cause  obesity.

Dear Maskin 

Greetings.

Good evident exist regarding the use of E2 in urinary and hot flushes in menopausal women from WHI. I do not think that this was endorsed by any agency.

In non diabetic group, blood pressure would be pretty much independent. Ageing can’t be correlated with hypertension all the time even in the case of menopausal women. The best way to correlate would be by external factors like lifestyle, usage of sex hormones (pills), alcohol etc.

Ciao,

I point out these two articles that seem to respond to your question . Mostly the data seem in favor of the combined HRT therapy.

Vittorio

Effect of hormone replacement therapy on inflammation-sensitive proteins in post-menopausal women with Type 2 diabetes.

Manning PJ, Sutherland WH, Allum AR, de Jong SA, Jones SD.

Diabet Med. 2002 Oct;19(10):847-52.

PMID:

12358873

Similar articles

Select item 11821303 4.

Hormone replacement therapy can augment vascular relaxation inpost-menopausal women with type 2 diabetes.

Perera M, Petrie JR, Hillier C, Small M, Sattar N, Connell JM, Lumsden MA.

Hum Reprod. 2002 Feb;17(2):497-502.

PMID:

11821303

Dear Shilpakala,,

I think that there is definitely a relationship . In  hyperinsulinemic/diabetic patients  the epimerase enzyme activity increased . This implies an increase of the conversion of myo - inositol to D - chiro - inositol . This represents a defense mechanism to reduce insulin resistance . At the same time , however, the reduction of myo - inositol determines a reduction of myo - inositolphsphoglycan promoters of the signals for both FSH and TSH . This results in a resistance of the thyroid to TSH with consequent increase of the same . I hope to be liked . BR Vittorio

 

Dear Howieda

The use of oral contraceptives in the treatment of menopausal disorders is definitely reason for being . On the other hand having a number of therapeutic alternatives available with fewer side effects I find no indication for the use of OC in these paziento .

See you soon

Vittorio

Perimenopausal hormonal contraception--can we do better?

Panay N, Fenton A.

Climacteric. 2014 Oct;17(5):517-9

an interesting and new aspect is the fact that both the coorelato ? FSH and TSH have a common second Myo - inositol dependent messenger. The increase in FSH typical of menopause could lead to a thyroid functional impairment related to a epimerase action induced .

The key is the protection factor coming from Estrogen. The Estrogen receptor stimulates nitric oxide production in the endothelium, decreasing BP; also, the receptor is present in the kidney, increasing the release of sodium and water, thus reducing the BP at long-term. At the menopause, no estrogen is produced at all, so this protection factor ais abolished, thus increasing BP. In additon, during the menopause, the balance between estrogen-testosterone is affect because of the estrogen reduction, so there's more free testosterone than estrogen. This increase in testosterone is highly related to increases in BP.

This article is punctual to demonstrate this differences.

I hope you understand.

I prefer HRT with tailored dosage, as this permits the possibility of pregnancy in the unlikely event of recovery.  Of course, the patient must be warned that pregnancy is a possibility, and if this is not desired, other methods must be employed.

It remains of concern that I am starting a treatment that will be continued for 20-30 years. This also mandates considerable discussion with the patient.

Regards

CJ van Gerlderen

Hello Mr. Jose.

I think this would be helpful

Regards!

Dear Robert thank you very much for your help and effort.

Sevil

Dear M Kechida,

I assume it is a osteoporotic fracture. ( would like some more details like which bone is fractured? How was the fracture sustained? Is it traumatic injury or related to Osteoporosis? T score?)

Conventionally one would treat enterobehcets with high dose steroids and immunosuppressives. However, steroids may impair fracture healing and one might want to avoid it. The alternatives might be Infliximab with or without Thalidomide. 

For the osteoporotic fracture, teriparatide (recombinant parathormone) might be indicated for 18 months. 

regards

Ideally the SHBG concentration should fluctuate inversely towards the serum levels of estrogens. But  low serum estrogen levels are not the only factor which lowers SHBG concentration. High levels of prolactin, growth hormone and insulin are shown to effect the SHBG concentration negatively. Obesity has also been shown to reduce SHBG concentrations.

Dear Miss Bahari,

 As you know cross cultural studies could be conducted between different countries. So we can not collaborate in this case. However menopause is my main interest and I can cooperate in another projects.

