Categories:

Harm of Prenatal Exposure to Radiation

Also see:
Inflammation from Radiation
Radiation Increases Breast Cancer Incidence
Maternal Ingestion of Tryptophan and Cancer Risk in Female Offspring
Nutrition and Brain Growth in Chick Embryos
Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring
PUFA, Estrogen, Obesity and Early Onset of Puberty
Fukushima Fallout Damaged the Thyroids of California Babies
We Are Giving Ourselves Cancer

Radiat Res. 1998 Sep;150(3):330-48.
Mortality in beagles irradiated during prenatal and postnatal development. II. Contribution of benign and malignant neoplasia.
Benjamin SA, Lee AC, Angleton GM, Saunders WJ, Keefe TJ, Mallinckrodt CH.
To evaluate the lifetime carcinogenic hazards of exposure to ionizing radiation during development, 1,680 beagles received whole-body exposures to 60Co gamma rays or sham exposures. Eight groups of 120 dogs each received mean doses of 15.6-17.5 or 80.8-88.3 cGy in early, mid- or late gestation, at 8, 28 or 55 days postcoitus or at 2 days after birth. Another group of 120 dogs received a mean dose of 82.6 cGy as 70-day-old juveniles and one group of 240 dogs received a mean dose of 81.2 cGy as 365-day-old young adults. Sham irradiations were given to 360 controls. Sexes were equally represented. In 1,343 dogs allowed to live out their life span, neoplasia was a major disease, contributing to mortality in 40% of the dogs. There was a significant increase in benign and malignant neoplasms occurring in young dogs (<4 years old), including fatal malignancies, after irradiation in the perinatal (late fetal and neonatal) periods. The lifetime incidence of fatal neoplasms was also increased in dogs irradiated perinatally. Three malignancies-lymphomas, hemangiosarcomas and mammary carcinomas-accounted for 51% of all fatal tumors. There was an apparent lifetime increase and earlier onset of lymphomas in dogs exposed as fetuses. Fatal hemangiosarcomas were increased in dogs irradiated early and late in gestation. Fatal mammary carcinomas were not increased by irradiation, although non-fatal carcinomas were increased after perinatal exposure. Myeloproliferative disorders and central nervous system astrocytomas appeared to be increased in perinatally irradiated dogs. These data suggest that irradiation in both the fetal and neonatal periods is associated with increased early onset and lifetime cancer risk.

Health Phys. 1988 Aug;55(2):295-8.
Intrauterine radiation exposures and mental retardation.
Miller RW.
Small head size and mental retardation have been known as effects of intrauterine exposure to ionizing radiation since the 1920s. In the 1950s, studies of Japanese atomic-bomb survivors revealed that at 4-17 wk of gestation, the greater the dose, the smaller the brain (and head size), and that beginning at 0.5 Gy (50 rad) in Hiroshima, mental retardation increased in frequency with increasing dose. No other excess of birth defects was observed. Otake and Schull (1984) pointed out that the period of susceptibility to mental retardation coincided with that for proliferation and migration of neuronal elements from near the cerebral ventricles to the cortex. Mental retardation could be the result of interference with this process. Their analysis indicated that exposures at 8-15 wk to 0.01-0.02 Gy (1-2 rad) doubled the frequency of severe mental retardation. This estimate was based on small numbers of mentally retarded atomic-bomb survivors. Although nuclear accidents have occurred recently, new cases will hopefully be too rare to provide further information about the risk of mental retardation. It may be possible, however, to learn about lesser impairment. New psychometric tests may be helpful in detecting subtle deficits in intelligence or neurodevelopmental function. One such test is PEERAMID, which is being used in schools to identify learning disabilities due, for example, to deficits in attention, short- or long-term memory, or in sequencing information. This and other tests could be applied in evaluating survivors of intrauterine exposure to various doses of ionizing radiation. The results could change our understanding of the safety of low-dose exposures.

Br J Radiol. 1984 May;57(677):409-14.
In utero exposure to A-bomb radiation and mental retardation; a reassessment.
Otake M, Schull WJ.
The prevalence of mental retardation in children exposed in utero to the atomic bombs in Hiroshima and Nagasaki has been re-evaluated in reference to gestational age and tissue dose in the fetus. There was no risk at 0-8 weeks post-conception. The highest risk of forebrain damage occurred at 8-15 weeks of gestational age, the time when the most rapid proliferation of neuronal elements and when most, if not all, neuroblast migration to the cerebral cortex from the proliferative zones is occurring. Overall, the risk is five or more times greater in these weeks than in subsequent ones. In the critical period, damage expressed as the frequency of subsequent mental retardation appears to be linearly related to the dose received by the fetus. A linear model is not equally applicable to radiation-related mental retardation after the 15th week, the observed values suggesting that there a threshold may exist. The data are consistent with a probability of occurrence of mental retardation of 0.40% per cGy or 40% per gray.

