Puberty occurs when areas within the brain awaken beginning a cascade of hormone signals which conclude with the gonads (ovaries and testicles) increasing their production of the female and male sex hormones estrogen and testosterone. Under the influence of these hormones a child begins the transition from childhood to sexual maturity. In boys puberty is associated with a growth spurt, the appearance of facial, axillary (arm pit) and pubic hair, acne, deepening of the voice, growth of the testicles and penis while girls undergo a growth spurt, develop breasts, acne, pubic and axillary hair, and growth of the clitoris.
Historical data shows the average age of puberty today is many years sooner than in previous generations. Most experts attribute earlier puberty to better nutrition. A recent article in metabolism.com reviewed how “over-nutrition” accelerates obese children into puberty sooner (referred to as precocious puberty) than normal weight children. The latest studies on causes of precocious puberty suggests that a child’s social environment also exerts an important influence on the timing of puberty. Researchers in Madrid publishing in The Journal of Clinical Endocrinology and Metabolism 95:4305 2010 analyzed the age of puberty in normal children, adopted children and children whose families immigrated (children not adopted but subject to high levels of personal stress) to Spain. Adopted children were 25 times more likely than other groups of children to undergo precocious puberty (breast development before the age of 8 years in girls, and boys under 9 years of age with testicular growth). Over-all girls were 11 times more likely than boys to demonstrate precocious puberty.
Researchers speculate that socio-emotional stresses early in life of children who are later adopted result in changes in the brain that cause premature maturation of vital nerve pathways. This early brain maturation later results in stimulation of the pituitary gland, turning on the hormone pathways that cause puberty. This seems strange to me because various forms of deprivation in childhood can also delay puberty. For example, girls who have anorexia remain child-like in their body development and may fail to menstruate even into their late teens. A decade ago I studied hormone levels in adults during the stress of illness and surgery and found this lowered the sex hormone levels in their blood. This makes sense from an evolutionary point of view because during stressful conditions nature wisely cuts off the reproductive hormones. Why make babies if the environment is hostile in some way? Why the opposite occurs in children under stress of adoption is an interesting but unanswered question.
Gary Pepper, M.D.,
Editor-in-Chief, metabolism.com
In a recent blog at metabolism.com (https://metabolism.com/2007/11/12/estrogencant-live-with-it-cant-live-without-it/) we reviewed information suggesting women who had their ovaries removed or who began early menopause before the age of 50 may preserve brain function as they age by using estrogen replacement. I have just reviewed new research which could help explain why. Researchers gave post-menopausal women one dose of inhaled estrogen while measuring blood flow to their brain. They discovered that the estrogen caused an increase in blood flow to the brain. Diminished blood flow to the brain is one reason people develop impaired memory and thinking as they get older. Could estrogen prevent or slow this process?
In other areas of estrogen research it was found that daily estrogen use can significantly lower blood pressure in post-menopausal women. Healthy post-menopausal women without high blood pressure were given sequential estrogen/progesterone treatment for one year. At the end of the year blood pressure was significantly lower in women using estrogen compared to those who did not. The fall in blood pressure was equal to the benefits of some popular blood pressure medications such as verapamil (Verelan, Calan, Isoptin).
Stay abreast of further estrogen related developments at metabolism.com.
Be advised that this information is not meant as medical advice. Starting or changing medications should be done only under the supervision of your own physician or medical provider.
Over the past few years the use of estrogen to treat post menopausal women has plunged in popularity. This occurred after the release of several major studies showing that instead of helping older women avoid arteriosclerosis (hardening of the arteries) and heart attacks the opposite was true. Recent studies showed that women taking estrogen after menopause were more likely to have heart attacks. Additionally, there has been a persistent concern that estrogen use is tied to increased risk of certain cancers, particularly breast and uterine cancer.
For most women, this knowledge was sufficiently convincing for them to stop using estrogen or to decide not to start.
