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What does high lh levels mean: Purpose, High vs. Low vs. Normal Levels


Purpose, High vs. Low vs. Normal Levels

What Is a Luteinizing Hormone Test?

A luteinizing hormone test measures how much luteinizing hormone (LH) is in your blood.

LH helps your reproductive system: specifically, a woman’s ovaries and a man’s testes. It’s also called lutropin and interstitial cell stimulating hormone. It’s made in your pituitary gland, which is about the size of a pea and sits just behind your nose.

Why Would I Get a Luteinizing Hormone Test?

There are different reasons you might get a luteinizing hormone test. Your doctor might order an LH test as part of an infertility workup or to check for a pituitary gland problem.

Signs of a pituitary gland disorder include:

  • Fatigue
  • Unexplained weight loss
  • Weakness
  • Decreased appetite

Other reasons for doing an LH test can differ depending on your sex and sometimes, your age.


An increase in LH during the middle of your cycle causes your ovaries to release eggs (ovulation).

Your doctor might order an LH test if:

  • You’re having trouble getting pregnant
  • Your periods aren’t regular
  • To see if you are in menopause

If you are trying to become pregnant, your doctor might want you to get an LH test several times to pinpoint when your body releases an egg. The amount of LH in your blood surges with ovulation.

There are at-home LH tests that help pinpoint when during your cycle you’re most likely to get pregnant. You can buy these types of tests in drug stores. During the middle of your cycle, you pee on the test stick. If the test is positive, that means there’s an LH surge. This could mean you’ll ovulate within the next day or two, but that might not be the case for everyone. These tests aren’t as accurate as the ones done at a doctor’s office.


For men, your doctor might order an LH test if:


For children, a doctor might order an LH test if:

  • Your child seems to be going through puberty early
  • Your child seems to be going through puberty late

Low LH levels are linked to late puberty, and high levels are linked to early puberty. Signs of early puberty include these things happening before age 8 in girls and 9 in boys:

What Happens During a Luteinizing Hormone Test?

You don’t need to do anything special to prepare for this test.

The health care worker who takes blood for your test will wipe the inside of your elbow with a germ-killing liquid. You’ll have an elastic band around the upper part of your arm.

To collect the sample for the test, the health care worker inserts a thin needle into a vein in your arm, and the blood flows into a vial. You might feel a sting when the needle goes in.

When the vial is full, the tech or nurse will remove the needle and the tourniquet. You’ll get a bandage to stop the bleeding. The whole thing takes only a few minutes.

You might feel lightheaded after the test. You also might develop a bruise at the puncture site.

Your doctor may also check your level of something called follicle-stimulating hormone – or FSH – at the same time.

Luteinizing Hormone Test Results

Your doctor will probably have the results in a few days.

Normal LH numbers depend on a few things, like your sex and age. For women, normal results are:

  • 5-25 international units per liter (IU/L) before menopause
  • 14.2-52.3 IU/Ll after menopause

The level peaks higher during the middle of your cycle.

For men, the normal levels are around 1.8-8.6 IU/L.

For children, LH levels are generally low.

Keep in mind that the “normal” value ranges can differ depending on the lab, so you should always talk to your doctor about what your result means for you.

For women

High levels of LH in a woman’s blood can be a sign of what’s called “primary ovarian failure,” which means that the problem is with the ovaries themselves.

Doctors often can’t pinpoint why primary ovarian failure happens. But it can happen if:

  • You have a metabolic disorder, a genetic disorder, like Turner syndrome, or an autoimmune disorder, like Addison disease
  • You have a low number of follicles, the tiny sacs in your ovaries
  • You’ve gone through chemotherapy or radiation therapy
  • You were exposed to toxins like chemicals, pesticides, or smoke from cigarettes in the past

Low levels of LH may be a sign of “secondary ovarian failure,” which means the problem starts with the pituitary gland or hypothalamus (a part of the brain).

For men

In men, high levels of LH in the blood are a sign of a problem with the testicles and can be a sign of primary testicular failure.

Primary testicular failure isn’t common, but it can happen if you:

It can also happen if your testicles are injured or if you do activities that cause low-level injury to your scrotum, like when you ride a bike or a motorcycle.

Low levels of LH mean the issue is with the pituitary gland or hypothalamus.

For children

If your child has high LH levels, it could mean they’re about to go through puberty or that it’s already started. But if they’re a girl younger than 8 years old or a boy younger than 9, it could be a sign of something like:

  • An injury to their brain
  • A central nervous systems disorder

If your child has low LH levels, they might have delayed puberty, which is where they go through puberty much later than expected. This could happen because of:

  • An eating disorder
  • A disorder of the ovaries or testicles
  • A genetic disorder, like Turner syndrome in girls or Klinefelter’s syndrome in boys
  • A hormone deficiency
  • An infection

Your LH level, by itself, isn’t enough to make a diagnosis. So you may get other tests too.

What This Women’s Hormone Test Can Reveal About Your Health – Blog

Medically reviewed by Neka Miller, PhD on March 27, 2020. Written by Kathryn Wall. To give you technically accurate, evidence-based information, content published on the Everlywell blog is reviewed by credentialed professionals with expertise in medical and bioscience fields.

Hormones have such a powerful effect on your body that they can influence things like weight, energy levels, mood, sex drive, and more. Ever wonder why you’re tired all the time, for example? Your hormones might be one reason why.

Hormone levels can thus reveal a lot about your overall wellness, and checking a variety of hormones can give you more specific insights into your body’s well-being. For example, if you’re experiencing high estrogen symptoms or you’re having symptoms of a low progesterone level, taking an at-home hormone test will allow you to check for imbalances in these hormones and potentially find the cause of your symptoms.

And that’s exactly why our hormone test for women can be informative for a woman at any stage of life: it measures more than 10 hormones involved in reproductive health, weight, energy, and more.

Because the Everlywell Women’s Health Test measures more than 10 hormones involved in reproductive health, weight fluctuation, energy, and more, it can be informative for a woman at any stage of life.

Here’s a breakdown of the hormones this test checks, what they do in your body, and symptoms of hormone levels that may be out of balance.


What Estradiol Does in Your Body:

Estradiol – the main type of estrogen – supports the functions of female sex organs like the vagina, uterus, and breasts. Your estrogen level plays an important role in ovulation (release of an egg from an ovary) during the menstrual cycle.

If your blood estrogen levels are normal, then there is a good chance ovulation has taken place during the month of your sample collection. Testing your blood estrogen levels can help you see if this sex hormone is balanced to support reproductive health. If you’re experiencing low estrogen levels, your healthcare provider may recommend hormone replacement therapy to correct your body’s estrogen imbalance.

What If Estradiol Levels Are Out of Balance?

Low estrogen levels – which often occur during and after menopause – can result in menstrual irregularities, vaginal dryness, and reduced bone strength. If you have high estrogen levels, you might experience stomach pain and bloating, breast tenderness, mood swings, headaches, weight gain, and sleep disturbance. Estradiol levels that remain chronically high can also increase the risk of serious conditions like breast or uterine cancer. That’s why it can be a good idea to check if you have normal estrogen levels for your age.


What Progesterone Does in Your Body:

Your progesterone level is important for regulating menstrual cycles. Progesterone—another sex hormone—is also a top “pregnancy hormone” because it causes the uterine lining to thicken in preparation for a fertilized egg. The right level of progesterone is thus essential for a successful pregnancy.

What If Progesterone Levels Are Out of Balance?

If progesterone levels fall too low, you may have irregular bleeding during your menstrual cycle, your cycles might become more spaced apart, or you might not have any menstrual cycle at all. Miscarriage and ovulation problems are a couple other possible consequences of a progesterone hormone imbalance, as well as headaches, hot flashes, mood changes, and reduced libido.

And if you have high progesterone levels? You might experience common high progesterone symptoms like vaginal dryness, mood changes, and fatigue. To address these symptoms, your healthcare provider may recommend hormone therapy through progesterone supplements of some kind.

Luteinizing Hormone (LH)

What Luteinizing Hormone Does in Your Body:

The pituitary gland, a part of the brain, releases varying amounts of luteinizing hormone (LH) throughout the menstrual cycle. LH levels help control the menstrual cycle. An LH surge in the middle of your cycle triggers ovulation (egg release), and LH levels typically drop after ovulation.

What If Luteinizing Hormone Levels Are Out of Balance?

A low LH level suggests that your pituitary gland might be malfunctioning, preventing the LH surge that’s involved with menstruation. Higher-than-normal LH levels – when seen with high FSH levels – can be a sign of ovarian failure (which can result in infertility. Another possible cause of an elevated LH concentration can be a syndrome known as polycystic ovarian syndrome – or PCOS.

Follicle-Stimulating Hormone (FSH)

What Follicle-Stimulating Hormone Does in Your Body:

Follicle-stimulating hormone, or FSH, prepares ovarian follicles (which house the ovary’s eggs) for ovulation. FSH secretion (and thus levels) tend to increase as egg quantity decreases throughout your life. This is because FSH is involved in ovarian stimulation – as ovarian function declines, higher FSH levels are needed to support ovulation.

What If FSH Levels in Women Are Out of Balance?

There are several possible causes of a low FSH level. Certain kinds of pituitary disorder can cause low FSH secretion. A high FSH level suggests that your ovaries may not have very many eggs left. If high FSH levels occur alongside high LH secretion, your ovaries may have stopped working normally – which may indicate a depleted ovarian reserve, a sign that you may be nearing menopause.

Learn More Here: Why Measure FSH?


What DHEAS Does in Your Body:

Your adrenal glands and ovaries make DHEA, which is then quickly converted to DHEAS. DHEAS helps your body produce other hormones – like testosterone and estrogen. DHEAS is also important for sustaining a healthy amount of muscle mass.

What If DHEAS Levels Are Out of Balance?

DHEAS levels that are too low can result in chronic fatigue, low libido, and mood changes. High DHEAS levels – often accompanied by acne, infertility, an absence of a menstrual cycle, or increased body and facial hair – can be a sign of polycystic ovary syndrome (PCOS) or other problems with the adrenal glands.


What Testosterone Does in Your Body:

Testosterone helps control your body’s muscle-making and fat-burning activities, as well as other aspects of metabolism. EverlyWell’s Women’s Health Test measures free testosterone as opposed to total testosterone.

What If Your Testosterone Level Is Out of Balance?

Your testosterone level needs to fall within a normal range – not too high or too low – for optimal wellness. When testosterone gets too low, you might experience thinning hair, dry skin, mood changes, and – over the long-term – sexual dysfunction and bone loss.

What about too much testosterone? In this case, you might experience acne, menstrual irregularities, and hair growth in parts of your body that hair normally doesn’t grow. Over time, too much testosterone in a woman can contribute to diabetes, obesity, infertility, and more.

Learn More Here: Unhealthy Testosterone Levels In Women: Some Causes And Symptoms


What Cortisol Does in Your Body:

Cortisol is known as the “stress hormone” because it aids in the fight-or-flight response. It provides the body with energy by controlling how much sugar your body burns for fuel. Well-balanced cortisol levels help you fall asleep at night and wake up in the morning.

What If Cortisol Levels Are Out of Balance?

When cortisol levels are too low, you’re more likely to be fatigued, have a loss of appetite (as well as weight loss), and sexual dysfunction. Too much cortisol can result in an irregular menstrual cycle, acne, weight gain, headaches, mood changes, and a hard time concentrating.

Learn More Here: Why Understanding Your Metabolism Is A Key To Better Health

Thyroid Hormones

What Thyroid Hormones Do in Your Body:

The thyroid gland pumps two hormones into your bloodstream: T3 and T4. These thyroid hormones are extremely important to the body because they regulate key functions like metabolism and body temperature. They also help support normal menstrual cycles.

What If Thyroid Hormone Levels Are Out of Balance?

An underfunctioning thyroid gland – a condition known as hypothyroidism – can cause low thyroid hormone levels. Women are 5 to 8 times more likely than men to develop a thyroid disorder. A low amount of thyroid hormones can produce symptoms like weight gain, menstrual cycle irregularities, hair loss, constipation, and feeling cold.

Learn More Here: Low Thyroid Hormone Levels

If thyroid hormone levels get too high, your heart might beat faster, you may have a hard time sleeping, and you may feel more restless or nervous – among other symptoms, like weight loss and thinning hair.

Learn More Here: High Thyroid Hormone Levels

Thyroid-Stimulating Hormone (TSH)

What Thyroid-Stimulating Hormone Does in Your Body:

The thyroid gland releases hormones that control many of the body’s functions, such as metabolism (as mentioned above). Thyroid-stimulating hormone (TSH), which also comes from the pituitary gland in our brains, regulates the amount of hormones the thyroid makes.

What If Thyroid-Stimulating Hormone Levels Are Out of Balance?

Abnormal TSH levels suggest that the thyroid is releasing too many or too few hormones – which can harm a woman’s fertility. Signs of a TSH imbalance include anxiety, trouble sleeping, weight loss or gain, fatigue, and an irregular menstrual cycle.

Learn More Here: What TSH Levels Indicate


What TPOab Does in Your Body:

Thyroid peroxidase antibodies (TPOab) are a kind of antibody. The immune system uses antibodies to eliminate germs that invade your body. TPOab, however, can attack your thyroid gland – hurting or destroying its function – if your immune system malfunctions (this is known as an autoimmune disease).

What If TPOab Levels Are Out of Balance?

Elevated amounts of TPOab – along with low thyroid hormone levels – can mean that your thyroid gland isn’t working well because of an autoimmune disorder called Hashimoto’s disease. Weight gain, an irregular menstrual cycle, fatigue, and hair loss are all clues that an autoimmune condition might be hurting your thyroid gland.

Learn More Here: TPO Antibodies

Why Take This Women’s Hormone Test?

An excellent starting point for understanding how hormone imbalances might be affecting your wellness, the Everlywell at-home Women’s Health Test can give you the insights you need to help your body and feel great. Our test checks key hormone levels to see if they’re within range for your age group.

Because it measures a lot of different hormones – at different points in your cycle – this test lets you check in on many aspects of your health (like weight, energy, and reproductive and sexual health). So it can help you discover areas of your health that might deserve more attention (from you and/or your doctor) – as well as give you peace of mind in other areas. If testing does reveal a hormonal imbalance, your healthcare provider may recommend replacement therapy to help balance your levels.