Yours

Dorothy, thanks for the suggestions, will explore the possibility.

according to my experience these patients had two phase:

1- their condition get aggravated in one year after start of menopausal sign and symptom 

2- after one year their condition gradually will be better.

The presence of depression next to the menopause is a phenomenon linked much more to psychological factors, social and environmental, and biological.

  If in fact the lack of estrogen can cause mood swings and problems related to the imbalance of the autonomic nervous system and the consequent metabolic alterations, the pressure of social stereotypes can lead to the onset of depression as a response to the cultural environment.

Menopause itself is for the woman who experiences a moment of transition and transformation, such as adolescence or motherhood, but unlike the latter is seen as a symbol of order and bereavement, deprivation and loss of femininity. In fact, Western society binds the image of women in the physical beauty and procreation, not recognizing the mature woman those qualities considered ancestrally wealth of males: the wisdom, experience, awareness.

In fact, in certain ethnic groups where menopause is celebrated and even celebrated as a time of initiation and input of women in the age group that most influence the life of the group, the climacteric syndrome practically does not exist.

How to say that in every culture is to establish the social roles and meanings of the individual, regardless of his feelings and his values .

In post menopausal women without bleeding endometrial thickness >11 mm should require a biopsy to be taken to exclude endometrial cancer. 

< or =11 mm is associated with low risk for endometrial cancer.

Following article explains in more detail 

I think estrogen dominance and decreased progesterone plays a key role.

There are no true optimal levels but there are general guides to optimise individual treatment regimens.

For oestradiol, the benchmark is a CURE of vasomotor symptoms and vaginal dryness which could be achieved by levels around 200pmol/l.  Bone protection, however while can be helped at lower doses, maintaining levels above 250pmol/l can cover over 94% of women.  Levels of up 1200pmol/l are sometimes required to maintain symptom free state.  As to the progesterone, levels are generally not helpful but if the withdrawal bleeding occurs at the end of the progesterone phase without intermenstrual bleeding and in the absence of adverse effect then the dose is adequate for endometrial protection.  We have published menstrual diaries recordings and interpretations with various progestins, including a dose ranging study of trimegestone.

As to the testosterone, it is effective on Free Androgen Index of around 4-7% provided adequate oestrogen levels preceed the introduction of testosterone.  Therefore measurement of oestradiol, SHBG and testosterone are required in the management of patients requiring testosterone supplementation.

Beta-cross laps is a product of collagen degradation and a biomarker of bone resorbtion, P1NP serves as an indicator of collagen formation, osteocalcin measurement is recommended to perform in postmenopausal women for risk assessment of osteoporosis.

This is quite true that endogenous estrogens protect female hearts and vessels prior to onset of menopause, they act as vasodilators, similarly to calcium channel blockers, have favorable effect on lipid metabolism and coagulation. But as for the application of HRT for primary or secondary prevention of CVD, it remains questioable due to the results of recent studies like HERS, WHI, PEPI, NHS, etc. which had demonstrated that selective beneficial effects of HRT on CVS doesnt overweight the possible risk of certain types of cancer, like invasive breast cancer, though decreasing the risk of colon cancer. Besides, HRT increses the overall risk of arterial and venous thrombosis in patients with trombophillia, EVTET trial.

To the question of possible factors which might impact the clinical course of the postmenopausal period. Some of the factors are well established, like smoking which leads to early menopause, surgical or so called artificial menopause, radiation therapy and chemotherapy, Stein-Levental syndrome, endometriosis. There are as well factors which are believed to have some impact, like the respected author of the question have mentioned, e.g. living in the areas >3500 meters over the sea level, chronic inflammatory pelvic diseases, intake of oral contraceptive pills, stress, etc.

Concerning ethnicity, it was noted that in Asian countries with high intake of food containing soybean early symptoms of menopause are postponed and frequently less extensive compared to the Western female population.

But also I would suggest following references worth mentioning with an insight on cardiovascular system:

1. Bello N. Epidemiology of coronary heart disease in women / N. Bello, L. Mosca // Prog Cardiovasc Dis. – 2004. – Vol. 46. – Р.287-295.

2. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: the Women's Health Initiative randomized controlled trial / Anderson G.L., Limacher M., Assaf A.R. [et al.] // JAMA. – 2004. – Vol. 291. – P.1701-1712.

