articles
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Daniel Ledda
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raypeat-articles/processed/growth-hormone.html
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raypeat-articles/processed/growth-hormone.html
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<html>
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<head><title></title></head>
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<body>
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<h1></h1>
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<p></p>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-large"
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><span style="font-size: large"><blockquote>
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<strong>Growth hormone: Hormone of Stress, Aging, & Death?</strong>
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</blockquote></span><span style="font-size: medium">
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<blockquote>
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The name "growth hormone" is misleading; stress produces somatic growth, in a process called
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"hormesis." Exercise produces muscle edema, to a degree similar to that produced by GH;
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edema stimulates growth, but GH effect isn't limited to bone and muscle.
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>Identity of GH: Molecular ambiguity, complex modifications change one substance
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into many; its evolution suggests a role in water regulation. Doctrine of a
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"specific molecule" and "specific receptor" and specific effects is a
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myth.</span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>The osmoregulatory problem--keeping water under control--is centrally involved
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in stress.</span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>In mammals, the kidneys and bowel are the main regulators of water
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balance.</span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>GH is a stress hormone. Its effects can be produced osmotically, for example
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inducing milk production and cartilage growth, by osmotic (dilution)
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shock.</span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>Estrogen produces increased GH, and increases its production in stress.</span
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></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>Nitric oxide is a pro-aging free radical induced by estrogen, releasing GH; all
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three produce edema.</span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>Behind edema, hypoxia, hypocarbia; free fatty acids, diabetes, vascular
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leakiness, degenerative kidney changes, connective tissue changes,
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thickened.basement membrane, retinal degeneration. The same changes occur in
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aging: increased permeability; kidney disease, connective tissue
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changes.</span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>The absence of GH protects kidneys against degeneration. Osteoarthritis, a
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characteristic aging condition, is caused by estrogen and GH.</span></span
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></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: xx-medium"
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><span style="font-size: medium"
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>Some studies found that heart failure and bone repair aren't improved by GH; GH
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is very high during heart failure, in which edema contributes to the
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problem; carpal tunnel syndrome, myalgia, tumor growth, gynecomastia, and
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many other problems have been produced by GH treatments.</span><span
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style="font-family: Lucida Grande"
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><span style="font-size: medium"></span></span><span
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style="font-size: medium"
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><hr /></span><span style="font-family: Lucida Grande"><span
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style="font-size: medium"
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></span></span><span style="font-size: medium"
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>Bovine Growth Hormone is used to make cows give more milk.</span><span
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style="font-family: Lucida Grande"
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><span style="font-size: medium"></span></span><span style="font-size: medium"
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>Human Growth Hormone is supposed to make men lean and muscular, not to increase
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their milk production.</span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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><hr /><span style="font-family: Lucida Grande"></span>Recently I heard Robert
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Sapolsky interviewed, and he was describing the changes that prepare the body
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for short-term stress. He said the energy-mobilizing hormones, adrenalin and
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cortisol, increase, while the hormones that don't contribute to meeting the
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immediate problem, including the sex hormones and growth hormone, are
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suppressed, to save energy; growth and reproductive processes can be suspended
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for the few minutes of acute stress, to make the body more able to meet its
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acute needs. He reiterated: Growth hormone is suppressed by stress.</span></span
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></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>Sapolsky has done very interesting work on the suppression of testosterone by
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stress, and on the way in which brain cells are killed by prolonged exposure to
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glucocorticoids. He showed that if extra glucose is supplied, the brain cells
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can survive their exposure to cortisol. In the body, adrenalin and the
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glucocorticoids increase the availability of glucose.</span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>In the radio interview, he didn't have time for much detail, but it seemed to me
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that he wasn't talking about the same growth hormone that I have been reading
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about, and trying to understand, for years. Since people have asked me to write