J Radiat Res. 1991 Mar;32 Suppl:249-64.
A review of forty-five years study of Hiroshima and Nagasaki atomic bomb survivors. Brain damage among the prenatally exposed.
Otake M, Schull WJ, Yoshimaru H.
Significant effects on the developing brain of exposure to ionizing radiation are seen among those individuals exposed in the 8th through the 25th week after fertilization. These effects, particularly in the most sensitive period, 8-15 weeks after fertilization, manifest themselves as an increased frequency of severe mental retardation (SMR), a diminution in IQ score and in school performance, and an increase in the occurrence of seizures. Of 30 SMR cases, 18 (60%) had small heads. About 10% of the individuals with small head sizes observed among the in utero clinical sample were mentally retarded. When all of the cases of mental retardation are included in the analysis, a linear dose-response model fits the data adequately and no evidence of a threshold emerges; however, if the two probable nonradiation-related cases of Down’s syndrome are excluded from the 19 SMR cases exposed 8-15 weeks after fertilization, the evidence of a threshold is stronger. The 95% lower bound of the threshold based on the new dosimetry system appears to be in the range of 0.12-0.23 Gy. In the 16-25 week period, the 95% lower bound of the threshold is 0.21 Gy both with and without inclusion of two probable nonradiation-related retarded cases. In a regression analysis of IQ scores and school performance data, a greater linearity is suggested with the new dosimetry (DS86) than with the old (T65DR), but the mean IQ score and the mean school performance of those exposed in utero to doses under 0.10 Gy are similar, and not statistically different from the means in the control group. The risk ratios for unprovoked seizures, following exposure during the 8th through the 15th week after fertilization, are 4.4 (90% confidence interval: 0.5-40.9) after 0.10-0.49 Gy and 24.9 (4.1-191.6) after 0.50 Gy or more when the mentally retarded are included and 4.4 (0.5-40.9) and 14.5 (0.4-199.6), respectively, when they are excluded.

Nihon Eiseigaku Zasshi. 1991 Aug;46(3):747-54.
[Effect on school performance of prenatal exposure to the Hiroshima atomic bomb].
[Article in Japanese]
Yoshimaru H, Otake M, Fujikoshi Y, Schull WJ.
As a part of the continuing assessment of the effects on the developing embryonic and fetal brain of exposure to ionizing radiation, the school performance of prenatally exposed survivors of the atomic bombing of Hiroshima and a suitable comparison group have been studied. In this report, the changes in performance in seven school subjects according to dose are compared under the dosimetry system (DS86) instituted in 1986 at the Radiation Effects Research Foundation. The sample involves 929 children whose fetal absorbed dose are known and includes 14 severely mentally retarded persons. The findings can be summarized as follows: 1) Damage to the 8-15 week fetal brain appears to be linearly related to the absorbed dose, as judged by the simple regression of average school-performance score on dose. Damage to the fetus exposed at 16-25 weeks after fertilization appears similar to that seen in the 8-15 week group. Canonical and multiple correlations also show a highly significant relationship of exposure 8-15 weeks and 16-25 weeks after fertilization to achievement in school. This trend is stronger, however, in the earliest years of schooling. 2) In the group exposed within 0-7 weeks following fertilization, or 26 or more weeks after fertilization, there was no evidence of a radiation-related effect on scholastic performance. 3) These results parallel those previously found in prenatally exposed survivors with respect to achievement in standard intelligence tests in childhood and development of severe mental retardation.

Stem Cells. 1997;15 Suppl 2:129-33.
Brain damage among individuals exposed prenatally to ionizing radiation: a 1993 review.
Schull WJ.
Mental retardation as a result of prenatal exposure to ionizing radiation is not a common phenomenon when compared to the incidence of cancer, but it has nevertheless been well-documented. This article describes results from studies of individuals who were exposed prenatally to radiation in Hiroshima and Nagasaki. The critical time of exposure, when the most significant damage was done, was during the 8th-15th week of gestation, with a lesser effect at 16-25 weeks. Individuals in the study were assessed by measurement of an intelligence quotient and by examination of school performance. Studies show that the period of 8-15 weeks of gestation coincides with a key time for neuronal cell migration in the developing brain. There is continuing investigation of the mechanism of this migration and how it might be disrupted by ionizing radiation.