When it comes to a hormone as complex in its action as estrogen there is a lot more to this story, however. A recently published study in the journal Neurology from the Mayo Clinic shows that women who undergo premature menopause due to surgical removal of one or both ovaries and who don’t receive estrogen replacement, have a significantly higher risk of developing memory loss, dementia (senility) and Parkinson’s Disease in later years. The younger the woman at the time of menopause the greater the risk of later brain dysfunction.
The benefit of estrogen use on brain function seems to end around the age of 50 years. The study did not address women who have spontaneous menopause before the age of 50. Is it possible that this group of women need to take estrogen to reduce the risk of developing brain damage as they grow older?
I am unaware of any study which answers this question. For any woman who wants to know if they should take estrogen, it is advised they confer with their own physician since the controversy and personal issues are so complex.
(This article is not meant to provide medical advice or treatment. Please read the Terms of Use for metabolism.com in this regard.)
Let’s face it, nature wants us dead. We were born to die. That may seem a bit harsh but I don’t make the rules. Can the use of human growth hormone and sex steroids help us delay this inevitability? Maybe.
After birth most living things are programmed to develop physically and sexually, to rise to dominance in their environment, pass on their genetic material as fast and as frequently as they can…then die. The species which masters these simple principles rules the earth. As well they have. I refer to cockroaches, ants and other creepy crawlers. Then comes us, the humans. We lag behind because we are slow reproducers and possess a stubborn refusal to die.
I am imagining most of you nodding your head in agreement as you read the programmed stages of life…develop sexually (yes), dominance (yes, yes), pass on genetic material fast and furious (oh yes, oh yes). Then comes the frown and gnashing of teeth… death you say? Death can’t be part of the plan. How could we be programmed to die?
Scientific support for a natural death wish comes from several angles. For example, there is a suicide gene in our cells. The term for programmed cell suicide is apoptosis. When the genes for apoptosis are turned on in a cell, the cell dies. These genes (some are termed “reaper” genes) are responsible for cell suicide. From another perspective we learn that the machinery for cell repair and replication has a built in limit. After a certain amount of replication the cell machinery runs out of supplies and the cell will die. Together these irreversible features of cells guarantee death.
During the development years (up to age 25 or so) the apoptosis genes mostly serve constructive purposes like removing tissues that stand in the way of growth or to prevent cancer cells from reproducing. The chemical messages of growth and development produced in our endocrine glands (known as hormones) are released into our blood in abundant amounts. These hormones include growth hormone, sex hormones (testosterone and estrogen), and adrenal hormones such as DHEA. After that these hormones gradually decrease and our abilities and physical attributes begin to decline.
The role of growth hormone in the adult remains controversial. Once the bones have grown to full adult size some experts claim that there is no other important role for growth hormone. I disagree. There are many tissues in the body that have “receptors” for HGH so that growth hormone can continue to play a role in maintenance of bone, muscle, brain, immune cells and other tissues. I believe that nature intended “growth” hormones to maintain, sustain and repair the body that it helped create during the development years. Without them the aging process through cell suicide, starvation, or disrepair is unopposed, and decline and death are not far behind.
To cripple the body a good starting place would be elimination of the machinery for making the caretaking hormones. The onset of menopause is the most obvious example of natural ending of the hormone making process. The changes of menopause due to estrogen deficiency that occur in the skin, hair, bone, arteries (arthrosclerosis), are all very well known. Not to mention hot flashes, moodiness and loss of libido which reduce the quality of life. Less obvious but just as critical hormonal declines associated with aging are the steady dwindling of testosterone in men, and the reduction of growth hormone and DHEA levels in both sexes.
The questions before us are whether or not replacement of these hormones will delay aging or improve the quality of our lives.
Important Notice: Hormones such as growth hormone, testosterone, and T3 are prescription drugs to be prescribed by a licensed professional within a doctor patient relationship. Prescribing or using growth hormone for the purpose of enhancing athletic performance, or using these hormones without a prescription is illegal and punished by fines and possibly jail. Metabolism.com and Dr. Pepper continue to support a lively debate about the appropriate use of these medications to help patients with true medical needs.