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about the current anti-aging uses of GH, and its use in the dairy industry,
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Sapolsky's statements made me decide to think about some of the issues around
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the hormone.*</span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>________________________________________________________________________________<span
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style="font-family: Lucida Grande"
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></span>*If Sapolsky had been talking about just mice and rats, his statement
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would have been generally accurate. Adrenaline stimulates rat pituitary cells to
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secrete GH, and since both increase the amount of free circulating fatty acids,
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it could be that rats' GH is suppressed by a fatty acid excess.</span></span
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></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>The "growth hormone" was named long before it was actually found, and the substance
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with that name turns out to be involved in many processes other than growth. It
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is being given to cows to make them produce more milk, and it is being given to
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people with the purpose of making them lean and muscular, and with the hope of
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building stronger bones.<span style="font-family: Lucida Grande"></span>It isn't
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surprising that the Growth Hormone helps breasts develop and promotes milk
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production, since it is very similar to prolactin. GH and prolactin are members
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of a family of proteins that have diverged from each other in evolution, but
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they still have many overlapping effects.</span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>When GH is treated as a drug, it is supposed to have a discrete identity, based on
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the sequence of its amino acids. But the natural hormone (disregarding the
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existence of a variety of closely related peptides with slightly different amino
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acid composition) varies with time, being chemically modified even before it is
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secreted. For example, its acidic amino acids may be methylated, and its lysine
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groups may combine with sugars or carbon dioxide. The history of the protein in
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the body determines its exact structure, and therefore its biological
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effects.</span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>Male animals secrete GH in pulses, but females secrete it more steadily. This
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pattern of secretion "masculinizes" or "feminizes" the liver (and other organs),
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determining the pattern of enzyme activity. It would be possible (though very
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difficult) to arrange a system for delivering doses in a pulsed, intermittent
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manner. In cows, this apparently isn't necessary, since the purpose of the
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growth hormone is presumably to "feminize" the milk-producing system. But the
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normal pattern of secretion is much more complex than simply being "pulsed" or
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"continuous," since it, like prolactin secretion, is responsive to changes in
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thyroid, estrogen, diet, stress, and many other factors.<span
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style="font-family: Lucida Grande"
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></span>For example, hormones in this family are, as far back in evolution as
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they have been studied, involved in the regulation of water and minerals. It is
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well established that increased water (hypotonicity) stimulates prolactin, and
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increased sodium inhibits its secretion. Growth hormone is also closely involved
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with the regulation of water and salts.</span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>One of the best known metabolic effects of GH is that, like adrenalin, it mobilizes
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fatty acids from storage. GH is known to antagonize insulin, and one of the ways
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it does this is simply by the ability of increased free fatty acids to block the
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oxidation of glucose. At puberty, the increased GH creates a mild degree of
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diabetes-like insulin resistance, which tends to increase progressively with
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age.<span style="font-family: Lucida Grande"></span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>In his book, Why Zebras Don't Get Ulcers, Sapolsky acknowledges some situations in
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which GH is increased by stress in humans, but I think he misses the real ways
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in which it operates in stress. One of the interesting features of cortisol,
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which Sapolsky showed killed brain cells by making them unable to use glucose
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efficiently, is that it makes cells take up unsaturated fatty acids more easily,
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interfering with their energy production. Since growth hormone also has this
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kind of "diatebetogenic" action, it might be desirable to suppress its secretion
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during stress, but in fact, there are several kinds of stress that clearly
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increase its secretion, and in animals as different as fish, frogs, cows, and
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people it can be seen to play roles in water and salt regulation, growth and
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development, stress, and starvation.<span
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style="font-family: Lucida Grande"
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></span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>Heat, hypoglycemia, running, and some types of shock are known to stimulate growth
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hormone secretion, sometimes to levels ten or twenty times higher than normal.