Int J Radiat Biol. 1998 Aug;74(2):159-71.
Radiation-related brain damage and growth retardation among the prenatally exposed atomic bomb survivors.
Otake M, Schull WJ.
Many studies of prenatally exposed survivors of the atomic bombings of Hiroshima and Nagasaki have shown that exposure to ionizing radiation during gestation has harmful effects on the developing human brain. Data on the occurrence of severe mental retardation as well as variation in intelligence quotient (IQ) and school performance show significant effects on those survivors exposed 8-15 and 16-25 weeks after ovulation. Studies of seizures, especially those without a known precipitating cause, also exhibit a radiation effect in survivors exposed 8-15 weeks after ovulation. The biologic events that subtend these abnormalities are still unclear. However, magnetic resonance imaging of the brains of some mentally retarded survivors has revealed a large region of abnormally situated gray matter, suggesting an abnormality in neuronal migration. Radiation can induce small head size as well as mental retardation, and a review of the relationship between small head size and anthropometric measurements, such as height, weight, sitting height and chest circumference, shows that individuals with small head size have smaller anthropometric measurements than normocephalics. This suggests that radiation-related small head size is related to a generalized growth retardation. Finally, the issue of a threshold in the occurrence of one or more of these effects, both heuristically and from a regulatory perspective, remains uncertain. Simple inspection of the data often suggests that a threshold may exist, but little statistical support for this impression can be advanced, except in the instance of mental retardation.

Int J Radiat Biol. 1993 Feb;63(2):255-70.
Radiation-related small head sizes among prenatally exposed A-bomb survivors.
Otake M, Schull WJ.
Of 1566 individuals prenatally exposed to the atomic bombings of Hiroshima and Nagasaki, 1473 had the circumference of their head measured at least once between ages 9 and 19. Among these 1473 individuals, 62 had small heads–the circumference of the heads was two standard deviations or more below the observed specific-age-at measurement mean. Of 26 cases with severe mental retardation, 15 (58%) had small heads. Most (86%) of the individuals with small heads were exposed in the first trimester (about < 12 weeks postovulation) or second trimester (about 12-24 weeks postovulation)–55% in the former period and 31% in the latter. Various dose-response relationships, with and without a threshold, have been fitted to the data grouped by the trimester or postovulatory age (weeks after ovulation) at which exposure occurred. A significant effect of radiation on the frequency of individuals with atypically small heads is observed only in the first and second trimesters and for the intervals postovulation of 0-7 weeks and 8-15 weeks. Although the risk of a small head at 0-7 weeks postovulation increases significantly with increasing dose, no increase in risk for severe mental retardation is noted in this period. No excess risk of a small head was seen in the third trimester (about > or = 25 weeks postovulation) or among individuals exposed at 16 weeks or more postovulation. The mean IQ values of mentally retarded cases with and without small heads were 63.8 and 68.9, respectively. No significant difference exists between these two IQ means, but both were significantly smaller than 96.4, the IQ value for individuals with small heads without severe mental retardation and 107.8, the value for the overall sample.

Teratology. 1999 Apr;59(4):222-6.
Cognitive function and prenatal exposure to ionizing radiation.
Schull WJ, Otake M.
It is clear from the many studies of the prenatally exposed survivors of the atomic bombing of Hiroshima and Nagasaki that exposure to ionizing radiation during gestation has harmful effects on the developing human brain, particularly if that exposure occurs at critical stages in the development of the neocortex. Data on a variety of measures of cognitive function, including the occurrence of severe mental retardation as well as variation in the intelligence quotient (IQ) and school performance, show significant effects on those survivors exposed 8-15 weeks and 16-25 weeks after ovulation. Studies of seizures, primarily those without known precipitating cause, also exhibit a radiation effect on those individuals exposed in the first 16 weeks after ovulation. The cellular and molecular events that subtend these abnormalities are still largely unknown although some progress toward an understanding has occurred. For example, magnetic resonance imaging of the brain of some of the mentally retarded survivors has revealed a large region of abnormally situated gray matter, suggesting an abnormality in neuronal migration, but cell killing could also contribute importantly to the effects on cognitive function that have been seen. The retardation of growth in stature observed in individuals exposed in the first and second trimesters of pregnancy suggests that the development of an atypically small head size, without conspicuously impaired cognitive function, may reflect a generalized retardation of growth.

Rinsho Byori. 1994 Apr;42(4):313-9.
[Health effects of atomic bomb radiation].
[Article in Japanese]
Shigematsu I.
The health effects of atomic bomb radiation have been studied by the Atomic Bomb Casualty Commission (ABCC) and its successor, the Radiation Effects Research Foundation (RERF) based on a fixed population of atomic bomb survivors in Hiroshima and Nagasaki which had been established in 1950. The results obtained to the present can be classified into the following three categories: (1) The effects for which a strong association with atomic bomb radiation has been found include malignant neoplasms, cataracts, chromosomal aberrations, small head size and mental retardation among the in utero exposed. (2) A weak association has been found in the several sites of cancers, some non-cancer mortalities and immunological abnormalities. (3) No association has been observed in some types of leukemia, osteosarcoma, accelerated aging, sterility and hereditary effects.

