Posted on 01/30/2002 10:46:32 AM PST by TopQuark
| Puberty Hitting Girls At Younger Age |
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Christine Miles, KOIN 6 News |
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PORTLAND -- If you think kids are growing up too fast these days, you may be right. Girls are hitting puberty at an earlier age, and scientists say it may be a sign of other health problems. Researchers at Oregon Health and Science University's Primate Research Center are trying to figure out why some girls as young as 4 or 5 are entering puberty. They say genetics plays a role, but they've also discovered that environmental factors, like certain plastics, could trigger early puberty. If you think young girls are growing up too fast and looking more mature than their age, it's not just the trendy clothes or makeup that they wear. Their bodies are changing -- entering puberty way before their parent's did. "Parents are having to learn to rethink what they think is normal," Daniel Mark of OHSU explains. Over the last century, the average age for girls entering puberty was age 13. But today, research shows that it's much younger. For Caucasian girls, the first signs of puberty come at age 7 or 8. For African-American girls, it's a little younger, between the ages of 6-8. At the Primate Center, researchers say genetics and environmental factors play a role in the early onset of puberty. For the last 30 years, Dr. Sergio Ojeda has been studying pre-mature puberty. He has a documented case of a girl, just 18 months old, fully developed, and a baby, not even a year old, menstruating. "She was menstruating at 7 months, and by 9 months, she was menstruating regularly," Ojeda says. Puberty is a function driven by the brain. The hypothalamus is an area at the base of the brain responsible for awakening part of the body to the process of puberty. Researchers believe that everyday environmental toxins trigger signals to the brain to begin puberty before the body is ready. "Chemicals that are used to make plastic that you see everyday -- plastic of soft drinks, the plastic that makes containers for milk, for baby formula," Ojeda says. Ojeda says that plastic toxins mimic hormones like estrogen, which play a key role in stimulating the brain. But if the body starts developing too early, it could be a warning sign for parents. "A 4-year-old having breast budding has a much high risk having something pathological going on like a CNS tumor or a cystic or a problem with their ovary." Those cases are rare, Marks says that parents need to be aware of possible problems their children could be facing so they can get treatment. "Medication is the treatment. And it's not a benign therapy, but it's an effective therapy once a monthly injections of a hormone," Marks says. Researchers hope to track down an exact cause in premature puberty, in hopes of slowing down the development process, so kids can enjoy being kids. Boys are also entering puberty earlier, but not as quickly as girls. Researchers also say that childhood obesity is also a trigger for premature puberty. |
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Posted: January 28, 2002 |
| All Material Copyright 2001, Emmis Television LP or by original content developer |
hmm argentina isn't too on top of things though...
Yeow! Not fun, I can imagine.
FEBS Lett 2000 Apr 28;472(2-3):276-82In other words, if a human growth hormone were given to cattle or chickens, it would activate their growth. However, non-primate growth hormones will have no effect on primates. Argentina was wrong. But, then, a lot of people let themselves get stampeded into doing things simply because they "sound" reasonable.
The species specificity of growth hormone requires the cooperative interaction of two motifs.
Peterson FC, Brooks CL.
Ohio State Biochemistry Program,
The Ohio State University,
1925 Coffey Road,
Columbus, OH 43210, USA.
Primate growth hormones (GH) activate both primate and non-primate somatotrophic receptors (GH receptors), but non-primate GHs do not activate primate GH receptors. Previous studies argued the interaction of Asp(171) of human GH and Arg(43) of the receptor produced an attractive ionic interaction. In non-primate GHs, His(170) replaces the homologous Asp(171), producing a repulsive interaction with Arg(43) of the primate receptor which was believed to reduce the attraction of non-primate GH for the human GH receptor, thus providing species specificity. In this report, H170D bovine GH had activity and affinity for human GH receptors approaching those of human GH. In contrast, replacing Asp(171) of human GH with His did not significantly reduce somatotrophic activity, indicating that species specificity is not wholly explained by this residue's interaction with Arg(43) of the receptor. Deletion of either Phe(44) (a residue present only in primate GHs) or residues 32-46 (20-kDa form of human GH) each only marginally reduced somatotrophic activities. But the combination of the D171H mutation with either DeltaPhe(44) or Delta32-46 in human GH reduced binding and activity in a greater than additive fashion, indicated a functional interaction between these distant structural features. In bovine GH addition of phenylalanine at position 44 increased the somatotrophic activity and receptor affinity in cells containing the human GH receptor. The combination of the H170D mutation and the addition of phenylalanine at position 44 created a bovine GH with activity indistinguishable from wild-type human GH. Based on evidence from both bovine and human GHs, the cooperative interaction of these two distant motifs determined the species specificity and indicated that structural plasticity was a critical feature necessary for the species specificity of somatotrophic activity.