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(Two kinds of stress that usually don't increase GH are cold and
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stimulus-deprivation.) I consider the growth hormone to be, almost as much as
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prolactin, a stress-inducible hormone. That's why I reasoned that, if an
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endocrinologist as good as Sapolsky can misunderstand GH to that degree, the
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public is even more likely to misunderstand the nature of the material, and to
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believe that it somehow acts just on muscle, fat, and bones.<span
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style="font-family: Lucida Grande"
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></span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>And the normally functioning pituitary appears to be unnecessary to grow to normal
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height. (Kageyama, et al., 1998.)<span style="font-family: Lucida Grande"></span
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></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>W. D. Denckla discovered that the pituitary hormones are in some way able to
|
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accelerate the process of aging. They block the actions of thyroid hormone,
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decreasing the ability to consume oxygen and produce energy. The diabetes-like
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state that sets in at puberty involves the relative inability to metabolize
|
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glucose, which is an oxygen-efficient energy source, and a shift to fat
|
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oxidation, in which more free radicals are produced, and in which mitochondrial
|
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function is depressed. Diabetics, even though it is supposedly an inability of
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their cells to absorb glucose that defines their disease, habitually waste
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glucose, producing lactic acid even when they aren't "stressed" or exerting
|
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themselves enough to account for this seemingly anaerobic metabolism. It was
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noticing phenomena of this sort, occurring in a great variety of animal species,
|
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in different phyla, that led Denckla to search for what he called DECO
|
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(decreasing consumption of oxygen) or "the death hormone." (Vladimir Dilman
|
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noticed a similar cluster of events, but he consistently interpreted everything
|
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in terms of a great genetic program, and he offered no solution beyond a
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mechanistic treatment of the symptoms.)<span
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style="font-family: Lucida Grande"
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></span></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
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style="font-size: medium"
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>Simply increasing the amount of free fatty acids in the blood will act like DECO or
|
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"the death hormone," but growth hormone has more specific metabolic effects than
|
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simply increasing our cells' exposure to fatty acids. The hormone creates a bias
|
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toward oxidizing of the most unsaturated fatty acids (Clejan and Schulz), in a
|
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process that appears to specifically waste energy.<span
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style="font-family: Lucida Grande"
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></span>Growth hormone plays an important role in puberty, influencing ovarian
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function, for example. <span style="font-family: Lucida Grande"></span
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></span></span></span>
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</blockquote>
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<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
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style="font-size: medium"
|
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>Removing animals' pituitaries, Denckla found that their aging was drastically
|
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slowed. He tried to isolate the death hormone from pituitary extracts. He
|
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concluded that it wasn't prolactin, although prolactin had some of its
|
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properties. In the last publication of his that I know of on that subject, he
|
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reported that he was unable to isolate the death hormone, but that it was "in
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the prolactin fraction." Since rats have at least 14 different peptides in their
|
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prolactin family, not counting the multitude of modifications that can occur
|
||||
depending on the exact conditions of secretion, it isn't surprising that
|
||||
isolating a single factor with exactly the properties of the chronically
|
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functioning aging pituitary hasn't been successful.<span
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style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
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||||
</blockquote>
|
||||
<blockquote>
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Denckla's experiments are reminiscent of many others that have identified changes
|
||||
in pituitary function as driving forces in aging and degenerative diseases.<span
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style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
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<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Menopause, for example, is the result of overactivity of the pituitary gonatropins,
|
||||
resulting from the cumulatively toxic effects of estrogen in the
|
||||
hypothalamus.<span style="font-family: Lucida Grande"></span></span></span
|
||||
></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>A. V. Everitt, in his book on the hypothalamus and pituitary in aging, reported on
|
||||
studies in which estrogen caused connective tissues to lose their elasticity,
|
||||
and in which progesterone seemed to be an antiestrogenic longevity factor.
|
||||
Later, he did a series of experiments that were very similar to Denckla's, in
|
||||
which removal of the pituitary slowed the aging process. Several of his
|
||||
experiments strongly pointed to the prolactin-growth hormone family as the aging
|
||||
factors. Removal of the pituitary caused retardation of aging similar to food
|
||||
restriction. These pituitary hormones, especially prolactin, are very responsive
|
||||
to food intake, and the growth hormone is involved in the connective tissue and
|
||||
kidney changes that occur in diabetes and aging. <span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>A mutant dwarf mouse, called "little," has only 5% to 10% as much growth hormone as
|
||||
normal mice, and it has an abnormally long lifespan.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Many experiments show that prolactin and estrogen have synergistic effects in
|
||||
causing tissue degeneration, including cancerization, and that their effects
|
||||
tend to operate with fewer protective restraining influences in old age.