JAMA. 1990 Aug 1;264(5):605-9.
Perinatal loss and neurological abnormalities among children of the atomic bomb. Nagasaki and Hiroshima revisited, 1949 to 1989.
Yamazaki JN, Schull WJ.
Studies of the survivors of the atomic bombing of Hiroshima and Nagasaki who were exposed to ionizing radiation in utero have demonstrated a significant increase in perinatal loss and the vulnerability of the developing fetal brain to injury. These studies have also helped to define the stages in the development of the human brain that are particularly susceptible to radiation-related damage. Exposure at critical junctures in development increases the risk of mental retardation, small head size, subsequent seizures, and poor performance on conventional tests of intelligence and in school. The most critical period, 8 through 15 weeks after fertilization, corresponds to that time in development when neuronal production increases and migration of immature neurons to their cortical sites of function occurs. The epidemiologic data are, however, too sparse to settle unequivocally the nature of the dose-response function and, in particular, whether there is or is not a threshold to damage. If a threshold does exist, it appears to be in the 0.10- to 0.20-Gy fetal-dose range in this vulnerable gestational period.

Adv Space Res. 1986;6(11):223-32.
Learning disabilities in individuals exposed prenatally to ionizing radiation: the Hiroshima and Nagasaki experiences.
Schull WJ, Otake M.
The brain, undoubtedly the most complex organ in the mammalian body, is the culmination of a long and interrelated sequence of molecular, cellular and tissue events. Brain function hinges on the orderly progression of these, each of which must occur correctly, temporally and spatially. Impingement on any one will give rise to a less developed system of cellular connections, and hence impaired function. Moreover, the neurons of the central nervous system are not self-renewing and thus neuronal loss cannot be repaired through repopulation. Reanalysis of the data on the prenatally exposed survivors of the atomic bombing of Hiroshima and Nagasaki suggests that severe mental retardation occurs primarily, if not exclusively in the period from the 8th through the 15th week following fertilization. Within this window of vulnerability, the increase in mental retardation appears linear with dose and without threshold. More subtle functional effects also occur as reflected in diminished performance on intelligence tests and in school. These findings and their implications for space travel and regulatory agencies charged with the specification of acceptable risks should not require further elaboration in this article given the focus of the radiobiological presentations at this meeting.

Health Phys. 1990 Jul;59(1):57-61.
Effects of prenatal exposure to ionizing radiation.
Miller RW.
Prenatal exposure to ionizing radiation induces some effects that are seen at birth and others that cannot be detected until later in life. Data from A-bomb survivors in Hiroshima and Nagasaki show a diminished number of births after exposure under 4 wk of gestational age. Although a wide array of congenital malformations has been found in animal experimentation after such exposure to x rays, in humans only small head size (exposure at 4-17 wk) and mental retardation (exposure primarily at 8-15 wk) have been observed. In Hiroshima, small head size occurred after doses of 0.10-0.19 Gy or more, and an excess of mental retardation at 0.2-0.4 Gy or more. Intelligence test scores were reduced among A-bomb survivors exposed at 8-15 wk of gestational age by 21-29 IQ points per Gy. Other effects of in-utero exposure to atomic radiation include long-lasting complex chromosome abnormalities.

JAMA. 2004 Apr 28;291(16):1987-93.
Antepartum dental radiography and infant low birth weight.
Hujoel PP, Bollen AM, Noonan CJ, del Aguila MA.
CONTEXT:
Both high- and low-dose radiation exposures in women have been associated with low-birth-weight offspring. It is unclear if radiation affects the hypothalamus-pituitary-thyroid axis and thereby indirectly birth weight, or if the radiation directly affects the reproductive organs.
OBJECTIVE:
To investigate whether antepartum dental radiography is associated with low-birth-weight offspring.
DESIGN:
A population-based case-control study.
PARTICIPANTS AND SETTING:
Enrollees of a dental insurance plan with live singleton births in Washington State between January 1993 and December 2000. Cases were 1117 women with low-birth-weight infants (<2500 g), of whom 336 were term low-birth-weight infants (1501-2499 g and gestation > or =37 weeks). Four control pregnancies resulting in normal-birth-weight infants (> or =2500 g) were randomly selected for each case (n = 4468).
MAIN OUTCOME MEASURES:
Odds of low birth weight and term low birth weight by dental radiographic dose during gestation.
RESULTS:
An exposure higher than 0.4 milligray (mGy) during gestation occurred in 21 (1.9%) mothers of low-birth-weight infants and, when compared with women who had no known dental radiography, was associated with an adjusted odds ratio (OR) for a low-birth-weight infant of 2.27 (95% confidence interval [CI], 1.11-4.66, P =.03). Exposure higher than 0.4 mGy occurred in 10 (3%) term low-birth-weight pregnancies and was associated with an adjusted OR for a term low-birth-weight infant of 3.61 (95% CI, 1.46-8.92, P =.005).
CONCLUSION:
Dental radiography during pregnancy is associated with low birth weight, specifically with term low birth weight.