(You can do the entire testing process from the comfort of home. After you’ve mailed your samples to the lab for analysis – a prepaid shipping label comes with this kit – you’ll receive your results online.)


Primary ovarian insufficiency. Mayo Clinic. URL. Accessed Mar 5, 2019.

Luteinizing Hormone (LH) | Lab Tests Online

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Chen, P. (2017 August 26, Updated). Luteinizing hormone (LH) blood test. MedlinePlus Medical Encyclopedia. Available online at https://medlineplus.gov/ency/article/003708.htm. Accessed on 5/05/19.

Eaton, J. et. al. (2016 November 4, Updated). Luteinizing Hormone Deficiency. Available online at https://emedicine.medscape.com/article/255046-overview. Accessed on 5/05/19.

(© 1995–2018). Luteinizing Hormone (LH), Serum. Mayo Clinic Mayo Medical Laboratories. Available online at https://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/602752. Accessed on 5/05/19.

Jabbour, S. (2018 March 12, Updated). Follicle-Stimulating Hormone Abnormalities. Medscape Endocrinology. Available online at https://emedicine.medscape.com/article/118810-overview#showall. Accessed on 5/05/19.

Straseski, J. and Young, B. (2018 May, Updated). Male Hypogonadism. ARUP Consult. Available online at https://arupconsult.com/content/hypogonadism-male?_ga=2.126530189.1479446145.1525530915-171446445. 1522145782. Accessed on 5/05/19.

Vogiatzi, M. (2018 February 11, Updated). Hypogonadism. Medscape Pediatrics: General Medicine. Available online at https://emedicine.medscape.com/article/922038-overview#showall. Accessed on 5/05/19.

Charbek, E. (2015 July 27, Updated). Luteinizing Hormone. Medscape Laboratory Medicine. Available online at https://emedicine.medscape.com/article/2089268-overview#showall. Accessed on 5/05/19.

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Corbett, JV. Laboratory Tests & Diagnostic Procedures with Nursing Diagnoses, 4th ed. Stamford, Conn.: Appleton & Lang, 1996. pp. 429-431, 726.

Clinical Guide to Laboratory Tests. 3rd ed. Tietz N, ed. Philadelphia: W.B. Saunders & Co; 1995: 248-249, 210-211.

The InterNational Council on Infertility Information Dissemination. PCOS in Pediatrics: When and How Does it Start? Originally written and presented by Silva Arslanian, MD, Children’s Hospital of Pittsburgh, Pittsburgh, PA; summarized in online version by Christine M. Schroeder, PhD. Available online at http://www.inciid.org/pcos/PCOS-pediatrics.html.

Gonadotropins: Luteinizing and Follicle Stimulating Hormones. Available online at http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/hypopit/lhfsh.html.

Blondell RD, Foster MB, Kamlesh CD. Disorders of Puberty. American Family Physician, July 1999 (online publication). Available online at http://www.aafp.org/afp/990700ap/209.html.

Hormone Society. Fact Sheet on Female Infertility. Available online at http://www.endo-society.org/pubrelations/patientInfo/infertility.htm.

The Hormone Foundation. Fact sheet on Polycystic Ovary Syndrome (PCOS). Available online at http://www.hormone.org/pcos_factsheet.html.

Laurence M. Demers, PhD. Distinguished Professor of Pathology and Medicine, The Pennsylvania State University College of Medicine, The M. S. Hershey Medical Center, Hershey, PA.

A Manual of Laboratory & Diagnostic Tests. 6th ed. Fischbach F, ed. Philadelphia: Lippincott Williams & Wilkins; 2000.

Pagana K, Pagana T. Mosby’s Manual of Diagnostic and Laboratory Tests. St. Louis: Mosby; 1998.

Davis B, Mass D, Bishop M. Principles of Clinical Laboratory Utilization and Consultation. Saunders; 1999.

Thompason, Sharon. LH response to GnRH. (Updated Aug 2005) MedlinePlus (online information). Available online at http://www.nlm.nih.gov/medlineplus/print/ency/article/003709.htm.

Neely EK, Wilson DM, Lee PA, Stene M, Hintz RL (July 1995). Spontaneous serum gonadotropin concentrations in the evaluation of precocious puberty. J Pediatric 127(1):47-52 from PubMed. Available online at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=7608810.

Nirupama Kakarla, M.D.; Karen D. Bradshaw, M.D. (Posted 03/05/2004.) Disorders of Pubertal Development: Precocious Puberty. From Seminars in Reproductive Medicine 21(4):339-351 from Medscape. Available online at http://www. medscape.com/viewarticle/468259.

Brito VN, Batista MC, Borges MF, Latronico AC, Kohek MB, Thirone AC, Jorge BH, Arnhold IJ, Mendonca BB. (1999 Oct) Diagnostic value of fluorometric assays in the evaluation of precocious puberty. J Clin Endocrinol Metab. 84(10):3539-44.

Sheehan, M (Dec 2003). Polycystic Ovarian Syndrome: Diagnosis and Management. Clinical Medicine and Research, 2(1): 13-27. Available online at http://www.pubmedcentral.gov/articlerender.fcgi?artid+1069067.

Pagana, K. D. & Pagana, T. J. (© 2007). Mosby’s Diagnostic and Laboratory Test Reference 8th Edition: Mosby, Inc., Saint Louis, MO. Pp 629-631.

Wu, A. (© 2006). Tietz Clinical Guide to Laboratory Tests, 4th Edition: Saunders Elsevier, St. Louis, MO. Pp 694-697.

Vorvick, L. (Updated 2009 July 29). LH. MedlinePlus Medical Encyclopedia [On-line information]. Available online at http://www.nlm.nih.gov/medlineplus/ency/article/003708.htm. Accessed February 2010.

Giannios, N. et. al. (Updated 2008 February 12). Luteinizing Hormone Deficiency. eMedicine [On-line information]. Available online at http://emedicine.medscape.com/article/255046-overview. Accessed February 2010.

Meikle, A. W. et. al. (Updated 2009 November). Amenorrhea. ARUP Consult [On-line information]. Available online at http://www.arupconsult.com/Topics/Amenorrhea.html#. Accessed February 2010.

Brzyski, R. and Jensen, J. (Revised 2007 March) Female Reproductive Endocrinology, Introduction. Merck Manual for Healthcare Professionals [On-line information]. Available online at http://www.merck.com/mmpe/sec18/ch343/ch343a.html?qt=FSH&alt=sh. Accessed February 2010.

Clarke, W. and Dufour, D. R., Editors (© 2006). Contemporary Practice in Clinical Chemistry: AACC Press, Washington, DC. Pp 360-361.

Barker, N, et, al. (Updated 2012 March 23). Luteinizing Hormone Deficiency. Medscape Reference [On-line information]. Available online at http://emedicine.medscape.com/article/255046-overview. Accessed April 2014.

Dowshen, S. (2011 March). Blood Test: Luteinizing Hormone (LH). KidsHealth from Nemours [On-line information]. Available online at http://kidshealth.org/parent/system/medical/blood_test_lh.html. Accessed April 2014.

Kaplowitz, P. (Updated 2013 February 11). Precocious Puberty. Medscape Reference [On-line information]. Available online at http://emedicine.medscape.com/article/924002-overview. Accessed April 2014.

Meikle, A. and Straseski, J. (Updated 2013 November). Infertility. ARUP Consult [On-line information]. Available online at http://www.arupconsult.com/Topics/Infertility.html?client_ID=LTD#tabs=0. Accessed April 2014.

Bielak, K. and Popat, V. (Updated 2012 June 5). Amenorrhea. Medscape Reference [On-line information]. Available online at http://emedicine.medscape.com/article/252928-overview. Accessed April 2014.

(© 1995–2014). LH. Mayo Clinic Mayo Medical Laboratories [On-line information]. Available online at http://www.mayomedicallaboratories. com/test-catalog/Overview/8663. Accessed April 2014.

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Blood Test: Luteinizing Hormone (LH) (for Parents)

What It Is

Luteinizing hormone (LH) plays an important role in sexual development and is produced by the pea-sized pituitary gland in the brain. An LH test measures the level of this hormone in the bloodstream.

In kids, LH levels are high right after birth, but then fall, remaining low until puberty approaches (usually between ages 10 and 14). At this time the hypothalamus, an almond-sized area of the brain that links the nervous system with the hormone-producing endocrine system, releases gonadotropin-releasing hormone (GnRH) that starts the changes of puberty. GnRH signals the pituitary gland to release two puberty hormones into the bloodstream: LH and follicle stimulating hormone (FSH).

In boys, LH and FSH work together to get the testes to begin producing testosterone, the hormone responsible for the physical changes of puberty and the production of sperm.

In girls, LH and FSH prompt the ovaries to begin producing the hormone estrogen, which causes a girl’s body to mature and prepares her for menstruation.

Because LH and FSH work so closely with each other, doctors often perform these tests together, as well as tests for testosterone (the major male sex hormone) and estradiol (a form of estrogen, the major female sex hormone). Taken together, the results can often provide a more complete picture of a child’s sexual maturation, and the well-being of the glands that produce these hormones.

Why It’s Done

Doctors may order an LH test if a boy or girl appears to be entering puberty much earlier or much later than expected. High levels are associated with precocious (early) puberty, while low levels may indicate a delay in sexual development.

The test may also be used to check for damage or disease of the testes or ovaries, pituitary gland, or hypothalamus.

In adults and teens, LH levels can also help doctors evaluate fertility issues and menstrual problems.


No special preparations are needed for this test. On the day of the test, having your child wear a T-shirt or short-sleeved shirt can make things easier for the technician drawing the blood.

page 2

The Procedure

A health professional will clean the skin surface with antiseptic, and place an elastic band (tourniquet) around the upper arm to apply pressure and cause the veins to swell with blood. Then a needle is inserted into a vein (usually in the arm inside of the elbow or on the back of the hand) and blood is withdrawn and collected in a vial or syringe.

After the procedure, the elastic band is removed. Once the blood has been collected, the needle is removed and the area is covered with cotton or a bandage to stop the bleeding. Collecting the blood for the test will only take a few minutes.

What to Expect

Collecting a sample of blood is only temporarily uncomfortable and can feel like a quick pinprick. Afterward, there may be some mild bruising, which should go away in a few days.

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Getting the Results

The blood sample will be processed by a machine, and results are usually available in a couple of days.


The LH test is considered a safe procedure. However, as with many medical tests, some problems can occur with having blood drawn, like:

  • fainting or feeling lightheaded
  • hematoma (blood accumulating under the skin causing a lump or bruise)
  • pain associated with multiple punctures to locate a vein

Helping Your Child

Having a blood test is relatively painless. Still, many kids are afraid of needles. Explaining the test in terms your child can understand might help ease some of the fear.

Allow your child to ask the technician any questions he or she might have. Tell your child to try to relax and stay still during the procedure, as tensing muscles and moving can make it harder and more painful to draw blood. It also may help if your child looks away when the needle is being inserted into the skin.

If You Have Questions

If you have questions about the LH test, speak with your doctor.

Luteinizing hormone and its dilemma in ovulation induction

J Hum Reprod Sci. 2011 Jan-Apr; 4(1): 2–7.

Pratap Kumar

Department of Obstetrics and Gynaecology, Manipal University, Manipal, India

Sameer Farouk Sait

1Kasturba Medical College, Manipal University, Manipal, India

Department of Obstetrics and Gynaecology, Manipal University, Manipal, India

1Kasturba Medical College, Manipal University, Manipal, India

Address for correspondence: Dr. Pratap Kumar, Department of Obstetrics and Gynecology, Kasturba Medical College, Manipal University, Manipal – 576 104, Karnataka, India E-mail: [email protected]

Received 2010 Nov 24; Revised 2010 Nov 25; Accepted 2010 Nov 25.

Copyright © Journal of Human Reproductive Sciences

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC.


Concept of a ‘therapeutic window’ of luteinizing hormone (LH) for successful conception in assisted reproductive technology and ovulation induction has been reviewed in this literature. The separate but complementary roles of follicle stimulating hormone and LH in stimulating folliculogenesis and ovulation are well established. Levels under which low LH concentrations may be equally or suboptimally needed for oocyte quality and subsequent embryonic development competence has been reviewed along with the data related to the high levels of LH promoting follicular atresia.

Keywords: Effects on ovulation, LH ceiling, ovulation induction


Luteinizing hormone (LH): A hormone released by the pituitary gland in response to luteinizing hormone- releasing hormone. It controls the length and sequence of the female menstrual cycle, including ovulation, preparation of the uterus for implantation of a fertilized egg, and ovarian production of both estrogen and progesterone. Theca cells in the ovary respond to LH stimulation by secretion of testosterone, which is converted into estrogen by adjacent granulosa cells. In women, ovulation of mature follicles on the ovary is induced by a large burst of LH secretion – the preovulatory LH surge. Residual cells within ovulated follicles proliferate to form corpora lutea, which secrete the steroid hormones – progesterone and estradiol. Progesterone is necessary for the maintenance of pregnancy, and, in most mammals, LH is required for continued development and function of corpora lutea.


Before we proceed to explore the effects and the potential therapeutic applications of LH on ovulation induction, it is extremely important to first gain a clear understanding of not just the normal physiology of LH and ovulation but also certain basic principles involved in ovulation induction. The follicular phase features a series of sequential actions of hormones and autocrine–paracrine peptides on the follicle, leading the follicle destined to ovulate through a period of initial growth from a primordial follicle through the stages of pre-antral, antral and preovulatory follicle. The two-cell, two-gonadotrophin model is a fundamental concept in ovarian physiology that establishes a role for both LH and follicle stimulating hormone (FSH) in hormone production. Androgen production and release during folliculogenesis is dependent on the stimulation of the theca cells by LH. The theca cells are in close contact with the granulosa cells that proliferate during follicular growth and which are stimulated by FSH to induce the expression of the aromatase enzyme. Thus, androgens produced by the theca cells are then transferred to the granulosa cells where they can be converted to estradiol by aromatase action. Hence, both gonadotrophins are involved in estradiol production during folliculogenesis. The finding of LH receptors in granulosa cells during the intermediate follicular phase suggests that LH has a supplementary role at this time. Growth factors, such as insulin growth factors I and II, are expressed by both granulosa and theca cells during folliculogenesis and are important in promoting follicular maturation. It is believed that LH plays a role in inducing and maintaining this paracrine system by its action on both granulosa and theca cells. Thus, once granulosa cells express sufficient receptors for LH, the activity of FSH can be replaced by administering LH alone.[1] It is not clear when in the follicular phase this action of LH on granulosa cells begins, but the local production of factors is necessary for granulosa cell growth and regulation of oocyte maturation.