|
||||
Estrogen stimulates both prolactin and growth hormone secretion. Thirty years
|
||||
ago, people were warning that estrogen contraceptives might produce diabetes,
|
||||
because they caused chronic elevation of growth hormone and free fatty
|
||||
acids.<span style="font-family: Lucida Grande"></span>Since estrogen causes a
|
||||
slight tendency to retain water while losing sodium, producing hypotonic body
|
||||
fluids, and since hypotonicity is a sufficient stimulus to cause prolactin
|
||||
secretion, I have proposed that it is estrogen's effect on the body fluids which
|
||||
causes it to stimulate prolactin. In pregnancy, the fetus is exposed to fluids
|
||||
more hypotonic than can be accounted for by estrogen and prolactin alone; since
|
||||
GH lowers the salt concentration of fish when they enter the ocean from
|
||||
freshwater, it seems to be a candidate for this effect in pregnancy.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Growth itself is an intrinsic property of all cells, but the growth hormone does
|
||||
have its greatest influence on certain tissues, especially cartilage. Gigantism
|
||||
and acromegaly were what originally made people interested in looking for a
|
||||
growth hormone, and these are characterized by continued, exaggerated
|
||||
enlargement of bones and cartilage. In old age, cartilaginous structures such as
|
||||
the bones and ears keep enlarging. The fact that simply diluting the culture
|
||||
medium is sufficient to stimulate the growth of cartilage suggests that the
|
||||
growth hormone might be acting by its effects on water metabolism. In fish which
|
||||
enter fresh water from the ocean, pituitary hormones of this family help them to
|
||||
balance salts in this new environment, but in the process, they develop
|
||||
osteoporosis and skeletal deformity, of the sort that occur more gradually in
|
||||
other animals with aging.<span style="font-family: Lucida Grande"></span></span
|
||||
></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Growth hormone clearly causes edema, and this is probably involved in the
|
||||
pathological processes that it can produce. The expansion of extracellular water
|
||||
has been reported, but others have concluded that the increased weight of
|
||||
muscles following GH treatment must be the result of "growth," "because
|
||||
microscopic examination didn't show edema." Statements of that sort give
|
||||
incompetence a bad name, because any student of biology or biochemistry has to
|
||||
know, before he does almost any experiment, that the way to determine the water
|
||||
content of a tissue is to compare the wet weight to the weight after thorough
|
||||
drying. Looking for water under a microscope is the sort of thing they do at
|
||||
drug companies to pretend that they have done something.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Estrogen, growth hormone, and nitric oxide, which tend to work as a system, along
|
||||
with free fatty acids, all increase the permeability of blood vessels. The
|
||||
leaking of albumin into the urine, which is characteristic of diabetes, is
|
||||
promoted by GH. In diabetes and GH treatment, the basement membrane, the
|
||||
jelly-like material that forms a foundation for capillary cells, is thickened.
|
||||
The reason for this isn't known, but it could be a compensatory"anti-leak"
|
||||
response tending to reduce the leakage of proteins and fats.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Besides being involved in kidney degeneration, vascular leakiness contributes to
|
||||
brain edema, and probably contributes to the "autoimmune" diseases.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Whatever the exact mechanism may be, it is clearly established that GH contributes
|
||||
to kidney degereration, and the lack of GH, even the removal of the pituitary,
|
||||
is protective against kidney degeneration.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Denckla's and Everitt's experiments can be interpreted much more clearly now that
|
||||
GH's essential contribution to kidney degeneration is known. Growth Hormone may
|
||||
not be precisely the Death Hormone that Denckla was looking for, but it is very
|
||||
close to it. Anti-thyroid effects have been seen, and possibly even anti-growth
|
||||
effects during gestation, and in kidney disease. In newborns, high GH is
|
||||
associated with smaller size and slower growth; in one study, this was
|
||||
associated wtith rapid breathing, presumably hyperventilation which is
|
||||
associated with stress. The shift to the diabetes-like fatty acid oxidation