3. Elevated arterial stiffness in postmenopausal women with osteoporosis / H. Sumino, S. Ichikawa, S. Kasama [et al.] // Maturitas. – 2006. – Vol. 55. – Р. 212–218.

4. Eric Levens. Current opinions and understandings of menopausal women about hormone replacement therapy (HRT) — The University of Florida experience / Levens Eric, R. Stan Williams // American Journal of Obstetrics and Gynecology. – 2004. – Vol. 191, № 2. – Р. 641-646.

5. Estrogen plus progestin and the risk of coronary heart disease / Manson J.E., Hsia J., Johnson K.C. [et al.] // N Engl J Med. – 2003. – Vol. 349. – P. 523-534.

6. Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women: 2007 Update / L. Mosca [et аl.] // Circulation. – 2007. – Vol. 115. – Р. 1481-1501.

7. Evidence-based guidelines for cardiovascular disease prevention in women / Mosca L., Appel L.J., Benjamin E.J. [et al.] // Circulation. – 2004. – Vol. 109. – P. 672-693.

8. Female-specific aspects in the pharmacotherapy of chronic cardiovascular diseases / N. Jochmann, K. Stangl, E. Garbe [et al.] // Eur Heart J. – 2005. – Vol. 26, №16. – P. 1585-1595.

9. Gender differences in recovery after coronary artery bypass surgery / Vaccarino V., Lin Z.Q., Kasl S.V. [et al.] // J Am Coll Cardiol. – 2003. Vol. 41 – P. 307-314.

10. Gender-related effects on metoprolol pharmacokinetics and pharmaco-dynamics in healthy volunteers / A.B. Luzier, A. Killian, J.H. Wilton, M.F. Wilson // Clin Pharmacol Ther. – 1999. – Vol. 66. – P. 594-601.

11. Hormone replacement therapy and cardiovascular disease: a statement for healthcare professionals from the American Heart Association / Mosca L., Collins P., Herrington D.M. [et al.] // Circulation. – 2001. – Vol. 104. – P. 499–503.

12. Hyperhomocysteinemia in menopausal hypertension: an added risk factor and a dangerous association for organ damage / R. Noto, S. Neri, G. Molino [et al.] // Eur Rev Med Pharmacol Sci. – 2002. – Vol. 6, №4 – P. 81-88.

13. Igweh J.C. The effects of menopause on the serum lipid profile of normal females of South East Nigeria / J.C. Igweh, I.U. Nwagha, J.M. Okaro // Niger J Physiol Sci. – 2005. – Vol. 20, №1. – Р. 48-53.

14. Jacobs A.K. Coronary revascularization in women 2003. Sex revisited / A.K. Jacobs // Circulation. – 2003. – Vol.107. – P. 375-377.

15. Kannel W.B. Metabolic risk factors for coronary heart disease in women: perspective from the Framingham Study / W.B. Kannel // Am Heart J. – 1987. – Vol. 114, №2. – Р. 413-422.

16. Lifestyle intervention and coronary heart disease risk factor changes over 18 months in postmenopausal women: the Women On the Move through Activity and Nutrition (WOMAN study) clinical trial / L.H. Kuller, L.S. Kinzel, K.K. Pettee [et al.] // J Womens Health. – 2006. – Vol. 15, №8. – Р. 962-974.

17. Luboshitzky R. Cardiovascular risk factors in middle-aged women with subclinical hypothyroidism / R. Luboshitzky, P. Herer // Neuro Endocrinol Lett. – 2004. – Vol. 25, №4. – Р. 262-268.

18. Montalcini T. Endogenous testosterone and endothelial function in postmenopausal women / T. Montalcini, G. Gorgone, C. Gazzaruso // Coron Artery Dis. – 2007. – Vol. 18, №1. – Р. 9-13.

19. Nielsen N. E. Plasma lipoprotein particle concentrations in postmenopausal women with unstable coronary artery disease. Analysis of diagnostic accuracy using receiver operating characteristics / N. E. Nielsen, A. G. Olsson, E. Swahn // Journal of Internal Medicine. – 2000. – Vol. 247. – Р. 43-52.

20. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results from the Women’s Health Initiative randomized controlled trial / Rossouw J.E., Anderson G.L., Prentice R.L. [et al.] // JAMA. – 2002. – Vol. 288. – P. 321–333.