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By Team FPS – June 23, 2012

Salt Lowers Pituitary Stress Response

Peptides. 1990 Jan-Feb;11(1):59-63.
Long-term salt loading impairs pituitary responsiveness to ACTH secretagogues and stress in rats.
Dohanics J, Kovacs KJ, Folly G, Makara GB.
Male Wistar rats were allowed to drink tap water ad lib (W), 2% saline (S) or 2% saline containing dexamethasone (S+D, 1 mg/l) for 7 days. On the 8th day rats were subjected to a 3-min ether stress. Plasma ACTH, corticosterone and prolactin concentrations were determined before and after ether exposure. Prestress concentrations of plasma ACTH were low and did not vary among the three groups. In response to ether stress W rats exhibited twice as high plasma ACTH concentrations as did S rats. Rats of the S+D group exhibited a small but statistically significant ACTH response. Plasma corticosterone concentration in S rats was increased while in S+D rats was significantly decreased under resting conditions compared to that in W rats. Ether stress caused large increases in plasma corticosterone concentrations in W and S rats while a small but statistically significant increase was observed in S+D rats. Prolactin responses to ether were smaller in groups S and S+D than in group W. To test whether the decreased ACTH response to ether exposure was a result of a decreased sensitivity of corticotrope cells to corticotropin releasing factor (CRF)-41 or arginine vasopressin (AVP), adenohypophysial fragments from W, S and S+D rats were incubated in the presence of different doses of CRF-41 or AVP. Pituitary fragments obtained from W rats secreted larger amounts of ACTH than did pituitaries from S rats in response to either CRF-41 or AVP. CRF-41 caused only a slight increase and AVP caused no significant increase in ACTH release from pituitary fragments obtained from S+D rats. These results indicate that prolonged osmotic stimulation impairs ACTH and prolactin but not corticosterone responses to ether stress. We suggest that the decreased sensitivity of corticotropes to CRF-41 and AVP is a possible mechanism that could account for the deficient ACTH response to ether stress in S rats.

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By Team FPS – June 23, 2012

Arthritis and Hypothyroidism

Also see:
Hormone Balancing: Natural Treatment and Cure for Arthritis

Folia Med (Plovdiv). 2007;49(3-4):5-12.
Rheumatoid arthritis and thyroid abnormalities.
Staykova ND.
Relationships between rheumatoid arthritis (RA) and the thyroid gland have been studied extensively for a long time. The studies of this problem have focused mainly on: (a) the functional and immune thyroid gland abnormalities in patients with previous history of RA, and (b) joint changes in patients with previous autoimmune thyroid diseases. Thyroid dysfunctions in RA patients are most often of autoimmune nature; they are accompanied by elevated thyroid autoantibody titers. The RA patients usually present with eu-, hypo- or hyperthyroid manifestations. The concurrent affection of joints and thyroid gland is related most probably to a genetic predisposition determined by the affiliation to a certain HLA type, most often HLA-DR. Joint abnormalities in thyroid gland disorders may be of different character (generally polyarthritis) and they are due to hypothyroidism. One possible explanation of the presence of two or more autoimmune diseases in one individual is microchimerism – the presence of a small number of fetal cells in the mother as well as maternal cells in the fetus. These data provide grounds for tests to be performed in all cases of RA so that thyroid autoantibodies and thyroid dysfunctions can be detected early and treated adequately.