|
||||
would be expected to inhibit respiration, and the chronic elevation of serum
|
||||
free fatty acids will have a generalized antithyroid effect. Under the influence
|
||||
of GH, the proportion of unsaturated fatty acids is increased, as occurs under
|
||||
the influence of estrogen.<span style="font-family: Lucida Grande"></span></span
|
||||
></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Growth hormone blocks gonadotropin-stimulated progesterone production, and this
|
||||
could also affect thyroid and respiratory metabolism.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>The increase of GH during sleep might seem to be utterly incompatible with the idea
|
||||
that it is a stress hormone, but in fact the other stress hormones, adrenalin,
|
||||
cortisol, and prolactin also tend to increase during night-time sleep. Thyroid
|
||||
function and progesterone function decrease at night. As I have argued
|
||||
previously darkness is one of our major stressors. Considering GH's tendency to
|
||||
cause edema, tissue swelling, it could play a role in the nocturnal increase of
|
||||
the viscosity of blood, as the volume of blood is decreased by the leakage of
|
||||
fluid into the tissues. Another process with potentially deadly results that
|
||||
increase withaging and stress, is the passage of bacteria from the intestine
|
||||
into the blood stream; this process is increased under the influence of GH.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span></span></span></span>
|
||||
</blockquote>
|
||||
<blockquote>
|
||||
<span style="color: #222222"><span style="font-family: georgia, times, serif"><span
|
||||
style="font-size: medium"
|
||||
>Acute, short term studies definitely show growth hormone to be a stress hormone
|
||||
with some destabilizing effects. Over a lifetime, it is possible that such
|
||||
things as chronically increased levels of unsaturated fatty acids in the blood,
|
||||
and increased leakiness of the blood vessels, could cumulatively produce the
|
||||
effects that Denckla ascribed to the Death Hormone.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span><h3>REFERENCES</h3><span style="font-family: Lucida Grande"></span
|
||||
>Intern Med 1998 May;37(5):472-5. A hypopituitary patient who attained tall
|
||||
stature without growth hormone. Kageyama K, Watanobe H, Nasushita R, Nishie M,
|
||||
Horiba N, Suda T. "We describe an unusual patient with hypopituitarism who
|
||||
attained tall stature even without growth hormone (GH)." <span
|
||||
style="font-family: Lucida Grande"
|
||||
></span>Pediatr. Pulmonol. 1998 26(4):241-9. Sleep, respiratory rate, and growth
|
||||
hormone in chronic neonatal lung disease, D. Fitzgerald, et al.<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span>"Insulin resistance in puberty [editorial]," Anonymousm Lancet, 1991 May
|
||||
25, 337:8752, 1259-60. <span style="font-family: Lucida Grande"></span>"The
|
||||
gonadotropic function of insulin," Poretsky L; Kalin MF, Endocr Rev, 1987 May,
|
||||
8:2, 132-4.1.<span style="font-family: Lucida Grande"></span><hr /><span
|
||||
style="font-family: Lucida Grande"
|
||||
></span>Circulation 1991 Jun;83(6):1880-7. Pathogenesis of edema in constrictive
|
||||
pericarditis. Studies of body water and sodium, renal function, hemodynamics,
|
||||
and plasma hormones before and after pericardiectomy. Anand IS, Ferrari R, Kalra
|
||||
GS, Wahi PL, Poole-Wilson PA, Harris PC. "BACKGROUND. The pathogenesis of sodium
|
||||
and water accumulation in chronic constrictive pericarditis is not well
|
||||
understood and may differ from that in patients with chronic congestive heart
|
||||
failure due to myocardial disease. This study was undertaken to investigate some
|
||||
of the mechanisms. METHODS AND RESULTS. Using standard techniques, the
|
||||
hemodynamics, water and electrolyte spaces, renal function, and plasma
|
||||
concentrations of hormones were measured in 16 patients with untreated
|
||||
constrictive pericarditis and were measured again in eight patients after
|
||||
pericardiectomy. The average hemodynamic measurements were as follows: cardiac
|
||||
output, 1.98 l/min/m2; right atrial pressure, 22.9 mm Hg; pulmonary wedge
|
||||
pressure, 24.2 mm Hg; and mean pulmonary artery pressure 30.2 mm Hg. The
|
||||
systemic and pulmonary vascular resistances (36.3 +/- 2.5 and 3.2 +/- 0.3 mm
|
||||
Hg.min.m2/l, respectively) were increased. Significant increases occurred in
|
||||
total body water (36%), extracellular volume (81%), plasma volume (53%), and
|
||||
exchangeable sodium (63%). The renal plasma flow was only moderately decreased