During follicular growth, the selection of the dominant follicle occurs despite declining FSH levels because the selected follicle expresses FSH receptors with a lower threshold (i.e. higher receptivity) than the non-selected follicles. It has been suggested that LH has a third role by assisting in deselecting these non-dominant follicles. The rapid increase in LH levels at mid-cycle (LH surge) causes a suspension of further granulosa cell mitosis and permits final oocyte maturation to begin and luteinization of the cumulus-oophorus to occur. The high levels of LH prevent further growth of the non-dominant follicles. This concept has led to the proposal of the ‘LH ceiling’ hypothesis wherein each follicle has an upper limit of responsiveness to LH beyond which follicle maturation ceases and degeneration occurs.[2] Thus, the dominant follicle would have a much higher ceiling than the non-dominant ones, leading to their regression at the time of the LH surge. It has been shown that low-dose stimulation with low-dose LH enhances steroidogenesis without inhibiting cell proliferation whereas high dose LH suppresses granulosa proliferation, initiates atresia of immature follicles and premature luteinization of preovulatory follicles. Another important concept is that of the FSH threshold and window. Administration of gonadotrophins at levels below a threshold does not elicit any ovarian response even when prolonged therapy is used. The FSH threshold is exceeded in the normal cycle during the late luteal and early follicular phase as a result of reduced steroid production from the regressing corpus luteum. The duration of FSH elevation above the threshold levels is limited by a decrease in FSH concentrations around the mid-follicular phase due to the negative feedback exerted by increasing estradiol and inhibin production from growing follicles. This FSH window is important in the determination of the number of developing follicles. If this window is extended in ovulation induction cycles, the recruited cohort of follicles is enlarged and more follicles will eventually develop to the preovulatory stage.

A great deal of discussion has been dedicated to the gonadotrophin need of the developing follicles. As described in the classic “two-cells-two-gonadotrophin” theory, LH is needed to provide the granulosa cells with androgen precursors for estradiol biosynthesis. FSH alone can induce follicle growth, but without LH, estradiol levels remain low and pregnancy will not occur. There is no debate about the need for both hormones in women with hypogonadotropic hypogonadism, but there is significant disagreement about the need for LH in “endocrinologically normal” women. This review analyses whether or not all patients need LH for follicular growth stimulation and new opportunities for improved treatment as a result of the availability of recombinant human LH both in patients with ovulatory disorders (World Health Organization (WHO) groups I and II anovulatory patients) and those undergoing multiple follicular development for assisted reproduction.


The real or presumed benefits of various gonadotrophin preparations were brought up by a number of researchers. A study done on 50 young normal responders analysed results obtained with recombinant FSH (rFSH) and human menopausal gonadotrophin (HMG) during in-vitro fertilization (IVF). [3] They underwent intracytoplasmic sperm injection (ICSI) treatment for male factor infertility and were given either HMG or rFSH after luteal phase downregulation with depot gonadotrophin releasing hormone agonist (GnRHa). The researchers found that in the HMG group, the length of stimulation was shorter and fewer ampoules of gonadotrophin were needed to get the cycle to the retrieval stage. Serum LH and estradiol levels were also higher. On the other hand, with rFSH stimulation, more follicles were seen during stimulation, more oocytes were retrieved, more mature oocytes were obtained, and more embryos were available for transfer. There was no difference in the implantation and pregnancy rates, however. The same study[3] also discussed the results of midcycle LH measurements in GnRHa-downregulated IVF cycles that resulted in conception and those that did not. They did not find a significant difference between LH levels measured in conception and non-conception cycles. Further, they did not find a difference in LH levels between cycles that resulted in ongoing pregnancies and pregnancy loss.

Another study[4] also evaluated the role of recombinant LH (rLH) during IVF cycles. They randomly assigned women who were undergoing IVF treatment, following luteal phase GnRHa downregulation and stimulation with rFSH, to either receive additional placebo or rLH once the largest follicles reached 14 mm in diameter. Although peak estradiol levels were higher in the rLH group, the number of eggs, mature eggs, number and quality of embryos, and pregnancy rates were similar between the two groups. However, these investigators did not measure midcycle LH levels. Rather than supplementing everybody with LH or measuring LH levels, they recommended that the decision to supplement be based on estradiol levels and endometrial thickness. When estradiol levels are low and there is poor endometrial development, they would recommend supplementation with exogenous LH. Similar to the outcome for the luteal phase GnRHa-downregulated cycles, there was not much benefit in adding LH to stimulation in cycles for which the GnRH antagonist is used.

To review the discussion about LH supplementation during IVF, a study[5] analysed the combined results of two studies that their group had performed, which showed significantly higher clinical pregnancy and delivery rates (49% vs 36%) among women who received HMG following luteal GnRHa downregulation, when cycle day 1 LH level was below 1.2 IU/L. The level 1.2 IU/L was used as the cut-off because this is the mean endogenous LH level in women with hypogonadotropic hypogonadism who were shown to benefit from LH supplementation. He attributed the group’s findings to lower fertilization rate, poorer embryo quality, and increased rate of spontaneous abortion when LH levels were low.

Although FSH is essential to stimulate ovarian folliculogenesis, increasing physiological and clinical evidence suggests that moderate LH stimulation may also be critical for optimal follicle and oocyte development.

To assess the endocrine and clinical effects of LH activity supplementation administered in the mid-follicular phase during controlled ovarian hyperstimulation to poor responders who were candidates for in vitro fertilization (IVF) embryo transfer, a prospective, controlled, non-randomized trial with historical controls was done. [6] Twenty-five IVF patients who had shown a poor response to standard, long-protocol GnRHa and FSH only in a preceding cycle (cycle A), were stimulated in the next cycle after six months with hCG supplementation (50 I.U. subcutaneously daily) starting on day 7 during standard, long-protocol GnRHa and FSH (cycle B). The comparative analysis of clinical effects (duration of stimulation, total highly purified (HP)-FSH dose, number of oocytes retrieved and pregnancy rate) and endocrine responses (serum E2, follicular E2 and androstenedione levels) were determined between cycles A and B. Maximum serum E2 levels and clinical pregnancy rate were higher in cycle B, with hCG supplementation. Also, the follicular E2 and androstenedione levels were higher in cycle B. No differences were noted between cycles as regards to the duration of stimulation, total HP-FSH dose and number of oocytes retrieved and the study concluded that the LH activity supplementation in the mid-follicular phase yields favorable pregnancy results in low responders. This may be due to enhanced release of follicular precursors for greater synthesis of E2.

Another study showed how LH plays critical roles in the control of folliculogenesis and ovarian function in humans.[7] LH activity administration during gonadotrophin ovulation induction can enhance ovarian response and optimize treatment. More specifically, LH activity (both LH and low-dose hCG) can support the growth and stimulate the maturation of larger ovarian follicles as a result of specific granulosa cell receptors that develop after a few days of FSH priming. This action of LH is independent of FSH, and it has been shown recently that the last stages of follicular development can be supported by sole administration of LH activity in the form of low-dose hCG, without causing premature luteinization.

Although the role that LH plays in folliculogenesis is still controversial, recent evidence points toward facilitatory actions of LH activity in ovulation induction. Thus, a study[8] compared the response to either highly purified FSH (75 IU FSH/ampoule; group A, 25 subjects) or human menopausal gonadotrophin (75 IU FSH and 75 IU LH/ampoule; group B, 25 subjects) in normoovulatory GnRH agonist-suppressed women, who were candidates for intrauterine insemination. A fixed regimen of two daily ampoules of highly purified FSH or human menopausal gonadotrophin was administered in the initial 14 days of treatment; menotropin dose adjustments were allowed thereafter. Treatment was monitored with daily blood samples for the measurement of LH, FSH, 17beta-estradiol E(2), progesterone, testosterone, hCG, inhibin A, and inhibin B, and transvaginal pelvic ultrasound was performed at two-day intervals. Although preovulatory E(2) levels were similar, both the duration of treatment (16.1±0.8 vs. 12.6±0.5 days; P<0.005) and the per cycle menotropin dose (33.6±2.4 vs. 23.6±1.1 ampoules; P<0.005) were lower in group B. The study concluded that ovulation induction with LH activity-containing menotropins is associated with shorter treatment duration, lower menotropin consumption, and reduced development of small ovarian follicles. These features can be exploited to develop regimens that optimize treatment outcome, lower costs, and reduce occurrence of complications such as multiple gestation and ovarian hyperstimulation.

A number of clinical trials have compared the efficacy of r-hFSH and urinary FSH in women undergoing assisted reproductive technology (ART). In general, these have shown that fewer FSH ampoules are required to achieve ovarian stimulation with r-hFSH, while the number of oocytes retrieved and embryos produced are higher than with urinary FSH, clinical pregnancy rate per cycle started is significantly higher, higher implantation rates were seen in patients treated with r-hFSH than in those treated with urinary FSH, suggesting that embryo viability is increased. The finding that FSH preparations produce effective ovarian stimulation compared to human menopausal gonadotrophins in women undergoing ART raises the question of whether LH is required for ovarian stimulation. Results have suggested that implantation rates may actually be lower in women who received exogenous LH. Such studies suggest, therefore, that in normogonadotropic women, the addition of LH to an r-hFSH regimen does not add any further clinical benefit and may actually be detrimental. [9] However, the addition of LH should still be considered in individual patients on a case by case basis, particularly in candidates who are poor responders.


The introduction of the GnRH agonist into the ovarian stimulation regimen resulted in a significant improvement in outcome with IVF treatment because cycle cancellation resulting from a premature surge in LH levels was reduced significantly and pregnancy rates were increased. However, GnRH agonist administration results in levels of LH during the phase of follicular development that are lower than in spontaneous cycles raising concerns that the levels of LH may be insufficient to support folliculogenesis particularly when recombinant FSH alone is used for ovarian stimulation. Measurement of serum LH levels on day 7 of stimulation in normogonadotropic women permitted the evaluation of different threshold levels on reproductive outcome using receiver operator characteristic curves. [10] It was evident that regardless of the cut-off level selected (i.e. 0.5, 0.7 or 1.0 IU/L), no adverse effect was observed on pregnancy and miscarriage rates. Similarly, in another study on day 8 of stimulation levels of LH, 1.5 IU/L were not associated with any detrimental effect on clinical pregnancy rates.[11] However, when the cut-off level was >1.5 IU/L, reduction in fertilization and clinical pregnancy rates was observed. Collectively, these observations indicate that although GnRH agonist is very effective in preventing an LH surge, the resulting low levels LH are sufficient to permit folliculogenesis despite the fact that no exogenous LH is administered.


Adverse outcomes from elevated serum LH levels have been observed in a variety of studies. A significant reduction in the rate of fertilization was observed in women with raised basal LH levels (greater than one standard deviation from the mean) undergoing treatment with IVF with ovarian stimulation using clomiphene citrate (CC), hMG or a combination of the two. [12] In another study, in women undergoing IVF treatment with a combination of CC and hMG, there were no pregnancies recorded if the urinary output of LH was elevated when measured two days prior to the day of hCG administration.[13] In women with polycystic ovary syndrome, the effect on outcome of the high endogenous levels of LH was observed in a study using pulsatile GnRH to induce ovulation; basal LH levels were lower in women who conceived compared to those who did not, and the rate of miscarriage was higher in those who had elevated levels of LH compared to those who had ongoing pregnancies.[14] The effect of raised LH levels in the follicular phase of spontaneous menstrual cycles was also investigated and found to be detrimental. A higher likelihood of pregnancy was observed when the LH level was <10 IU/L and the miscarriage rate was significantly higher in women with LH levels >10 IU/L.[15]


Polycystic ovary syndrome (PCOS), a relatively common reproductive endocrine disorder often associated with high endogenous LH secretion, menstrual cycle disorders, infertility and high rates of spontaneous abortion, was considered the paradigm condition that proved the potential untoward actions of LH. LH-stimulated theca cell androgen secretion may be involved in the promotion of atresia of non-dominant follicles in the normal menstrual cycle. Growing evidence is pointing towards defining PCOS as a mostly metabolic disorder, with limited untoward effects directly linked to high LH secretion. Excessive insulin levels appear to be causing the majority of the reproductive endocrine disruptions of PCOS. Patients with PCOS have increased LH relative to FSH, but LH is modified by body mass index (BMI). A study was conducted on 24 women to determine whether the impact of BMI on neuroendocrine dysregulation in PCOS is mediated at the hypothalamic or pituitary level.[16] The results of the study showed that BMI was negatively correlated with mean LH, LH/FSH, and LH pulse amplitude but there was no effect of BMI on LH pulse frequency. Percent inhibition of LH was decreased in PCOS, compared with normal women, suggesting an increase in the amount of endogenous GnRH, but was not influenced by BMI.