Ann Rheum Dis. 2008 Feb;67(2):229-32. Epub 2007 Jun 8.
Rheumatoid arthritis is associated with a high prevalence of hypothyroidism that amplifies its cardiovascular risk.
Raterman HG, van Halm VP, Voskuyl AE, Simsek S, Dijkmans BA, Nurmohamed MT.
OBJECTIVE:
Rheumatoid arthritis (RA) patients have an increased risk of developing cardiovascular diseases (CVD). Other autoimmune diseases such as hypothyroidism are also associated with an enhanced risk for CVD. Our objective was to determine first, the prevalence of hypothyroid disorders in RA patients, and second, the risk of CVD in RA patients with hypothyroid abnormalities.
METHODS:
SUBJECTS:
were RA patients who participated in an ongoing prospective cohort study of cardiovascular mortality and morbidity (n = 358) in which hypothyroid abnormalities were assessed. CVD was defined as a verified medical history of coronary, cerebral or peripheral arterial disease.
RESULTS:
Clinical hypothyroidism was observed in 16 of 236 female RA patients (6.8%), which is significantly higher than in the general population of The Netherlands. Subclinical hypothyroidism was detected in 6 out of 236 RA women (2.5%). In female RA patients, CVD was present in 6 out of 16 (37.5%) of all hypothyroid women. The odds ratio for CVD comparing female hypothyroid RA patients with female euthyroid RA patients was 4.1 (95% CI 1.2-14.3) after adjustment for sex, age, diabetes, smoking (ever), hypertension and statin use.
CONCLUSIONS:
Clinical hypothyroidism was observed three times more often in female RA patients than females in the general population. In female RA patients, clinical hypothyroidism was associated with a fourfold higher risk of CVD in comparison with euthyroid female RA patients independently of the traditional risk factors.

Semin Arthritis Rheum. 1995 Feb;24(4):282-90.
Bone and joint manifestations of hypothyroidism.
McLean RM, Podell DN.
Hypothyroidism is frequently accompanied by musculoskeletal manifestations ranging from myalgias and arthralgias to true myopathy and arthritis. A case is presented in which an arthropathic process in the hip was the isolated finding in a young man who was severely hypothyroid. Previous literature on bone and joint manifestations of hypothyroidism is reviewed, with emphasis on cases where such manifestations were the presenting symptoms of thyroid dysfunction. Most cases of arthropathic changes in adult-recognized hypothyroidism involved the knees and hands, while the hip and the epiphysis of the femoral head appear more commonly involved in children. Thyroid hormones have known effects at the cellular level on proliferation and differentiation of bone and cartilage. The hypothyroid state appears to induce abnormalities in these tissues, which result in such clinical manifestations as epiphyseal dysgenesis, aseptic necrosis, possibly crystal-induced arthritis, and an arthropathy characterized by highly viscous noninflammatory joint effusions primarily affecting the knees, wrists, and hands. Neuropathic and myopathic symptoms accompanying hypothyroidism may manifest as joint region abnormalities when in fact there is no underlying arthropathy.

Postgrad Med J. 1985 Feb;61(712):157-9.
Hypothyroidism presenting as destructive arthropathy of the fingers.
Gerster JC, Quadri P, Saudan Y.
A patient presenting with destructive arthropathy of the proximal interphalangeal (PIP) joints of the hands is described. She was initially believed to have rheumatoid arthritis but non-steroidal anti-inflammatory drugs were of no help. The patient was subsequently found to have hypothyroidism and erosive osteoarthritis of the fingers. Joint swelling, pain and stiffness responded dramatically to thyroid hormone substitution. The PIP joint spaces reappeared on the radiographs within 9 months. This case suggest that hypothyroidism may induce destructive arthropathy of the finger joints. As thyroxine replacement may reverse the rheumatic complaints, hypothyroidism should be considered in the differential diagnosis of a destructive arthropathy of unclear aetiology.

Isr J Med Sci. 1987 Nov;23(11):1110-3.
Musculoskeletal symptoms as a presenting sign of long-standing hypothyroidism.
Krupsky M, Flatau E, Yarom R, Resnitzky P.
Muscle and joint pains and/or weakness are not usually stressed as central symptoms in hypothyroidism. Two cases of long-standing hypothyroidism presenting with prominent myopathic symptoms are described. The first patient presented with a 12-year history of proximal myopathy, arthropathy and skin abnormalities, and florid primary myxedema was diagnosed. No evidence for a systemic autoimmune process was found. The second patient had been treated with irradiation to the neck 23 years before admission and presented with clinical and laboratory signs of both proximal myopathy and hypothyroidism. Thyroid hormone replacement resulted in a complete recovery of all the musculoskeletal symptoms, with reversion to normal of the very high muscle enzyme levels in both patients. The cases presented illustrate that hypothyroidism can lead to the development of a variety of muscular, rheumatic and dermatologic syndromes easily confused with dermatomyositis or other collagen diseases.

J Pediatr. 1993 Oct;123(4):586-8.
Rheumatic symptoms associated with hypothyroidism in children.
Keenan GF, Ostrov BE, Goldsmith DP, Athreya BH.
We describe five children with varied rheumatic manifestations, including fibromyalgia and arthralgias, ultimately proved to be associated with hypothyroidism. All musculoskeletal symptoms improved after thyroid replacement therapy. We conclude that rheumatic manifestations of hypothyroidism can be as varied in children as in adults.