J Pediatr Endocrinol Metab 2000 Jul;13 Suppl 1:717-22
Body fat mass, leptin and puberty.
Kiess W, Muller G, Galler A, Reich A, Deutscher J, Klammt J, Kratzsch J.
Children's Hospital,
University of Leipzig,
Germany.
kiw@server3.medizin.uni-leipzig.de
Leptin, the ob gene product, provides a molecular basis for the lipostatic theory of the regulation of energy balance. Leptin circulates as a monomeric 16 kDa protein in rodent and human plasma and is also bound to leptin binding proteins that may form large high molecular weight complexes. Initial models of leptin action included leptin-deficient ob/ob mice and leptin-insensitive db/db mice. Peripheral or central administration of leptin reduced body weight, adiposity, and food intake in ob/ob mice but not in db/db mice. In ob/ob mice leptin treatment restored fertility. Leptin interacts with many messenger molecules in the brain. For example, leptin suppresses neuropeptide Y (NPY) expression in the arcuate nucleus. Increased NPY activity has an inhibitory effect on the gonadotropin axis and represents a direct mechanism for inhibiting sexual maturation and reproductive function in conditions of food restriction and/or energy expenditure. By modulating the hypothalamo-pituitary-gonadal axis both directly and indirectly, leptin may thus serve as the signal from fat to the brain about the adequacy of fat stores for pubertal development and reproduction. Normal leptin secretion is necessary for normal reproductive function to proceed and leptin may be a signal allowing for the point of initiation of and progression toward puberty.
Both daughters are gone. Wife is old. All is well.
But by are the most likely driving force for early puberty (for both BOYS and girls) is superior nutrition, both pre-natal and early childhood. This has been known for decades--in a poor nutritional scenario, puberty is delayed, with excellent nutrition, it happens much earlier.
I haven't had time to research it all and read all the material, but what I have been struck with initially is that those who are raising a cautious red flag and saying "wait a minute, we need to study this more" are being shouted out by the soy lobby and all the "health Nazi's" who tell us that soy is the answer for all of lifes ills. The pro-soy advocates don't seem to answer science with science, but rather rely on (seemingly) unsubstantiated claims about how the much soy that certain nationalities eat and how healthy they all are.
It may turn out that there is not a problem, but I think (at least from what I've seen) there has been a real rush to make all things soy part of our daily regimen. (Also interesting to note, a lot of the high-protien feeds that dairy farmers give their cows to help them produce more milk are soy based).
Anyway, it could be some interesting research and I'll bet that on a forum of this quality we will soon have plenty of info both pro and con.
I know that this decreasing age of sexual maturity phenomenon is a fact.
I first learned about it about 10 years ago, when I was an undergrad. I was in the library looking for psychiatry textbooks for something that had nothing to do with school. One of the books I came across was a very extensive edocrinology text from the 50's. I found alot of interesting stuff in there so I took it home.
One thing that struck me quite memorably(as the father of a little girl) was the bland statement that, since the turn of the century, the age at which females achieved sexual maturity has declined by approximately six months per generation.
It was in a paragraph in a section about puberty, and specifically precocious puberty. It was a very succint paragraph. It said in about three sentences that the age of female sexual maturity had been declining by six months per generation, there was little or no such decline in boys and that there was not a decline in the females measured mental maturity.
Like babies playing with shotguns.
But, for the last few thousand years, an unmarried girl was an old maid at 18. I seem to recall that New Mexico raised the age of consent from thirteen to something older, about fifteen or so years ago. Elvis, Romeo and Juliet... The 18/21 thing is recent. So I just don't know what I think.
Precocious pubery is rare. If simple plastics caused it, it would be common. Besides, if I were looking for a cause, I would look first at petrochemicals and solvents.
While I seriously doubt the story of the 18 month old baby menstrating, I would also not be surprised if it were true. Stranger things have happened.
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