Some studies tend to imply that LH excess worsens hyperandrogenism through ovarian stimulation of androgenesis. This is unlikely to be valid despite the fact that a major neuroendocrine component of PCOS involves alterations in LH secretion, and primary LH excess has long been considered the cause of the excess ovarian androgen secretion in PCOS. This concept simply arose because of the known stimulatory effect of LH on theca cell function and the elevation of serum LH levels at baseline and in response to GnRH in classic PCOS. In hyperandrogenemic girls destined to develop PCOS, the nocturnal increase in ovarian steroids may not be adequate to suppress the GnRH pulse generator, leading to a persistently rapid LH pulse frequency, impaired FSH production, and inadequate follicular development.[17]

Circulating levels of LH are essential for the production of steroid hormones that regulate the timing of ovulation and target tissue responses, as well as maintenance of the corpus luteum and therefore early pregnancy. Clinical and basic science observations show that elevated levels of serum LH during the follicular phase of the menstrual cycle are not only unnecessary for follicular maturation but are deleterious to normal reproductive processes. These elevations may occur as a result of administration of exogenous LH or through an endogenous pathological process like in PCOS. Resting levels of LH, synergizing with locally produced IGFs, inhibin and perhaps other growth factors, are adequate for normal follicular growth and steroidogenesis. Elevations in serum LH above these resting levels may result in increased androgen production that diminishes follicular function and reduces early embryo viability. Elevated LH levels during the preovulatory period may also negatively influence post-ovulatory events such as conception and implantation. With these facts in mind, the best results for ovulation induction would be expected with purified FSH administration to women following GnRH downregulation. One may, therefore, envisage the role of LH during the follicular phase of the menstrual cycle to be a crescendo: of little importance during the early follicular phase and most important at the time of ovulation. FSH, on the other hand, has a reversed pattern of importance: essential for early events and having a relatively minor role at the time of ovulation.[18] Although LH receptors have not yet been identified in oocytes, excessive LH may disrupt granulosa cell communication in the cumulus-oophorus, which is critical to maintain the oocyte in the dictyate stage of meiosis until ovulation.[19,20] Thus, according to this theory, abnormal oocyte maturation could be responsible for the reduced fertility and increased miscarriage rates frequently encountered in PCOS. Growing evidence is pointing towards defining PCOS as a mostly metabolic disorder, with limited untoward effects directly linked to high LH secretion. Excessive insulin levels appear to be causing the majority of the reproductive endocrine disruptions of PCOS. Furthermore, insulin-lowering drugs improve glycodelin levels (an endogenous compound linked to embryo implantation) and significantly reduce the incidence of miscarriage in patients at risk. [21] These positive effects cannot be achieved by reductions of endogenous LH secretion, for instance with GnRH analogs. Thus, it appears that the hypersecretion of LH in PCOS is simply an epiphenomenon, possibly related to chronic anovulation and reduced progesterone secretion, relative increments of estrogens such as estrone and unbound 17b-estradiol, or a combination of these factors. Recently, it was also shown that excessive LH secretion alone is not the cause of ovarian hyperandrogenism. The lack of any cause±effect relationship between LH hypersecretion and reproductive system disorders, particularly in PCOS, clearly undermines theories of detrimental actions of LH on fertility.

The defect in steroidogenesis must be the result of escape from normal downregulation of thecal cell secretion rather than over-stimulation by LH. If we accept these results, then the fundamental defect underlying the androgen excess of PCOS is ovarian hyper-responsiveness to gonadotrophin action because of escape from downregulation and not a primary result of excess LH per se. Taken together, all these observations suggest that dysregulation of androgen biosynthesis is an intrinsic property of PCOS theca cells. Hence, the evidence suggests that LH is not a major player in the hyperandrogenism of PCOS, and excess LH may be a consequence of the metabolic alterations in PCOS.

From a clinical point of view it is axiomatic that LH supplementation must be used for the induction of ovulation in WHO Group I patients. Nevertheless, this may not be valid for WHO group II patients and for patients under ART for different reasons.


The separate but complementary roles of FSH and LH in stimulating folliculogenesis and ovulation are well established. However, it is not known if there are levels under which low LH concentrations may be equally or suboptimal for oocyte quality and subsequent embryonic development competence. On the other hand, there are some conflicting data related to the high levels of LH promoting follicular atresia and early miscarriage. This has lead to the concept of a ‘therapeutic window’ of LH for successful conception in ART and ovulation induction. As can be seen from the opposing results presented by various groups, the controversy surrounding the role of LH in ovarian stimulation has certainly not been resolved. Although FSH is universally recognized as the key driver of ovarian follicle growth and maturation, the role of LH in these processes is more controversial. Future studies are needed to better identify those who would benefit from the addition of LH.


Source of Support: Nil

Conflict of Interest: None declared.


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Luteinising hormone | You and Your Hormones from the Society for Endocrinology

Alternative names for luteinising hormone

Interstitial cell stimulating hormone; luteinizing hormone; lutropin; LH

What is luteinising hormone?

Luteinising hormone, like follicle stimulating hormone, is a gonadotrophic hormone produced and released by cells in the anterior pituitary gland. It is crucial in regulating the function of the testes in men and ovaries in women.

In men, luteinising hormone stimulates Leydig cells in the testes to produce testosterone, which acts locally to support sperm production. Testosterone also exerts effects all around the body to generate male characteristics such as increased muscle mass, enlargement of the larynx to generate a deep voice, and the growth of facial and body hair.

In women, luteinising hormone carries out different roles in the two halves of the menstrual cycle. In weeks one to two of the cycle, luteinising hormone is required to stimulate the ovarian follicles in the ovary to produce the female sex hormone, oestradiol. Around day 14 of the cycle, a surge in luteinising hormone levels causes the ovarian follicle to tear and release a mature oocyte (egg) from the ovary, a process called ovulation. For the remainder of the cycle (weeks three to four), the remnants of the ovarian follicle form a corpus luteum. Luteinising hormone stimulates the corpus luteum to produce progesterone, which is required to support the early stages of pregnancy, if fertilisation occurs.

How is luteinising hormone controlled?  

The secretion of luteinising hormone from the anterior pituitary gland is regulated through a system called the hypothalamic-pituitary-gonadal axis. Gonadotrophin-releasing hormone is released from the hypothalamus and binds to receptors in the anterior pituitary gland to stimulate both the synthesis and release of luteinising hormone (and follicle stimulating hormone). The released luteinising hormone is carried in the bloodstream where it binds to receptors in the testes and ovaries to regulate their hormone secretions and the production of sperm or eggs.   

The release of hormones from the gonads can suppress the secretion of gonadotrophin-releasing hormone and, in turn, luteinising hormone from the anterior pituitary gland. When levels of hormones from the gonads fall, the reverse happens and gonadtrophin-releasing hormone and hence luteinising hormone rise. This is known as negative feedback.  

In men, testosterone exerts this negative feedback and in women oestrogen and progesterone exert the same effect except at the midpoint in the menstrual cycle.  At this point, high oestrogen secretions from the ovary stimulate a surge of luteinising hormone from the pituitary gland, which triggers ovulation. 

The fine tuning of luteinising hormone release is vital to maintaining fertility. Because of this, compounds designed to mimic the actions of gonadotrophin-releasing hormone, luteinising hormone and follicle stimulating hormone are used to stimulate gonadal function in assisted conception techniques such as in vitro fertilisation (IVF). Measuring the levels of luteinising hormone present in urine can be used to predict the timing of the luteinising hormone surge in women, and hence ovulation. This is one of the methods employed in ovulation prediction kits used by couples wishing to conceive.

What happens if I have too much luteinising hormone?

Too much luteinising hormone can be an indication of infertility. Since the secretion of luteinising hormone is tightly controlled by the hypothalamic-pituitary-gonadal axis, high levels of luteinising hormone in the bloodstream can indicate decreased sex steroid production from the testes or ovaries (for example, as in premature ovarian failure).  

Polycystic ovary syndrome is a common condition in women associated with high levels of luteinising hormone and reduced fertility. In this condition, an imbalance between luteinising hormone and follicle stimulating hormone can stimulate inappropriate production of testosterone.

Genetic conditions, such as Klinefelter’s syndrome and Turner syndrome, can also result in high luteinising hormone levels. Klinefelter’s syndrome is a male-only disorder and results from carrying an extra X chromosome (so that men have XXY, rather than XY chromosomes). As a result of this, the testes are small and do not secrete adequate levels of testosterone to support sperm production. Turner syndrome is a female-only disorder caused by a partial or full deletion of an X chromosome (so that women have XO, rather than XX). In affected patients, ovarian function is impaired and therefore luteinising hormone production increases to try to stimulate ovarian function.  

What happens if I have too little luteinising hormone?

Too little luteinising hormone will also result in infertility in both men and women, as a critical level of luteinising hormone is required to support testicular or ovarian function.

In men, an example of a condition where low levels of luteinising hormone are found is Kallmann’s syndrome, which is associated with a deficiency in gonadotrophin-releasing hormone secretion from the hypothalamus.

In women, a lack of luteinising hormone means that ovulation does not occur and menstrual periods may not occur regularly. An example of a condition which can be caused by too little luteinising hormone is amenorrhoea.

Last reviewed: Feb 2018

Hormone Levels and PCOS

Remember that PCOS cannot be diagnosed by symptoms alone.  PCOS is a very complicated endocrine disorder.  Blood tests to measure hormone levels, an ultrasound to look at your reproductive organs and thorough personal and family histories should be completed before a PCOS diagnosis is confirmed. Depending on your symptoms, your physician will determine exactly which tests are necessary. Assessing hormone levels serves two major purposes. First of all, it helps to rule out any other problems that might be causing the symptoms. Secondly, together with an ultrasound and personal and family histories, it helps your doctor confirm that you do have PCOS. Most often, the following hormone levels are measured when considering a PCOS diagnosis:

  • Lutenizing hormone (LH)
  • Follicle-stimulating hormone (FSH)
  • Total and Free Testosterone
  • Dehydroepiandrosterone sulfate (DHEAS)
  • Prolactin
  • Androstenedione
  • Progesterone.

Other hormones that may be checked include:

  • estrogen
  • thyroid stimulating hormone (TSH)

In addition, glucose, cholesterol (HDL, LDL and triglicerides) levels might also be assessed.

Lutenizing Hormone (LH) and Follicle Stimulating Hormone (FSH)

LH and FSH are the hormones that encourage ovulation. Both LH and FSH are secreted by the pituitary gland in the brain. At the beginning of the cycle, LH and FSH levels usually range between about 5-20 mlU/ml. Most women have about equal amounts of LH and FSH during the early part of their cycle. However, there is a LH surge in which the amount of LH increases to about 25-40 mlU/ml 24 hours before ovulation occurs. Once the egg is released by the ovary, the LH levels goes back down.

While many women with PCOS still have LH and FSH still within the 5-20 mlU/ml range,  their LH level is often two or three times that of the FSH level. For example, it is typical for women with PCOS to have an LH level of about 18 mlU/ml and a FSH level of about 6 mlU/ml (notice that both levels fall within the normal range of 5-20 mlU/ml).  This situation is called an elevated LH to FSH ratio or a ratio of 3:1. This change in the LH to FSH ratio is enough to disrupt ovulation. While this used to be considered an important aspect in diagnosing PCOS, it is now considered less useful in diagnosing PCOS, but is still helpful when looking at the overall picture.


All women have testosterone in their bodies. There are two methods to measure testosterone levels:

  • Total Testosterone
  • Free Testosterone

Total testosterone refers to the total amount of all testosterone, including the free testosterone, in your body.  The range for this is 6.0-86 ng/dl.  Free testosterone refers to the amount of testosterone that is unbound and actually active in your body.  This amount usually ranges from 0.7-3.6 pg/ml.  Women with PCOS often have an increased level of both total testosterone and free testosterone.  Furthermore, even a slight increase in testosterone in a woman’s body can suppress normal menstruation and ovulation.


DHEA-S or dehydroepiandrosterone is another male hormone that is found in all women. DHEA-S is an androgen that is secreted by the adrenal gland. It is normal for women to have DHEA-S levels anywhere between 35-430 ug/dl.  Most women with PCOS tend to have DHEA-S levels greater than 200 ug/dl.


Prolactin is a pituitary hormone that stimulates and sustains milk production in nursing mothers. Prolactin levels are usually normal in women with PCOS, generally less than 25 ng/ml. However, it is important to check for high prolactin levels in order to rule out other problems, such as a pituitary tumor, that might be causing PCOS-related symptoms.  Some women with PCOS do have elevated prolactin levels, typically falling within the 25-40 ng/ml range.

Androstenedione (ANDRO)

ANDRO is a hormone that is produced by the ovaries and adrenal glands. Sometimes high levels of this hormone can affect estrogen and testosterone levels. Normal ANDRO levels are between 0.7 ­ 3.1 ng/ml.


Progesterone is produced by the corpus luteum after ovulation occurs.  Progesterone helps to prepare the uterine lining for pregnancy.  For women with PCOS, especially those who are trying to become pregnant using fertility medications, Progesterone levels are checked about 7 days after it is thought that ovulation occurred.  If the Progesterone level is high (usually greater than 14 ng/ml) this means that ovulation did indeed occur and the egg was released from the ovary.  If the progesterone level is low the egg was probably not released. This test is especially important because sometimes women with PCOS can have some signs that ovulation is occurring however, when the progesterone test is done, it shows that ovulation did not occur. If this happens, your body is may be producing a follicle and preparing you to ovulate, but for some reason the egg is not actually being released from the ovary.   This information helps your physician possibly adjust fertility medication for the next cycle to encourage the release of the egg.


Estrogen is the female hormone that is secreted mainly by the ovaries and in small quantities by the adrenal glands.  The most active estrogen in the body is called estradiol.  A sufficient amount of estrogen is needed to work with progesterone to promote menstruation. Most women with PCOS are surprised to find that their estrogen levels fall within the normal range (about 25-75 pg/ml).  This may be due to the fact that the high levels of insulin and testosterone found in women with PCOS are sometimes converted to estrogen.


TSH stands for Thyroid Stimulating Hormone and is produced by the thyroid, a gland found in the neck. Women with PCOS usually have normal TSH levels (0. 4-3.8 uIU/ml).  TSH is checked to rule out other problems, such as an underactive or overactive thyroid, which often cause irregular or lack of periods and anovulation.

Insulin and Glucose

Due to the recent research that PCOS is probably caused by insulin resistance, physicians are beginning to check glucose levels as a factor when diagnosing PCOS.   Most women with polycystic ovary syndrome should have an Fasting Plasma Glucose Test and a Glucose Tolerance Test at diagnosis and periodically thereafter, depending on risk factors.  A high glucose level can indicate insulin resistance, a diabetes-related condition that contributes to PCOS.