Muscle Nerve. 2002 Jul;26(1):141-4.
Hypothyroid myopathy with a strikingly elevated serum creatine kinase level.
Scott KR, Simmons Z, Boyer PJ.
Although serum creatine kinase (CK) levels are frequently modestly elevated in patients with hypothyroid myopathy, elevations in serum CK to the levels usually seen in inflammatory myopathies or dystrophies are rare. We report a patient with progressive proximal weakness and a serum CK level of over 29,000 IU/L, in whom subsequent laboratory evaluation identified profound hypothyroidism. Thyroid hormone replacement therapy resulted in resolution of clinical symptoms and a marked reduction in the serum CK level. Such a high serum CK level in a patient with hypothyroidism underscores the importance of assessing thyroid function in patients with weakness, regardless of serum CK levels, even when systemic symptoms and signs of hypothyroidism are minimal or absent.

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By Team FPS – June 23, 2012

Edema in Hypothyroidism

Probl Endokrinol (Mosk). 1987 Jan-Feb;33(1):18-21.
[Characteristics of the hydration status of patients with hypothyroidism].
[Article in Russian]
Nazarov AN, Lobachik VI, Zhidkov VV, Borisov GI, Abrosimov SV.
The hydratation status of 15 patients of various age groups with hypothyrosis was studied using nuclear physical methods. Their body composition was calculated. All the examinees demonstrated considerable hyperhydratation of the extracellular water sector with prevailing liquid accumulation in the interstitial space. Some changes in the infrastructure of the hydratation status including those in the nature of interrelationships of liquid media, were noted. The dependence of the hydratation status and its infrastructure in patients with hypothyrosis on age and gravity of disease but not on its duration was revealed.

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By Team FPS – June 23, 2012

Melatonin Lowers Body Temperature

Also see:
Inflammation from Decrease in Body Temperature
Menopausal Estrogen Therapy Lowers Body Temperature
Tryptophan, Sleep, and Depression
Carbohydrate Lowers Free Tryptophan
Gelatin > Whey
Serotonin, Fatigue, Training, and Performance
Gelatin, Glycine, and Metabolism
Whey, Tryptophan, & Serotonin

Am J Psychiatry. 1976 Oct;133(10):1181-6.
Negative effects of melatonin on depression.
Carman JS, Post RM, Buswell R, Goodwin FK.
In order to test the efficacy of the pineal neurohumor melatonin on depression, the hormone was administered in varying doses to six moderately to severely depressed patients and two patients with Huntington’s chorea in double-blind crossover study. Melatonin exacerbated symptoms of dysphoria in these patients, as well as causing a loss of sleep and weight and a drop in oral temperature. Melatonin increased cerebrospinal fluid 5-hydroxyindoleacetic acid and calcium in three of four patients studied. The authors discuss the implications of this finding.

Physiol Behav. 1996 Jan;59(1):133-9.
Nonsteroidal anti-inflammatory drugs alter body temperature and suppress melatonin in humans.
Murphy PJ, Myers BL, Badia P.
Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis in humans. Prostaglandins are involved in thermoregulation, melatonin synthesis, and sleep. To determine effects of NSAIDs on body temperature (BT) and melatonin synthesis (MT) in humans, and to elucidate mechanisms by which NSAIDs may alter sleep patterns, a series of experiments using the NSAIDs aspirin and ibuprofen was conducted. Seventy-five subjects were tested under several experimental protocols. BT after NSAID or placebo was assessed in both between- and within-subjects designs at night and during the day. MT levels were assessed after NSAID or placebo at night in a within-subjects design. The normal nocturnal BT decrease was attenuated and MT was suppressed after NSAID relative to after placebo administration. Lower MT levels were associated with a relative flattening of BT. Daytime BT was not affected by NSAIDs. These results are compatible with the hypothesis that some of the behavioral changes associated with NSAIDs, including changes in sleep, are due to changes in BT and MT. We speculate that NSAID effects on sleep and BT are related to prostaglandin synthesis inhibition and/or suppression of MT.

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By Team FPS – June 23, 2012

Toxic substances in plants and the food habits of early man

Science. 1972 May 5;176(4034):512-4.
Toxic substances in plants and the food habits of early man.
Leopold AC, Ardrey R.
The widespread occurrence of toxic substances in plants must have greatly restricted their usefulness as food for primitive man. The development of cooking of plant products is suggested to have been a major evolutionary advance, making a major increase in the vegetable materials palatable to man; this technical advantage apparently occurred only in the most recent 2 percent of the anthropological record.