|
||||
(49%), and the glomerular filtration rate was normal. Significant increases also
|
||||
occurred in plasma concentrations of norepinephrine (3.6 times normal), renin
|
||||
activity (7.2 time normal), aldosterone (3.4 times normal), cortisol (1.4 times
|
||||
normal), growth hormone (21.8 times normal), and atrial natriuretic peptide (5
|
||||
times normal)." "The arterial pressure is maintained more by the expansion of
|
||||
the blood volume than by an increase in the peripheral vascular
|
||||
resistance." <span style="font-family: Lucida Grande"></span>J Clin
|
||||
Endocrinol Metab 1991 Apr;72(4):768-72 Expansion of extracellular volume and
|
||||
suppression of atrial natriuretic peptide after growth hormone administration in
|
||||
normal man. Moller J, Jorgensen JO, Moller N, Hansen KW, Pedersen EB,
|
||||
Christiansen JS. University Department of Endocrinology and Internal Medicine,
|
||||
Aarhus Kommunehospital, Denmark. "Sodium retention and symptoms and signs of
|
||||
fluid retention are commonly recorded during GH administration in both
|
||||
GH-deficient patients and normal subjects." "GH caused a significant increase in
|
||||
ECV (L): 20.45 +/- 0.45 (GH), 19.53 +/- 0.48 (placebo) (P less than 0.01),
|
||||
whereas plasma volume (L) remained unchanged 3.92 +/- 0.16 (GH), 4.02 +/- 0.13
|
||||
(placebo)."<span style="font-family: Lucida Grande"></span>Edema of cardiac
|
||||
origin. Studies of body water and sodium, renal function, hemodynamic indexes,
|
||||
and plasma hormones in untreated congestive cardiac failure. Anand IS, Ferrari
|
||||
R, Kalra GS, Wahi PL, Poole-Wilson PA, Harris PC. "This study provides data on
|
||||
plasma hormone levels in patients with severe clinical congestive cardiac
|
||||
failure who had never received therapy and in whom the presence of an
|
||||
accumulation of excess water and sodium had been established." "Total body water
|
||||
content was 16% above control, extracellular liquid was 33% above control,
|
||||
plasma volume was 34% above control, total exchangeable sodium was 37% above
|
||||
control, renal plasma flow was 29% of control, and glomerular filtration rate
|
||||
was 65% of control. Plasma norepinephrine was consistently increased (on average
|
||||
6.3 times control), whereas adrenaline was unaffected. Although plasma renin
|
||||
activity and aldosterone varied widely, they were on average above normal (renin
|
||||
9.5 times control, aldosterone 6.4 times control). Plasma atrial natriuretic
|
||||
peptide (14.3 times control) and growth hormone (11.5 times control) were
|
||||
consistently increased. Cortisol was also increased on average (1.7 times
|
||||
control). Vasopressin was increased only in one patient." <span
|
||||
style="font-family: Lucida Grande"
|
||||
></span>J Pediatr Endocrinol 1994 Apr-Jun;7(2):93-105. Studies on the renal
|
||||
kinetics of growth hormone (GH) and on the GH receptor and related effects in
|
||||
animals. Krogsgaard Thomsen M, Friis C, Sehested Hansen B, Johansen P, Eschen C,
|
||||
Nowak J, Poulsen K. "Growth hormone (GH) is filtered through the kidney, and may
|
||||
exert effects on renal function when presented via the circulation.
|
||||
Investigations on kidney-related aspects of GH are increasing in number." "Short
|
||||
term administration of GH to rats and humans elicited electrolyte and water
|
||||
retention that may cause edema in adults."<span
|
||||
style="font-family: Lucida Grande"
|
||||
></span>Mech Ageing Dev 1983 Jul-Aug;22(3-4):233-51 The anti-aging action of
|
||||
hypophysectomy in hypothalamic obese rats: effects on collagen aging,
|
||||
age-associated proteinuria development and renal histopathology. Everitt AV,
|
||||
Wyndham JR, Barnard DL Hypophysectomy in young male Wistar rats aged 70 days,
|
||||
like food restriction begun at the same age, retarded the life-long rate of
|
||||
collagen aging in tail tendon fibres and inhibited the development of
|
||||
age-associated proteinuria and renal histopathology. Hypothalamic lesions which
|
||||
increased the food intake of hypophysectomized rats from 7 g to 15 g/day and
|
||||
produced obesity did not alter the rate of either collagen aging or proteinuria
|
||||
development, nor reduce life expectancy, but increased the incidence of abnormal
|
||||
glomeruli. In the intact rats elevation of food intake from 7 g to 15 g/day
|
||||
increased the rate of proteinuria development, but did not affect the rate of
|
||||
collagen aging. Hypophysectomy was found to have a greater anti-collagen aging
|
||||
effect than food restriction, when food intakes were the same in both groups.