Researchers are also beginning to notice a connection between PCOS and heart disease; therefore, some physicians may want to look at your cholesterol levels when diagnosing and treating PCOS. Women with PCOS have a greater tendency to have high cholesterol, a major risk factor for developing heart disease. Cholesterol is a fat-like substance normally used by the body for form cell membranes and certain hormones.  A high cholesterol level is considered greater than 200. Also, since the levels of good (high-density lipoproteins or HDL) and bad (low-density lipoproteins or LDL) are sometimes more indicative of a woman’s risk for developing heart disease, these levels might also be assessed.

Too much bad cholesterol tends to increase the risk for plaque to build up in the arteries which can lead to a heart attack. Too much good cholesterol is believed to remove the cholesterol from building up in the arteries.  Women with PCOS tend to have less good cholesterol and more bad cholesterol.  In addition, triglyceride levels, another component of cholesterol, tend to be high in women with PCOS which further contributes to the risk of heart disease.   Even if your physician does not check your cholesterol levels when diagnosing PCOS, it is a good idea to have these levels checked periodically since women with PCOS have a greater chance of developing high cholesterol which can lead to heart disease.

More About Hormone Levels

It is important to remember that with all women, hormone levels can very greatly.  It is also important to mention that since the “normal” ranges vary greatly for some hormones (especially since each lab sets its own “normal” values for these hormones), some women with PCOS have hormone levels that appear within the “normal” range, but still suffer from symptoms and still might have PCOS. This is especially true with Testosterone , DHEAS, and LH levels.  Unfortunately, many physicians are not familiar enough with PCOS to understand that even small changes in hormone levels can cause PCOS-related symptoms.   If you have a Testosterone level of >40 ng/ml, DHEAS level of >200 ug/dl or a LH level that is two or three times that of your FSH level (LH and FSH levels should be roughly equal), seek the advice of a specialist since there is still a good possibility you might have PCOS.


Angela Best-Boss and Evelina Weidman Sterling, authors of Living with PCOS with Richard Legro MD (Editor)

90,000 ovarian dysfunction, menstrual irregularities


A set of tests to help identify hormonal causes of reproductive system dysfunction in women (cycle disorders, infertility).


In the morning on an empty stomach. Check the date of the study with the attending physician (usually on the 6-7th day of the menstrual cycle). On the eve, exclude excessive physical activity, alcohol intake, emotional stress.


This profile includes the following analyzes:

Cortisol (Hydrocortisone)

Adrenal cortex steroid hormone; the most active of the glucocorticoid hormones.

Regulator of carbohydrate, protein and fat metabolism. Cortisol is produced by the fascicular area of ​​the adrenal cortex under the control of ACTH. In the blood, 75% of cortisol is associated with corticosteroid-binding globulin (transcortin), which is synthesized by the liver. Another 10% is weakly bound to albumin. Cortisol is metabolized in the liver, the hormone has a half-life of 80-110 minutes, it is filtered in the renal glomeruli and excreted in the urine.

This hormone plays a key role in the body’s defense responses to stress.It has a catabolic effect. Increases the concentration of glucose in the blood by increasing its synthesis and decreasing utilization at the periphery (insulin antagonist). Reduces the formation and increases the breakdown of fats, contributing to hyperlipidemia and hypercholesterolemia. Cortisol has a slight mineralocorticoid activity, but when it is excessively formed, sodium retention in the body, edema and hypokalemia are observed; a negative calcium balance is formed. Cortisol potentiates the vasoconstrictor effect of other hormones, increases urine output.Cortisol has an anti-inflammatory effect and reduces the body’s hypersensitivity to various agents, suppressing cellular and humoral immunity. Cortisol stabilizes lysosomal membranes. It helps to reduce the number of zosinophils and lymphocytes in the blood while increasing neutrophils, erythrocytes and platelets.

The daily rhythm of secretion is characteristic: maximum in the morning hours (6-8 hours), minimum – in the evening (20-21 hours). The secretion of cortisol changes little with age.During pregnancy, there is a progressive increase in concentration associated with an increase in the content of transcortin: in the late stages of pregnancy, a 2-5-fold increase is noted. The circadian rhythm of the secretion of this hormone may be disrupted. In the case of a partial or complete block in the synthesis of cortisol, an increase in the concentration of ACTH and the total concentration of corticoids occurs.

Limits of determination: 27.6 nmol / L-6599.6 nmol / L.

Thyroid stimulating hormone (TSH, thyrotropin)

Glycoprotein hormone that stimulates the formation and secretion of thyroid hormones.

Produced by basophils of the anterior pituitary gland under the control of thyroid-stimulating hypothalamic releasing factor, as well as somatostatin, biogenic amines and thyroid hormones. Strengthens the vascularization of the thyroid gland. Increases the flow of iodine from blood plasma into thyroid cells, stimulates the synthesis of thyroglobulin and the release of T3 and T4 from it, and also directly stimulates the synthesis of these hormones. Enhances lipolysis.

There is an inverse logarithmic relationship between the concentrations of free T4 and TSH in the blood.

For TSH, daily fluctuations in secretion are characteristic: the highest values ​​of TSH in the blood reach 2 – 4 a.m., a high level in the blood is also determined at 6 – 8 a. m., the minimum TSH values ​​fall on 17 – 18 p.m. The normal rhythm of secretion is disturbed when awake at night. During pregnancy, the concentration of the hormone rises. With age, the concentration of TSH increases slightly, the amount of hormone release at night decreases.

Limits of determination: 0.0025 mU / L-100 mU / L.

Follicle stimulating hormone (FSH)

Glycoprotein gonadotropic hormone of the pituitary gland. Stimulator of the development of seminiferous tubules and spermatogenesis in men and follicles in women.

Synthesized by basophilic cells of the anterior pituitary gland under the control of gonadoliberin, sex hormones and inhibin. FSH is released into the blood in pulses at intervals of 1 to 4 hours. The concentration of the hormone during the release is 1.5-2.5 times the average level; the burst lasts about 15 minutes.There are seasonal fluctuations in the concentration of the hormone in the blood: in summer, the level of FSH in men is higher than in other seasons.

In women, FSH stimulates the formation of follicles. Achieving a critical level of FSH leads to ovulation. In men during puberty, FSH triggers spermatogenesis, and then participates in its maintenance. FSH is the main stimulant of the growth of the vas deferens. FSH increases the concentration of testosterone in plasma, thereby facilitating the process of sperm maturation.

The LH / FSH ratio is important. Normally, before menarche, it is equal to 1; a year after menarche – from 1 to 1.5; in the period from two years after the onset of menarche and before menopause – from 1.5 to 2.

Limits of determination: 0.05 mU / ml-750 mU / ml.

Due to the pulsating nature of the release of FSH and LH, in conditions leading to a decrease in the level of these hormones, it may be useful to study three consecutive blood samples, every 30 minutes. In conditions associated with an increased level of FSH (as, for example, with dysfunctions of the gonads during menopause), taking one sample is adequate.

Luteinizing hormone (LH)

Glycoprotein gonadotropic hormone. It is synthesized by basophilic cells of the anterior pituitary gland under the influence of hypothalamic releasing factors.

Stimulates the synthesis of estrogen in women; regulates the secretion of progesterone and the formation of the corpus luteum. Reaching a critical level of LH leads to ovulation and stimulates the synthesis of progesterone in the corpus luteum. In men, by stimulating the formation of sex hormone binding globulin (SHBG), it increases the permeability of the seminiferous tubules for testosterone.This increases the concentration of testosterone in the blood plasma, which contributes to the maturation of sperm. In turn, testosterone re-inhibits the release of LH. In men, LH levels increase by the age of 60 to 65.

The release of the hormone is of a pulsating nature and in women depends on the phase of the ovulation cycle. During puberty, the LH level rises, approaching the values ​​typical for adults. In the menstrual cycle in women, the peak LH concentration falls on ovulation, after which the level of the hormone falls and keeps the entire luteal phase at values ​​lower than in the follicular phase.During pregnancy, the concentration decreases. In the postmenopausal period, there is an increase in the concentration of LH, as well as FSH (follicle-stimulating hormone). In women, the concentration of LH in the blood is maximum in the interval from 12 to 24 hours before ovulation and is retained throughout the day, reaching a concentration 10 times higher than in the non-ovulation period.

The LH / FSH ratio is important. Normally, before menarche, it is equal to 1; after a year of menarche – from 1 to 1.5; in the period from two years after the onset of menarche and before menopause – from 1.5 to 2.

Limits of determination: 0.09 mU / ml-1000 mU / ml.


Polypeptide hormone that stimulates breast proliferation and milk secretion.

Prolactin is produced in the anterior pituitary gland, a small amount is synthesized by peripheral tissues. During pregnancy, it is also produced in the endometrium. During pregnancy, prolactin supports the existence of the corpus luteum and the production of progesterone, stimulates the growth and development of the mammary glands and the formation of milk.It is one of the hormones that contribute to the formation of sexual behavior. Prolactin regulates water-salt metabolism, delaying the excretion of water and sodium by the kidneys, and stimulates calcium absorption. In general, prolactin activates anabolic processes in the body. Other effects include stimulating hair growth. Prolactin also has a modulating effect on the immune system.

The daily secretion of prolactin has a pulsating character. During sleep, its level rises. After awakening, the concentration of prolactin decreases sharply, reaching a minimum in the late morning hours.In the afternoon, the hormone levels rise. In the absence of stress, daily fluctuations in levels are within the normal range. During the menstrual cycle in the luteal phase, the level of prolactin is higher than in the follicular phase. From the 8th week of pregnancy, the prolactin level rises, reaching a peak by 20-25 weeks, then decreases immediately before childbirth and increases again during lactation.

The test for the presence of macroprolactin is carried out as an additional study to the determination of prolactin when an increased level of prolactin is detected (according to the relevant recommendations – for all patients with a prolactin result> 700 mU / l).Prolactin can be present in the blood in different molecular forms.

Macroprolactin is a prolactin bound in immune complexes with antibodies and is present in the blood in varying amounts. It is cleared from the blood more slowly than monomeric prolactin and can accumulate in high concentrations. This form of prolactin is less bioactive; patients with high levels of macroprolactin may not have the classic symptoms associated with an increase in prolactin concentration.

The results of this study should be taken into account when interpreting the increased values ​​of the prolactin index, the discrepancy between the study results and the general clinical picture, the lack of reproducibility when conducting studies in different laboratories. We draw your attention to the fact that performing a study for macroprolactin does not increase the cost of determining prolactin. Identification of the possible significant presence of macroprolactin in samples of hyperprolactinemic patients is necessary to exclude diagnostic errors, the need to prescribe unnecessary biochemical and X-ray examinations, as well as to prevent inadequate drug therapy or surgery.

Limits of determination: 12.6 mU / l-172200 mU / l.


The most active estrogenic (female) sex steroid hormone.

In women, it is produced in the ovaries, in the placenta and in the reticular adrenal cortex under the influence of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin. In small quantities, estradiol is formed during the peripheral conversion of testosterone. In men, estradiol is formed in the testes, in the adrenal cortex, but most of it in peripheral tissues due to the conversion of testosterone.

In women, estradiol ensures the formation of the female reproductive system, the development of female secondary sexual characteristics in puberty, the formation and regulation of menstrual function, the development of the egg, the growth and development of the uterus during pregnancy; responsible for the psychophysiological characteristics of sexual behavior. Provides the formation of female-type subcutaneous adipose tissue. By reducing the resistance of the vessels of the uterus, it increases blood flow in it and stimulates endometrial hyperplasia.Ovulation occurs 24 to 36 hours after the onset of a suprathreshold level of estradiol. A prerequisite for the realization of the effects of estradiol is the correct ratio with the level of testosterone. Estradiol has an anabolic effect, enhances bone metabolism and accelerates the maturation of skeletal bones. Promotes sodium and water retention in the body. Reduces cholesterol levels and increases blood clotting activity. Estradiol affects the release of neurotransmitters, contributing to increased nervous tension and irritability.

Daily fluctuations in serum estradiol concentration are associated with the rhythm of LH (luteinizing hormone) secretion: the maximum falls on the period from 15 to 18 hours, and the minimum is between 24 and 2 hours.In men, the level of estradiol increases progressively, in boys, the increase occurs to a lesser extent … In women of childbearing age, serum and plasma estradiol levels depend on the phase of the menstrual cycle. At the beginning of the cycle, the concentration of estradiol increases slowly. The highest level of estradiol is observed in the late follicular phase.After ovulation, the level of the hormone decreases, a second, smaller in amplitude, rise occurs. Then there is a decline in the concentration of the hormone, which continues until the end of the luteal phase. During pregnancy, the concentration of estradiol in serum and plasma increases by the time of delivery, and after delivery it returns to normal on the 4th day. With age, women experience a decrease in the concentration of estradiol. In postmenopausal women, the concentration of estradiol decreases to the level observed in men.

Limits of definition: 37.0 pmol / l-40370 pmol / l.

Dehydroepiandrosterone sulfate (DEA-S04)

Androgenic hormone of the adrenal glands.

Produced in the adrenal cortex. The level of this hormone is an adequate indicator of the androgen-synthetic activity of the adrenal glands. The hormone has only a weak androgenic effect, however, in the process of its metabolism, testosterone and dihydrotestosterone are formed in peripheral tissues. Does not detect noticeable daily fluctuations and has a low clearance rate.

During pregnancy, it is produced by the adrenal cortex of the mother and fetus and serves as a precursor for the synthesis of estrogen in the placenta. Its level rises to the period of puberty, and then gradually decreases as a person leaves reproductive age. During pregnancy, the level of this hormone also decreases.

The determination of DEA-SO4 replaces the determination of 17-KC in urine for the assessment of adrenal androgen production. In the ovaries, the synthesis of DEA-sulfate does not occur (therefore, the test is used to determine the source of hyperandrogenemia in a woman’s body).

Limits of determination: 0.08-81.42 μmol / L ..


Steroid androgenic hormone, which causes the development of secondary sexual characteristics, puberty and normal sexual function.

In men, the main part is synthesized in the testicle; a smaller number – by cells of the reticular layer of the adrenal cortex and during transformation from precursors in peripheral tissues. In women, testosterone is formed in the process of peripheral transformation, as well as during synthesis in the cells of the inner membrane of the ovarian follicle and the reticular layer of the adrenal cortex.