The mission of the The Thyroid Project is to encourage sharing of information and experience between the public and the medical community about the treatment of hypothyroidism (low thyroid function). For at least the past few decades there is a growing awareness of “something missing†in the way suffers of hypothyroidism are treated for their disease.
Too many patients, as documented in an on-line study of 12,000 individuals conducted by the American Thyroid Association published in June 2018, (https://doi.org/10.1089/thy.2017.0681) , complain of persistent symptoms of hypothyroidism despite what their doctors believe is successful treatment with levothyroxine (brands include Synthroid, Unithroid, Tirosent, Levoxl). We believe something needs to be done to resolve this conflict between patients and their doctors.
Without effective intervention the early stage of type 2 diabetes known as prediabetes carries a high risk of progressing to outright diabetes. Metabolism.com provides an up-to-date summary of recommendations from national authorities, for preventing and possibly reversing this life long affliction
Diabetes can be defined simply as elevated blood sugar levels. What exactly is high blood sugar and when should someone be concerned about their level? Does having prediabetes mean diabetes is around the corner? Metabolism.com tackles this tricky but important topic in this comprehensive review.
By Gary M. Pepper, M.D. Ozempic, Rybelsus, Trulicity, Wegovy, Saxenda are the central players in the weight loss craze sweeping across the globe. Metabolisim.com has been monitoring this phenomenon from its beginnings in 2008 with its report “Lizard Spit Reduces Blood Sugar and Appetite”, regarding the first drug in this class, Byetta (exenatide). Caught In the middle of the current chaos are the medical experts who treat diabetes and have been prescribing these medications for more than a decade. Here is a brief commentary from one such board certified endocrinologist; “I started treating Type 2 diabetics with GLP-1 agonists more than 10 years ago. In some respects, these medications have revolutionized the treatment of diabetes by lowering blood sugar effectively and promoting weight loss at the same time, a unique combination of benefits. Not everyone benefits from these drugs to the same degree unfortunately, and I have seen lots of patients experience unacceptable side effects from them. Nothing though, has prepared me for what is happening now. Too often, I find myself confronting someone who expects me to prescribe one of these drugs just so they can lose weight. Sadly, one extreme example was someone who, despite battling a life threatening medical condition, was insistent on getting a prescription. At the same time my diabetic patients are scrambling to find a place to buy their medications if they can even afford it. It is disheartening, to say the least, and I dread the negative interactions with some of my patients I now face almost daily.”
Off- Label Use
The FDA is the U.S. government’s department tasked with evaluating and approving drugs for specific medical conditions. When a new medication is approved for treating a medical condition by the FDA the agency will, at the same time, set strict guidelines for exactly which patients may use the newly approved drug. When a medication is used “off-label” it means that these limitations are being overridden by the provider for a potential benefit which outweighs the drugs risks. It is a general misconception that off-label means illegal; it does not. This practice has been going on for ages and more than 20% of prescriptions in the United States are prescribed off-label. A common example is the use of beta-blockers (approved for heart problems) for the treatment of performance anxiety.
GLP-1 agonist drugs, as discussed recently by metabolism.com. were originally approved for the treatment of Type 2 diabetes in adults. In the past few years most of these same medications have gained unprecedented popularity for their “off-label” weight loss benefit. Of the 5 GLP-1 agents presently in U.S. pharmacies only Wegovy (semaglutide) and Saxenda (liraglutide) are FDA approved for treating obesity. Of these two, Wegovy is the newer and had been much more popular that its sister drug Saxenda, probably due to being dosed only once weekly compared to daily for Saxenda and less likely to cause side effects. Due to Wegovy’s soaring popularity, its manufacturer, Novo Nordisk, increased the price of Wegovy two times since its initial release.