|
||||
These studies suggest a pituitary-hormonal effect on collagen aging and a
|
||||
food-pituitary-hormone-mediated effect on the development of age-associated
|
||||
proteinuria. <span style="font-family: Lucida Grande"></span>Growth Dev
|
||||
Aging 1992 Summer;56(2):85-93. Morphometrical analysis of the short-term effects
|
||||
of hypophysectomy and food restriction on skeletal muscle fibers in relation to
|
||||
growth and aging changes in the rat. Shorey CD, Manning LA, Grant AL, Everitt
|
||||
AV.<span style="font-family: Lucida Grande"></span>Metabolism of glomerular
|
||||
basement membrane in normal, hypophysectomized, and growth-hormone-treated
|
||||
diabetic rats," Reddi AS, Exp Mol Pathol, 1985 Oct, 43:2, 196-208. "The in vivo
|
||||
synthesis of the renal glomerular basement membrane (GBM) collagen was studied
|
||||
in normal, hypophysectomized (hypox), diabetic, and growth-hormone (GH)-treated
|
||||
diabetic rats...." "A significant decrease in both proline and hydroxyproline
|
||||
specific activities were observed in GBM of hypox rats at all periods of study.
|
||||
Administration of GH to hypox rats returned the GBM collagen synthesis to
|
||||
normal. Diabetic GBM had higher proline and hydroxyproline specific activities
|
||||
when compared to normal rats. Treatment of diabetic rats with GH for 10 days
|
||||
further increased both proline and hydroxyproline specific activities when
|
||||
compared either to diabetic or normal rats treated with GH. The activity of
|
||||
glucosyltransferase, an enzyme involved in the biosynthesis of the disaccharide
|
||||
unit of GBM collagen was found to be decreased in glomeruli of hypox rats. In
|
||||
contrast, the activity of N-acetyl-beta-glucosaminidase, a
|
||||
glycoprotein-degrading enzyme, was found to be significantly increased in hypox
|
||||
rats. GH treatment restored both enzyme activities to normal. The results of the
|
||||
present study show that GBM collagen synthesis is decreased in hypox rats and
|
||||
increased in diabetic rats. ....not only normalized GBM collagen synthesis in
|
||||
hypox rats but also caused significant increase in diabetic rats. This suggests
|
||||
that the renal GBM metabolism is influenced by GH, and this may be of particular
|
||||
significance in view of GH involvement in diabetic microvascular
|
||||
complications."<span style="font-family: Lucida Grande"></span>Ciba Found Symp
|
||||
1982;(90):263-78 Prolactin and growth hormone receptors. Friesen HG, Shiu RP,
|
||||
Elsholtz H, Simpson S, Hughes J The two hormones prolactin and growth hormone
|
||||
exhibit considerable structural homology as well as exerting similar biological
|
||||
effects, especially the primate hormones. One effect of prolactin that deserves
|
||||
greater attention is its action on the immune system including the stimulation
|
||||
of growth of experimental lymphomas, both in vivo and in vitro." <span
|
||||
style="font-family: Lucida Grande"
|
||||
></span>N Engl J Med 1999 Sep 9;341(11):785-92. Increased mortality associated
|
||||
with growth hormone treatment in critically ill adults.</span></span></span>
|
||||
</blockquote>
|
||||
<p> </p>
|
||||
</span></span></span></span>
|
||||
|
||||
© Ray Peat Ph.D. 2013. All Rights Reserved. www.RayPeat.com
|
||||
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|
||||
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|
||||
Reference in New Issue
Block a user