Testosterone has anabolic effects on muscle tissue, promotes the maturation of bone tissue, stimulates the formation of sebum by the skin glands, participates in the regulation of lipoprotein synthesis by the liver, modulates the synthesis of b-endorphins (“hormones of joy”), insulin. In men, it provides the formation of the male reproductive system, the development of male secondary sexual characteristics in puberty, activates sexual desire, spermatogenesis and potency, is responsible for the psychophysiological characteristics of sexual behavior.In women, it is involved in the mechanism of follicle regression in the ovaries and in the regulation of the level of pituitary gonadotropic hormones.

In men, testosterone levels increase during puberty and remain at a high level, on average, up to 60 years. The level of the hormone in the blood plasma fluctuates during the day. The maximum concentration is observed in the morning hours, the minimum – in the evening. In autumn, testosterone concentration rises. In women, the maximum testosterone concentration is determined in the luteal phase and during ovulation.In pregnant women, the concentration of testosterone increases by the third trimester, exceeding almost 3 times the concentration in non-pregnant women. During menopause, the concentration of testosterone decreases.

Limits of determination: 0.15 nmol / L-120 nmol / L.

Globulin binding sex hormones (SHBG)

Blood plasma protein involved in the binding and transport of sex hormones.

There are several synonyms for the name of this protein: sex steroid binding globulin, androgen binding globulin, sex steroid binding globulin, sex hormone-binding globulin.This glycoprotein is synthesized in the liver; its molecular weight is about 80,000 – 100,000 daltons, the molecule has 1 binding site for steroid hormones. SHBG binds testosterone and 5-dihydrotestosterone with high affinity and estradiol is somewhat weaker.

Testosterone circulates mainly in the form associated with SHBG, to a lesser extent with albumin and cortisol-binding globulin. Since variations in carrier protein levels can affect circulating testosterone levels, SHBG levels are usually measured in addition to measuring total testosterone.The level of SHBG synthesis in the liver depends on sex hormones: estrogens increase, and androgens decrease its production. Therefore, the content of SHBG in women is almost twice as high as in men. With a decrease in estradiol production, the total hormone content and the concentration of free hormone in the blood decrease in parallel.

With a decrease in the production of androgens, an increase in the production of SHBG causes the maintenance of a constant level of total testosterone, although the concentration of the free hormone decreases. Therefore, the level of total plasma testosterone may be paradoxically normal in the early stages of testicular disease. Decreased SHBG levels are often found in hirsutism, acne vulgaris, and polycystic ovary syndrome. With hirsutism, a decrease in SHBG is described in about 30% of the women surveyed.

The level of SHBG in the late stages of pregnancy or after the administration of estrogens can be significantly increased. Androgen administration is often combined with reduced SHBG levels. The Free Androgen Index (FAI), calculated as the ratio of total testosterone to SHBG in%, correlates with the content of biologically available free testosterone and is used as a useful indicator of the pathological status of androgens.

After 60 years, the content of SHBG increases by about 1.2% per year, thus, with age, the level of bioavailable testosterone decreases to a greater extent than the level of total testosterone.

17-OH progesterone (17-OP)

17-OH progesterone is an intermediate in the synthesis of cortisol in the adrenal glands.

17-OH-progesterone (17-hydroxyprogesterone) is a steroid produced in the adrenal glands, gonads and placenta, a product of metabolic transformations of progesterone and 17-hydroxypregnenolone. In the adrenal glands, 17-OH-progesterone (with the participation of 21-hydroxylase and 11-b-hydroxylase) is further converted into cortisol. Both in the adrenal glands and in the ovaries, 17-OH-progesterone can also be converted (by the action of 17-20-lyase) into androstenedione, a precursor of testosterone and estradiol.

For 17-OH-progesterone, ACTH-dependent daily fluctuations are characteristic (similar to cortisol, the maximum values ​​are detected in the morning, the minimum at night). In women, the formation of 17-OH-progesterone in the ovaries fluctuates during the menstrual cycle.The day before the peak of luteinizing hormone (LH), there is a significant rise in 17-OH-progesterone, followed by a peak that coincides with the LH peak in the middle of the cycle, followed by a short-term decrease, followed by a rise, correlating with the level of estradiol and progesterone. The content of 17-OH-progesterone increases during pregnancy. Levels of 17-OH-progesterone depend on age: high values ​​are observed during the fetal period and immediately after birth (in premature infants, the concentrations of 17-OH-progesterone are relatively higher). During the first week of life, 17-OH-progesterone levels fall and remain consistently low during childhood, progressively increasing during puberty, reaching adult concentration.

A deficiency of enzymes involved in the synthesis of steroids (in 90% of cases it is 21-hydroxylase deficiency) causes a decrease in the level of cortisol and aldosterone and the accumulation of intermediate products, which include 17-OH-progesterone. A decrease in cortisol levels by feedback mechanisms causes an increased production of ACTH, which in turn causes an increase in the production of precursor molecules, as well as androstenedione, since the course of synthesis is shifted (“shunted”) in the direction of this unblocked metabolic pathway.Androstenedione in tissues is converted into an active androgen – testosterone. Determination of 17-OH-progesterone (basal and ACTH-stimulated levels) is mainly used in the diagnosis of various forms of 21-hydroxylase deficiency and monitoring of patients with congenital adrenal hyperplasia (congenital adrenogenital syndrome).

Congenital adrenal hyperplasia is a genetically determined, autosomal recessive disease that develops in most cases due to a deficiency of 21-hydroxylase, as well as due to a deficiency of other enzymes involved in the synthesis of steroids.Enzyme deficiencies can vary in severity. With congenital adrenal hyperplasia in infancy, virilization develops due to an increase in the production of androgens by the adrenal glands, a violation of aldosterone synthesis in this case can be partially compensated by the activation of regulatory mechanisms. In more severe cases, 21-hydroxylase deficiency causes profound impairment of steroid synthesis, aldosterone levels are reduced, and salt loss is potentially life-threatening. Partial enzyme deficiency seen in adults can also be hereditary, but it is initially insignificant, not clinically apparent (“latent”).A defect in the synthesis of enzymes can progress with age or under the influence of pathological factors and cause functional and morphological changes in the adrenal glands, similar to congenital syndrome. It causes disturbances in sexual development in the prepubertal period, and can also be the cause of hirsutism, cycle disorders and infertility in postpubertal women.

Limits of determination: 0.1 nmol / L-606 nmol / L.

Based on materials from the site Invitro

Luteinizing hormone

The hormone LH (luteinizing hormone), produced by the pituitary gland, regulates the activity of the gonads: stimulates the production of progesterone in women and testosterone in men.

In men, LH stimulates the formation of proteins that bind sex hormones, increases the permeability of the seminiferous tubules for testosterone. Under the influence of luteinizing hormone, testosterone levels increase, due to which sperm maturation occurs.

In women, it stimulates the synthesis of estrogens, regulates the secretion of progesterone and the formation of the corpus luteum.

The release of the hormone is of a pulsating nature and depends in women on the phase of the ovulation cycle.

When the follicle and the egg inside it mature, a sharp increase in LH in the blood leads to rupture of the follicle and the release of the egg (ovulation).The concentration of L.G. in the blood is maximum in the interval from 12 to 24 hours before ovulation and is maintained throughout the day, reaching a concentration 10 times greater than the neovulatory period (follicular and luteal phases). The ruptured follicle then turns into a corpus luteum, which produces progesterone and estradiol.

Thus, the determination of the concentration of LH is necessary to determine the time of ovulation, in the diagnosis of infertility and diseases of the pituitary gland and gonads.To determine the period of maximum fertility (day of ovulation) in order to plan the time of intercourse or artificial insemination, the concentration of LH is determined daily.

During pregnancy, the concentration decreases. In the postmenopausal period or after oophorectomy, an increase in the concentration of both LH and FSH (follicle-stimulating hormone) occurs.

There is a close relationship between the production of hormones LH, FSH on the one hand and estradiol, progesterone and testosterone on the other.Therefore, it is important not only to measure the content of any one of them, but also to evaluate the ratio of their concentrations on a certain day of the menstrual cycle in order to understand whether the mechanism of their interaction is working correctly.

In reproductive age, deficiency of gonadotropins – LH, FSH, hCG (chorionic gonadotropin) and TSH (thyroid stimulating hormone) is usually an early sign of panhypopituitarism (a clinical syndrome that develops as a result of destruction of the adenohypophysis with subsequent persistent decrease in the production of tropic hormones ), while the concentrations of LH, FSH and steroid hormones decrease.

In some tumors of the hypothalamus and pituitary gland, on the contrary, there is an increase in the concentration of LH and FSH and a decrease in the concentration of sex hormones.

Indications for the study

  • Hirsutism (male type of hair growth in women)
  • Decreased libido and potency
  • Azoospermia (absence of sperm in the ejaculate)
  • Oligospermia (decrease in the number of sperm in the ejaculate)
  • Anovulation (change in the menstrual cycle, in which there is no release of a mature egg from the follicle)
  • Oligomenorrhea and amenorrhea (menstrual irregularities)
  • Anorexia
  • Infertility
  • Pituitary insufficiency
  • Dysfunctional uterine bleeding
  • Miscarriage
  • Premature puberty and delayed puberty
  • Growth retardation
  • Sexual infantilism
  • Polycystic ovary syndrome
  • Ovarian failure
  • Metrorrhagiai.e. with menstrual irregularities) 90 220
  • Endometriosis
  • Monitoring the effectiveness of hormone therapy

LH levels are normal
(these values ​​may vary depending on the test systems and devices used)


  • Concentration 0. 8-7.6 IU / L


  • Follicular phase – concentration 1.1-11.6 IU / L
  • Ovulatory peak – concentration 17-77 IU / L
  • Luteal phase – concentration
  • Reception OK – concentration
  • Menopause – Concentration 11.3-40 IU / L 90 220

Increased LH

  • Ovulation
  • Hypergonadotropic hypogonadism (women): ovarian wasting syndrome
  • Polycystic ovary syndrome
  • Endometriosis
  • Primary amenorrhea (absence of menstruation)
  • Menopause
  • Shershevsky-Turner syndrome
  • Basophilic pituitary adenoma
  • Fasting
  • Sports training
  • Renal failure
  • Testicular feminization
  • Dysgenesis of the seminiferous tubules (Klinefelter’s syndrome)
  • Insufficiency of Sertoli cells
  • Atrophy of the gonads in men after inflammation of the testicles due to mumps, gonorrhea, brucellosis (rare)
  • Taking medications (bombesin, bromocriptine, finasteride, goserelin (in the first month of treatment), ketoconazole, mestranol, naloxone, nilutamide, oxcarbazepine, phenytoin, spironolactone, tamoxifen, troleandomycin).

Decreased LH

  • Secondary (hypothalamic) amenorrhea
  • Hyperprolactinemia (increased prolactin in the blood)
  • Hypogonadotropic hypogonadism
  • Pituitary dwarfism (a disease characterized by growth retardation and physical development associated with impaired growth hormone secretion)
  • Sheehan’s syndrome (decreased function of the anterior pituitary gland due to massive bleeding)
  • Simmonds disease (primary pituitary insufficiency)
  • Denny-Marfan syndrome
  • Polycystic ovary syndrome (atypical form)
  • Insufficiency of the luteal phase
  • Obesity
  • Smoking
  • Surgical interventions
  • Stress
  • Taking medications (anabolic steroids, anticonvulsants, carbamazepine, conjugated estrogens, cyproterone, danazol, diethylstilbestrol, digoxin, dopamine, goserelin, megestrol, methandrostenolone, norethindrone, tamreotide, oral contracepidinatepine , torimefene, thioridazine, valproic acid) 90 220

Material for research: blood from a vein

Preparation for analysis

The conditions of preparation and the day on which blood should be donated are determined by the attending physician. If there are no special recommendations, blood for this study is donated on days 2-4 of the menstrual cycle.

On the eve of the study (for 3 days) exclude physical activity (sports training) and smoking.

It is recommended to donate blood in the morning, on an empty stomach. If you plan to donate blood in the afternoon or in the evening, then you must refrain from food 4-6 hours before donating blood and exclude fatty foods from the diet.

When donating blood, you must inform the nurse about taking medications that affect the level of hormones in the blood.

Terms of readiness: 2 working days. This analysis can be performed urgently (result – in 2 hours).

Research methods: chemiluminescent immunoassay on microparticles (CIAM)

Increased LH and FSH – significance, consequences. The ratio of LH and FSH

The role of hormones in our body can hardly be overestimated, since they regulate the work of almost all organs. The hormonal background affects behavior, emotional state, appearance, general health. Hormones have a particularly strong effect on the human reproductive system, responsible for the ability to reproduce. Gonadotropic hormones are actively involved in the regulation of the reproductive system: follicle-stimulating (FSH) and luteinizing (LH), therefore information about their increase, decrease or violation of the ratio will help eliminate serious diseases, as well as prevent their development.

FSH and LH: role in the body

There are several levels of hormonal regulation of the functioning of the reproductive system: the hypothalamus, pituitary gland and directly the ovaries and testes.FSH and LH are pituitary hormones produced by the central endocrine gland, the secretion of which depends on the liberins and statins of the hypothalamus.

Follicle-stimulating – is responsible for the formation of reproductive gametes, taking an active part in oogenesis and spermatogenesis. FSH promotes the appearance of a dominant follicle, ensures the growth of its membrane and the synthesis of estrogens, testosterone, and also increases the susceptibility of genital cells to LH. Luteinizing – affects the development of the genitals, as well as the synthesis of testosterone and estrogen.Elevated LH levels and high FSH in women in the ovulatory phase promote the release of the egg from the follicle, LH is also responsible for the formation of the corpus luteum and the production of progesterone.

The ratio of LH and FSH and the phase of the menstrual cycle

The reproductive function of the genitals is in direct proportion to the hormones of the pituitary gland. The normal ratio of FSH and LH is the main condition for the development of a full-fledged egg and sperm cell, the appearance of ovulation and the corpus luteum in women.Without these processes, pregnancy is impossible.