21. Rosano G.M. Hormone replacement therapy and cardioprotection: what is good and what is bad for the cardiovascular system / G.M. Rosano, C. Vitale, M. Fini // Ann N Y Acad Sci. – 2006. – Vol. 1092. – Р. 341-348.

22. Rossouw J.E. Implications of recent clinical trials of postmenopausal hormone therapy for management of cardiovascular disease / J.E. Rossouw // Ann N Y Acad Sci. – 2006. – Vol. 1089. – Р. 444-453.

23. Serum sex hormones in premenopausal women with coronary heart disease / M.J. Mohamad, M.Karayyem, M.A.Mohammad [et al.] // Neuro Endocrinol Lett. – 2006. – Vol. 27, №6. – Р. 758-762.

24. Some Thoughts on the Vasculopathy of Women With Ischemic Heart Disease / Carl J. Pepine, Richard A. Kerensky, Charles R. Lambert [et al.] // Journal of the American College of Cardiology. – 2006. – Vol. 47, №3. – Р. 30-35.

25. The Women’s Health Initiative Steering Committee. Effects of Conjugated Equine Estrogen in Postmenopausal Women with Hysterectomy: The Women’s Health Initiative Randomized Controlled Trial // JAMA. – 2004. – Vol. 291. – Р. 1701-1712.

26. Validation of the Framingham coronary heart disease prediction scores: results of a multiple ethnic groups investigation / D’Agostino R.B.Sr, Grundy S., Sullivan L.M. [et al.] // JAMA. – 2001.- Vol. 286. - P. 180–187.

27. Wenger N.K. Coronary heart disease: The female heart is vulnerable / N.K. Wenger // Prog Cardiovasc Dis. – 2003. – Vol. 46. – P. 199-229.

28. Wenger N.K. Menopausal hormone therapy and cardiovascular disease / N.K. Wenger // Rev Esp Cardiol. – 2006. – Vol. 59, №10. – P. 1058-1069.

Natural selection requires an advantage for replicators (genes) competing against alternatives; hence selection cannot favor traits that diminish the success of genes, regardless of potential benefits at the species level.

Menopause is a complex, organized physiological process -- evidence against a simple 'breakdown' hypothesis.

Other species with analogous reproductive cessation include pilot whales and elephants. In all cases, species with co-resident maternal kin, multi-generational overlaps, long periods of juvenile development and dependence, and important functions for old females.

The evolutionary logic here is that the reproductive value of additional offspring diminishes as a female ages -- she is increasingly likely to die before the offspring has been successfully raised. Conversely, older females can be useful as helpers for older offspring, and eventually, grandoffspring. So selection favored genes for menopause in hominins (and some whales & elephants) because females that stopped having babies got more genes into future generations than those females who continued to reproduce and were less able to help their existing kin because they died sooner (cost of making additional offspring, who were unlikely to survive to reproduce).

For review see:

Flinn, M.V., Quinlan, R.J., Ward, C.V., & Coe, M.K. (2007). Evolution of the human family: Cooperative males, long social childhoods, smart mothers, and extended kin networks. In: Family relationships, C. Salmon & T. Shackelford (Eds.) Chapter 2, pp. 16-38. Oxford: Oxford University Press.

Flinn, M.V. (2011a). Evolutionary anthropology of the human family. In Oxford handbook of evolutionary family psychology, C. Salmon & T. Shackleford (Eds.), chapter 2, pp. 12-32. Oxford: Oxford University Press.

Geary, D.C. & Flinn, M.V. (2001). Evolution of human parental behavior and the human family. Parenting: Science and Practice, 1 (1&2), 5-61.

Muehlenbein, M. & Flinn, M.V. (2011). Pattern and process of human life history evolution. In: Oxford handbook of life history, T. Flatt & A. Heyland (Eds.), chapter 23, pp. 153-168. Oxford: Oxford University Press.

Thank you very much for such brillient comment, still I think that atresia of the primordial follicles in the ovaries is timely life cycle, so the effects of extra genetic factors may play a minor role in prolonging their life span. Definately, better life style and better health will improve the basic circumstances and inviroments in the process of atresia of the follicles and may lead to less no of atresia each month and so delay the onset of menopause.