Normally, after birth, a high level of FSH and LH is recorded, which gradually decrease, an increase in the concentration of hormones is recorded from 8-9 years to puberty, during this period they contribute to the formation of secondary sexual characteristics and ensure the correct development of the genitals. After the onset of puberty in boys, the concentration of hormones stabilizes and remains approximately at the same level, providing the necessary conditions for the formation of sperm.But the indicators of hormones in the female body are subject to fluctuations throughout life, as well as throughout the menstrual cycle, which is divided into certain phases.

In the follicular phase of the cycle, a gradual increase in FSH is noted (its level is 3.5-12.5 mIU / ml), which ensures the maturation of the dominant follicle and the synthesis of estrogens. The concentration of LH in the blood is 1.8-2.7 mIU / ml. As soon as a sufficient level of estrogens has accumulated in the cells, they are released into the blood, which sends a signal to the central endocrine glands and a sharp increase in the concentration of LH occurs, which exceeds the initial value by 10 times (up to 19.5-115 mIU / ml).It should be noted that at this time a high level of FSH is observed (4.5-21 mIU / ml). All this contributes to the release of the egg from the mature follicle – ovulation occurs and the ovulatory phase begins, which lasts several days.

Then luteal phase begins. Gradually, the FSH level decreases to 1.5-7.5 mIU / ml, since it does not play a big role. The concentration of LH also decreases to 0.6-16 mIU / ml, but it prevails over follicle-stimulating hormone, since in this phase it provides the formation of the corpus luteum, which is necessary to prepare a woman for the onset of future pregnancy: progesterone is produced, which creates optimal conditions for the development of the embryo …If the embryo is successfully implanted into the endometrium, then the functionality of the corpus luteum is maintained further, but if it is rejected or fertilization was not, then the corpus luteum atrophies, the level of FSH in the blood will again increase and the cycle repeats again.

An increase in LH and FSH in different periods of development and in the phases of the menstrual cycle, their decrease or change in the ratio signals a malfunction of the reproductive system and the development of serious pathological conditions.

Normal ratio of LH and FSH

During the entire menstrual cycle, the concentration of LH and FSH changes, but their ratio should be from 1.5 to 2 in women during the reproductive period.Before puberty, the hormone ratio is 1, a year after the onset of the first menstruation, it increases to 1.5. 2 years after the onset of menarche, the ratio stabilizes, increasing, but does not exceed 2.

In men, LH and FSH perform an equally important function, but their concentration after puberty is more stable: LH reaches 0.9-8.8 mIU / ml, and FSH – 1.1-11.1 mIU / ml. At the same time, FSH most often slightly predominates in the male body.

But the balance should always be, an increase in one hormone (for example, an increase in FSH) invariably leads to an imbalance in others, which significantly disrupts the functioning of the reproductive system and reduces the likelihood of pregnancy. It is worth recalling that a change in the level of one of the hormones always affects the concentration of others. Therefore, during the diagnosis, deviations from the norm are observed in almost all hormones; although an increase in FSH or LH while maintaining a normal ratio is not a sign of pathology and indicates a favorable state of the female body.For this reason, it is not recommended to decipher the analyzes on your own, since only a qualified specialist can adequately evaluate the data. You can get tested for hormones and get their decryption at the “IVF Center” in Kaliningrad.

Increase FSH

The level of hormones depends on age, day of the cycle, individual characteristics and other external and internal factors. All these signs are taken into account when interpreting research results. Deviations can be detected as a result of laboratory errors, due to the influence of adverse factors or any disease.

Imbalance in the direction of increasing FSH signals the onset of pathological conditions. Normally, an increase in FSH is observed during menopause, since during this period the ovaries lose their functional activity, the amount of estrogen decreases, which leads to a high level of FSH.

But an increase in FSH at a young age speaks of endocrine disorders, ovarian depletion. High FSH is most often accompanied by uterine bleeding, menstrual disorders, and the complete absence of menstruation (amenorrhea) is not excluded.In addition, high FSH can be caused by neoplasms and gynecological diseases.

The higher the level of follicle-stimulating hormone and the lower the LH, the more likely endometrial hyperplasia, delayed menstruation, anovulation, uterine bleeding. It should be noted, however, that high FSH levels are a common cause of infertility and miscarriage.

Increased FSH in men indicates the presence of endocrine pathology, which adversely affects the process of spermatogenesis.

Increase LH

Most often, women have normal or decreased LH values. An increase in LH levels significantly reduces the likelihood of pregnancy, since such indicators indicate a serious hormonal imbalance, the appearance of endometriosis, polycystic disease, and renal failure. A high level of LH with a low concentration of FSH leads to dysfunction of the ovaries, the follicle cannot fully mature, ovulation does not occur, which ends with the formation of a cyst.

Often an increase in FSH and LH signals the onset of early menopause, ovarian depletion and infertility. Therefore, the determination of the level of these hormones is a mandatory study when diagnosing infertility and problems with bearing pregnancy, especially before preparing for the IVF protocol. Although low rates are also not favorable signs, such results require repeated tests, since the hormones FSH and LH enter the bloodstream in an impulse mode, therefore, studies can not always give an objective assessment of the state of a woman’s body.

In any case, having received the results of the analysis, you should contact your doctor so that he draws up a further plan for your observation, prescribes additional research methods and, if necessary, therapeutic measures.

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90,000 Luteinizing hormone (LH) – its role in the body

The anterior pituitary gland secretes a number of gonadotropic hormones: luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin. Luteinizing hormone is synthesized in both the male and female body. It is essential for the proper functioning of the reproductive organs. In a woman’s body, luteinizing hormone stimulates the production of estrogen by the ovaries, and at its maximum level in the blood serum, ovulation occurs. Under the influence of luteinizing hormone, testosterone is produced in a man’s body. The concentration of LH in different phases of the menstrual cycle is different. Its level varies with age. If the luteinizing hormone is elevated, a pathological condition is observed.

Why do you need luteinizing hormone

LH is a complex protein, a glycoprotein. It consists of α- and β-subunits. Its α-subunit is identical to those in follicle-stimulating and human chorionic hormones. The β-subunit is the unique particle that distinguishes LH from other hormones. The α-subunit is encoded by a gene located on the sixth chromosome, and the β-subunit – on the nineteenth. The activity of the β-subunit gene depends on the level of gonadotropin-releasing hormone synthesized by the hypothalamus. Men and women need luteinizing hormone for reproductive function. In a woman, during the menstrual cycle, follicle-stimulating hormone is a catalyst for follicular growth. Under its influence, differentiation and proliferation of cells of the granular layer of the ovary occurs. Under the influence of FSH, the follicles that mature produce more and more estrogen. Among these, the most important is estradiol. On the cells of the follicles, receptors are transcribed that perceive the luteinizing hormone.

By the time the dominant follicle matures, the concentration of estradiol rises so much that the hypothalamus is activated as a result. At this point, the pituitary gland actively releases luteinizing and follicle-stimulating hormones. There is a peak in LH concentration, which triggers ovulation. This leads not only to the release of the egg, but also to the transformation of the residual follicle into the corpus luteum, which synthesizes progesterone in order to prepare the endometrium for possible implantation. LH maintains the corpus luteum for about fourteen days. If pregnancy occurs, the luteal function will be supported by human chorionic gonadotropin, the level of which in the blood is its diagnostic sign. Due to the stimulation of certain cells in the ovaries with luteinizing hormone, androgens and estradiol precursors begin to be intensively produced. In men, LH is the main hormone in the body. It is responsible for the production of testosterone, without which normal spermatogenesis is impossible.The release of luteinizing hormone is controlled by the hypothalamus, which releases gonadoliberin with the same cyclicity.

Norm of luteinizing hormone

The lowest level of luteinizing hormone is observed in childhood and in women during menopause. So, in a child of fifteen days of age, the rate of concentration of luteinizing hormone is less than 0.7 milliunits per liter. By the age of twelve, its level rises to almost ten milliunits per liter, and at nineteen years, its upper figure should not exceed eleven milliunits.

LH concentration varies depending on the phase of the menstrual cycle. So, from the first to the sixth day of the cycle, its reference values ​​are in the range from 1.9 to 12.5 mMu / ml. In the proliferative phase, its concentration does not change. From the thirteenth to the fifteenth day of the cycle, during ovulation, the level of luteinizing hormone is highest (from 8.7 to 76.3 international milliunits per milliliter). After ovulation, the luteal phase begins, which lasts about two weeks. At this time, the level of LH is minimal (0.5 – 16.9).

The concentration of luteinizing hormone varies depending on the period of a woman’s life. It is minimal in the pre-reproductive period and during pregnancy, and increases almost tenfold in postmenopausal women. In men, LH reference values ​​vary with age. So, its level is minimal in adolescents under the age of eighteen, and the highest after seventy.

When the level of luteinizing hormone is elevated

A relative increase in the level of luteinizing hormone can be in children with precocious puberty. Also, an increased concentration of LH can be detected in patients with polycystic ovary disease. Luteinizing hormone is elevated in cases where the normal negative feedback between the sex glands and the hypothalamus is disrupted. This leads to the fact that the synthesis of LH and FSH by the pituitary gland is disinhibited. If such a phenomenon occurs during menopause, this is not a deviation from the norm, but during the reproductive period it is considered a pathology. Luteinizing hormone is elevated in such cases:

  • When removing the ovaries;
  • During premature menopause;
  • In case of gonadal dysgenesis;
  • In the presence of congenital adrenal hyperplasia;
  • In case of ovarian hypofunction.

When and how to get tested for LH content

If you need to take a blood test for the compliance of the luteinizing hormone content with the norm, it is better to donate its blood in the morning – from seven to nine o’clock. On the eve, you must not eat for at least twelve hours. In case of infectious diseases and fever, they do not take tests for luteinizing hormone – the norm is not determined there. The concentration of LH depends on the phase of the woman’s cycle. Peaks are normal during ovulation.

Ovarian hypofunction as a disease in which LH is elevated

With a decrease in the function of the ovaries, a whole complex of changes occurs in the female body, which are called their hypofunction. This syndrome is neither a diagnosis nor a disease. Gynecologists consider the following types of ovarian failure – primary and secondary. Primary disorders develop in utero and are associated with incomplete development of the ovary. Secondary insufficiency develops as a result of pathological changes in metabolism and hormonal imbalance due to a violation of the correlation of the pituitary gland and the hypothalamus.

What are the signs of ovarian hypofunction? Symptoms of ovarian hypofunction depend on when the failure occurs – before puberty, or after it. Congenital hypofunction of the ovaries is manifested by delayed puberty in girls over the age of seventeen, underdevelopment of the mammary glands, amenorrhea and oligomenorrhea. If the disease has developed in the reproductive period, the following manifestations should be expected:

  • Scanty, painful menses, which may disappear altogether;
  • Mental disorders;
  • Fluctuation of blood pressure numbers;
  • Symptoms characteristic of PMS;
  • A sharp decrease in the size of the uterus;
  • Development of dryness and atrophy of the vaginal mucosa;
  • Endometrial hypoplasia;
  • Infertility.

In order to confirm the diagnosis of ovarian hypofunction, it is necessary to perform an ultrasound of the uterus, draw up a chart of basal temperatures, determine the level of hormones of the ovary, pituitary gland and hypothalamus. With ovarian failure, luteinizing hormone is elevated.

How to treat ovarian hypofunction? In case of primary hypofunction of the ovaries, the regimen and nutrition should be normalized, therapeutic gymnastic exercises should be performed, aimed at normalizing blood circulation in the small pelvis, and hormone replacement therapy should be carried out with estrogens. In case of an increase in the level of luteinizing hormone in women, you can contact the “IVF Center” Tambov, where they will not only establish the reason for this increase, but also prescribe individual therapy.

What is type 2 diabetes? ⋆ Prof. Dr. Alper Celik

Diabetics are also classified within themselves. The most common type of diabetes in patients with type 2 diabetes. These patients usually consist of people aged 40 and over. In addition, overweight is another common characteristic of these patients.

Type 2 diabetes is usually noticed too late. People don’t notice until the pool of beta cells reaches -20. However, with the age factor, symptoms such as illness with a high fever, unprovoked and rapid weight gain, pregnancy or various surgeries appear.

What are the symptoms of type 2 diabetes?

As we just stated, type 2 diabetes is diagnosed later and more difficult than type 1. However, there are some symptoms that can be used for early diagnosis in patients with type 2 diabetes. Polyuria, which is the easiest to detect from these symptoms. When there is a frequent urge to urinate or excessive consumption of water and food, polydipsis is called. As a result, after a while, weight increases or, on the contrary, is lost. In addition to these symptoms, blood glucose levels increase.

Although there is frequent water intake in people with type 2 diabetes, dry mouth is still observed. In addition to these symptoms, different conditions are observed on the surface of the skin than usual.Most often, dryness and cracking occurs on the surface of the skin. These dryings are accompanied by itching after a while, and the deformation of the skin cannot heal for a very long time. As a risk group for type 2 diabetes, a certain segment is more interested. While it is not known exactly why this is generally caused, it has been observed that people with weight problems, those with long-term eating disorders, those who do not include exercise in the stream of life, and family members diagnosed with diabetes in their genetic background, mothers Those who experience gestational diabetes during pregnancy or who are over 4. 5 kg of birth weight are more common in those who have been at the center of stress all their lives.

What are the principles for treating type 2 diabetes?

The most important thing that people with diabetes should do during treatment; be decisive. In this context, the first step is a strict and regular diet. In order for this to happen, lifestyle changes need to be made. The new lifestyle should also include an exercise program. If blood sugar cannot be within the normal range with this planned new lifestyle, the pill should be taken as a reinforcement.These medications are usually oral pills. However, these tablets do not show the expected effect for some patients. In this case, insulin treatment can be started. Injection procedures are performed in doses that the doctor deems necessary for insulin treatment.

Why is high sugar important?

All hormones required in our body are produced by the pancreas. One of the hormones produced by the pancreas is the hormone insulin. The main job of this hormone is to carry sugar into cells through the blood.The cells provide the daily energy we need through these sugars. The problem of type 2 diabetes occurs when insulin is not secreted in the body. Sometimes cells go to reduce the sensitivity to the hormone insulin. Type 2 diabetes also occurs at this stage. Due to this resistance, the insulin hormone is unable to perform its duties. If you think about it in a general sense; Sugar enters the body, sugar is processed and passed into the blood, but when it passes from the blood to the cells and is converted into energy, there is a problem because insulin cannot do its job.Therefore, sugar, entering the body, remains in the blood. This increases blood sugar levels above normal, which destroys cells in the body. Generally speaking, blood sugar is equal to poison.

Place of metabolic surgery in the treatment of type 2 diabetes

Insulin resistance in patients with type 2 diabetes has precellular components as well as intracellular components. At this stage, resistance hormones, especially those caused by the digestive system, tightly surround the cells and prevent the penetration of insulin into the cell.As a result of the use of metabolic surgery, the problems that arise at this moment are solved, the resistance hormones are revealed and insulin penetrates into the cell quite easily. After this procedure, blood sugar levels improve rapidly, as do cholesterol and triglycerides. In addition, the problem of high blood pressure, overweight and obesity of the liver, as well as damage to the eyes, kidneys and legs are being addressed.

Who is a metabolic surgery candidate?

Various treatments are applied to patients prior to metabolic surgery.However, metabolic surgery procedures are suitable for patients who have problems with blood sugar control despite treatment. Patients who have experienced diabetes for some time may experience various damage to organs such as the chest, heart, kidneys, liver, and legs as a result of this period. Metabolic surgery procedures should also be tried out for patients who are experiencing organ damage. In addition, successful results are being produced for people who are struggling with obesity and diabetes.

How to set the volume level to one standard value for all input sources and broadcasters

Sound adjustments

The volume of the broadcast TV and external inputs can be adjusted with the Sound adjustments:

  • Advanced auto volume: allows all volume levels to be adjusted automatically
  • Volume offset: allows volume levels to be adjusted individually

Automatic volume control

Advanced auto volume can reduce large differences in volume levels in the following cases:

  • Advertising and TV programs
  • Various TV broadcasting stations
  • TV broadcasting (digital / analogue) * Only available in certain countries / regions
  • for each external input

input signal. This setting is effective, for example, when the volume of an advertisement appears to be higher than the volume of a TV broadcast.

  1. Switch to the TV broadcast (or input) for which you want to adjust the volume.
  2. Press the Home button on the remote control.
  3. Select Settings.
  4. Select Sound.
  5. Select Sound adjustments.
  6. Select Advanced settings.
  7. Select Common and press the → button to move the cursor to the option menu on the right.
  8. Press ENTER and set Advanced auto volume to Auto.
  9. Press the BACK button on the remote control to return to the main menu.

Individual volume control

This setting refers to the volume level of the BRAVIA TV speakers.The volume of the headphones and external outputs is not adjustable. Also, if the sound volume is low even when the surround function is on, turn off the surround function.

  1. Switch to the TV broadcast (or input) for which you want to adjust the volume level.
  2. Press the HOME button on the remote control.
  3. Select Settings.
  4. Select Sound.
  5. Select Sound adjustments.
  6. Select Advanced settings.
  7. Select Input related and press the → button to move the cursor to the option menu on the right.
  8. Select Volume offset.
  9. Adjust the volume using the ← / → button on the remote control, then press the ENTER button.
  10. Press the BACK button on the remote control to return to the main menu.

This completes the volume adjustment.

Type 2 diabetes mellitus

Diabetes mellitus as defined by WHO (World Health Organization) –
this is a whole group of metabolic diseases characterized by an increased content
blood glucose as a result of defects in insulin secretion and / or insulin action.
Uncompensated or poorly compensated diabetes mellitus can lead to
the development of complications: vessels, kidneys, nerve endings, retina, etc. are affected. 1.2

Glucose is the main source of energy in the body.Insulin, a hormone produced by the pancreas, plays the main role in glucose metabolism.

Insulin interacts with cells at the receptor level, opening channels in the cell membrane through which glucose enters the cells from the bloodstream. In the absence of insulin or when cell receptors are insensitive to it, glucose is “locked” in the bloodstream and cannot enter cells and tissues. This condition is sometimes called “hunger in abundance” 1 In the absence of insulin, one speaks of the development of type 1 diabetes mellitus.With the preserved production of insulin by the pancreas, but insensitivity of the receptors to it in insulin-dependent tissues, one speaks of insulin resistance: glucose cannot enter the cell despite a sufficient amount of insulin in the bloodstream. Insulin resistance is the basis for the development of type 2 diabetes mellitus . Glucose penetrates into the cells of non-insulin dependent tissues, including the nervous system (brain and spinal cord) without insulin: the higher its concentration in the blood, the more glucose enters these organs 2 .

What is type 2 diabetes mellitus,

how it differs from 1

As stated above, there are several types of diabetes mellitus: 1st and 2nd, respectively. There are also monogenic forms of diabetes mellitus, neonatal diabetes mellitus 4 , but this article will focus on the main two types of diabetes.

In type 1 diabetes mellitus (T1DM) , insulin secretion suffers due to damage to the tissues of the pancreas.The destruction of the insulin-producing cells in the pancreas is caused by an autoimmune process. In this case, there is an absolute insufficiency of insulin, which is manifested by a constant high level of glucose in the blood – hyperglycemia.

The kidneys try to excrete excess glucose in the urine, glucosuria appears – glucose in the urine. Glucose is an osmotically active substance, which means that when its level in urine rises, the volume of urine excreted will increase, and the frequency of urination will increase, which leads to the development of the so-called polyuria.The increased excretion of fluids, in turn, causes the feeling of thirst, and the volume of fluid intake increases, which is medically called polydipsia.

The above symptoms are characteristic (specific) signs of diabetes mellitus: hyperglycemia, glucosuria, polyuria, polydipsia 1 . Dramatic weight loss may occur (more common in type 1 diabetes) 1 .

Type 1 diabetes used to be often called insulin-dependent. It is detected in about 12-15% of all patients with diabetes mellitus and is more often diagnosed in children and adolescents 2 .It requires constant administration of insulin and develops very rapidly without proper treatment 2 . If type 1 diabetes is diagnosed in one of the parents, then the probability of developing the disease in a child is 3. 94% ((3-3.5% if the mother has diabetes mellitus and 4.5-5% if the child has diabetes father).) If both parents have diabetes, the child’s risk of developing the disease is 34% 7 .

In type 2 diabetes mellitus (T2DM) insulin can be produced in sufficient and even excessive amounts, however, due to the insensitivity of the receptors to insulin, as noted above, the latter cannot exert its effect.Therefore, in type 2 diabetes, they talk about relative insulin deficiency, and this type can be called insulin-independent. However, this is not entirely true, as the treatment of type 2 diabetes may also require the administration of insulin.
T2DM is diagnosed more often in middle and old age and accounts for 85-88% of the total number of patients with diabetes mellitus. Diabetes mellitus type 2 develops gradually 2 .

In 2015, the total number of patients with diabetes worldwide was 415 million people.Experts predict that by 2042 this figure could reach 642 million 2 . Therefore, prevention and timely detection of this disease is one of the important tasks of public health.

Increased bilirubin level during pregnancy

The main causes of type 2 diabetes are considered:

Obesity or overweight. Determined by body mass index (body weight in kg divided by height in meters squared). Normal BMI is 18.5 to 24.9 .When it rises from 25 to 29.9 , the risk of getting T2DM increases by 2 times, and with indicators from 30 to 34.9 – already 5 times, etc. 1

Insufficient physical activity (hypodynamia). A sedentary lifestyle also increases the risk of developing diabetes.

Incorrect power supply. An increased amount of easily digestible carbohydrates and fats in the diet, high-calorie foods lead to an imbalance between the amount of calories consumed and consumed by the body 6 .

Age. After age 40, the risk of the disease increases. In the group over 65, the number of people with diabetes reaches 10-20% 9 .

Mental illness. According to some authors, depressive and anxiety disorders can indirectly lead to the development of disorders of carbohydrate metabolism 8.10 .

At the same time, risk factors for DM2 are divided into non-modifiable, that is, those that cannot be influenced, and modifiable.The first group includes heredity, age, ethnicity. To the second – all the others.

Symptoms of type 2 diabetes mellitus

Since type 2 diabetes develops gradually, the diagnosis of this disease is often untimely. Often, type 2 diabetes is diagnosed accidentally during examination for other diseases (according to the literature, the disease is detected by chance in 50% of cases). Late diagnosis leads to the fact that patients come to the doctor with chronic complications of diabetes.

Classical signs of type 2 diabetes mellitus, which were already mentioned above, are considered 11 :

Polyuria –
increased formation of urine, frequent urination.

Nocturia –
excess of night diuresis over daytime.

Polydipsia –
those. increased fluid intake. Manifested by thirst and dry mouth.

Increased fatigue.

Itching of the skin and genitals.

Frequent infectious and inflammatory diseases.

Based on the clinical picture (symptoms of the disease), it is quite difficult to determine the type of diabetes, therefore, further thorough examination is necessary.

Diagnosis of type 2 diabetes mellitus

Diagnosis of type 2 diabetes mellitus involves the following laboratory tests
What tests are performed to detect diabetes:

  • blood glucose determination: fasting, 2 hours after a meal, oral glucose tolerance test (assessment of fasting blood glucose and 2 hours after the patient drank a solution with 75 g of glucose),
  • glycated hemoglobin (HbA1) – estimates the average blood glucose level over the last 3 months 1 ,
  • general urinalysis: with diabetes, glucosuria will be observed
  • insulin and C-peptide tests can also be prescribed by a doctor to determine the type of diabetes mellitus.

It is worth noting that some studies (for example, a quarterly study of the level of glycated hemoglobin) can be carried out to assess the compensation of the disease and the effectiveness of treatment. Some tests may be prescribed by a doctor in order to diagnose chronic complications of diabetes mellitus, for example, nephropathy, i.e. kidney damage: in this case, the doctor may prescribe a study of creatinine, urea and other biochemical parameters.Also for the purpose of diagnosing other chronic complications such as retinopathy, i.e. retinal vascular lesions, consultation of narrow specialists may be required.

According to the American Diabetes Association, the fasting glucose level should not exceed 5.6 nmol / L, and the glycated hemoglobin (average blood glucose level for the last 3 months) should not exceed 5.7% 3 .

Diagnostic Criteria for Diabetes Mellitus (American Diabetes Association 2005-2017 3 ):

fasting venous blood glucose (at least 8 hours after the last meal) –
7 mmol / L and more;

2 hours after eating or performing a glucose tolerance test – 11.1 mmol / l and more;

glycated hemoglobin –
6.5% and more.

With indicators exceeding normal values, but not yet high enough to establish the diagnosis of diabetes mellitus, they speak of prediabetes: with fasting glucose values ​​in the range of 5.6 – 7.1, there is a so-called impaired fasting glycemia, and with glucose values ​​through 2 hours after a meal or after glucose loading during an oral glucose tolerance test in the range from 7.8 to 11.1 indicate impaired glucose tolerance. Glycated hemoglobin values ​​in the range of 5.7 to 6.5% may also indicate the development of prediabetes 3 .

When diagnosing diabetes mellitus, doctors can send a patient to the study of “blood sugar”, having in mind the assessment of the glucose level.

In order to timely diagnose type 2 diabetes mellitus, experts recommend a regular annual dispensary examination with the obligatory determination of fasting glucose levels for all persons older
40 years 11 .

Living with diabetes

It has been proven that disease compensation and low glycemic variability, i.e.e low degree of dispersion of glycemic values ​​during the day can prevent the development of both acute and chronic complications of this disease 4.12 .

The most important thing is teaching patients self-control and diabetes management Education of patients with diabetes mellitus involves teaching the basics of proper nutrition in diabetes, teaching a set of necessary measures for planned and unplanned physical activity, teaching self-correction of doses of injected insulin if necessary, etc.

Recommendations for dietary therapy for patients with type 1 diabetes mellitus 4 :

  • The total intake of protein, fat and carbohydrates in type 1 diabetes should not differ from that of a healthy person.
  • Patients on insulin therapy require a Bread Units (XE) assessment of digestible carbohydrates to adjust the pre-meal insulin dose.

Recommendations for dietary therapy for patients with type 2 diabetes mellitus 4 :

All overweight / obese patients are advised to restrict caloric intake.

Fasting is contraindicated.

It is recommended to limit the consumption of fats (animal origin) and sugars. Increase the content of foods consisting mainly of complex carbohydrates (starches) and proteins, vegetables.

However, compensation of the disease can only be achieved if the patient listens to the doctor’s advice: when drawing up a treatment regimen for type 2 diabetes, the doctor focuses on blood glucose levels, the level of glycated hemoglobin and the presence of complications.The doctor may prescribe antihyperglycemic drugs and / or insulin to the patient.

Most of the risk factors for the development of T2DM are modifiable, so the primary prevention of the disease consists in weight loss, proper nutrition and an increase in the level of daily physical activity (brisk walking, swimming, cycling, dancing) for at least 30 minutes).

According to research, lifestyle changes do reduce the risk of developing type 2 diabetes: for example, a combination of diet and exercise can reduce the risk of developing the disease by 58% 15 .

Date of publication of the material: November 17, 2020

MAT-RU-2003445-1.00-11 / 2020

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  2. G.U. Nurdinova and others. Epidemiology of diabetes mellitus. International scientific review. 2016, pp. 93-95.
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  4. Algorithms for specialized medical care for patients with diabetes mellitus / Edited by I.I. Dedova, M.V. Shestakova, A. Yu. Mayorov. – 9th issue (amended). – M .; 2019
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  7. Genetics of diabetes mellitus in children and adolescents A manual for doctors II Dedov et al. Moscow 2003, Ministry of Health of the Russian Federation, State Institution Endocrinological Research Center of the Russian Academy of Medical Sciences, 74 pp.
  8. Garganeeva, N.P. (2011). Psychosocial aspects of type 2 diabetes mellitus: innovation in prevention. Siberian Medical Journal (Tomsk), 26 (4-2), 121-125.
  9. Early disorders of carbohydrate metabolism in cardiological practice: diagnosis and treatment: manual / M.N. Korneeva, E.A. Poddubskaya, B.U. Mardanov, E.N. Dudinskaya. Ed. M.N. Mamedov. Moscow: FGBU State Research Center for Preventive Medicine, 2017.108 p.
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MAT-RU-2003460-1.00-11 / 2020