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By Team FPS – June 22, 2012

Fermentable Carbohydrates, Anxiety, Aggression

Also see:
Ray Peat, PhD on the Benefits of the Raw Carrot
Estrogen, Serotonin, and Aggression
Endotoxin: Poisoning from the Inside Out
Scanning Electron Microscope (SEM) images of plant cell microparticles in urine sediment
THE PHENOMENON OF PERSORPTION: PERSORPTION, DISSEMINATION, AND ELIMINATION OF MICROPARTICLES

“The food industry is promoting the use of various gums and starches, which are convenient thickeners and stabilizers for increasing self-life, with the argument that the butyric acid produced when they are fermented by intestinal bacteria is protective. However, intestinal fermentation increases systemic and brain serotonin, and the short-chain fatty acids can produce a variety of inflammatory and cytotoxic effect. Considering the longevity and stress-resistance of germ-free animals, choosing foods (such as raw carrots or cooked bamboo shoots or cooked mushrooms) which accelerate peristalsis and speed transit through the bowel, which suppressing bacterial growth, seems like a convenient approach to increasing longevity.” -Ray Peat, PhD

Physiol Behav. 2004 Sep 15;82(2-3):357-68.
Anxiety and aggression associated with the fermentation of carbohydrates in the hindgut of rats.
Hanstock TL, Clayton EH, Li KM, Mallet PE.
Lactic acid accumulation in the caecum and colon resulting from the fermentation of carbohydrates can lead to deleterious effects in ruminant and monogastric animals, including humans. In the present study, we examined the behavioural effects of two types of commonly consumed foods: soluble and fermentable carbohydrates (FCs). Thirty-six male Wistar rats were fed either a commercial rat and mouse chow, a soluble carbohydrate (SC)-based diet or an FC-based diet. Social interaction, anxiety, aggression and locomotor activity were examined by employing a social interaction test and a light/dark emergence test, while physical parameters of hindgut fermentation were examined after sacrifice, either 3 or 21 h after feeding. Results showed that anxiety (spending less time in the light compartment during the light/dark emergence test) and aggression (increased fighting during the social interaction test) were increased following raised concentrations of fermentation end products, such as lactic acid and volatile fatty acids (VFAs) in the caecum of rats. These associations occurred regardless of dopamine and 5-HT concentrations in the prefrontal cortex (PFC) and provide evidence supporting a general effect of FCs on behaviour. Possible mechanisms of action along with similarities between a rat and human model of acidosis are discussed.

Asia Pac J Clin Nutr. 2003;12 Suppl:S12.
Anxiety following increased hind-gut fermentation.
Hanstock TL, Claytons EH, Mallet PE.
Background – Previous investigations into the effects of carbohydrate on behaviour have focussed on behavioural changes 2-4 hrs after consumption of the diet and have not considered the effect of site of digestion. Fermentation and lactic acid production in the caecum and colon can lead to detrimental effects in several animal models, including adverse behaviour in horses. Objective – To determine changes in anxiety promoted by the consumption of fermentable carbohydrate and increased fermentation in the hind-gut of rats. Design – Randomised control trial with 3 iso-energetic dietary treatment groups, a soluble carbohydrate diet containing wheat (n=12), a fermentable carbohydrate diet based on cooked and cooled rice (n=12) and a basal control rat and mouse Chow diet (n= 12). Behaviour was assessed 3 and 21 hrs after dietary consumption by the light dark emergence test. Outcomes – The 3 diets promoted different fermentation patterns in terms of pH and lactic acid concentrations in the caecum of rats 3 or 21 hrs after consumption. The length of time spent in the dark compartment of the light dark emergence test, indicating increased anxiety, was associated with increased concentrations of D- and L-lactic acid in the caecum (r(2)= 0.97 and 0.96 respectively; P <0.01) irrespective of dietary group. Conclusions – Fermentation of carbohydrate leading to increased concentrations of lactic acid in the caecum of rats was associated with increased anxiety in rats. This has important implications in terms of those diets promoting increased fermentation (eg. with a high intake of resistant starch) without considering any possible detrimental effects.
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Fermentable fibers raise ammonia.

J Nutr. 1989 Feb;119(2):235-41.
Independent effects of fiber and protein on colonic luminal ammonia concentration.
Lupton JR, Marchant LJ.
The potential interactive effects of protein and fiber on cecal and colonic surface areas, colonic luminal ammonia concentrations, luminal pH and blood indices of nitrogen metabolism were tested using two levels of protein (8% and 24%) and two types of fiber (8% pectin or cellulose). Pectin supplementation resulted in larger cecal surface areas and longer large intestines than those of rats fed fiber-free or cellulose-supplemented diets. All high protein diets resulted in total large bowel luminal ammonia (NH3 + NH4+) concentrations that were twice as high as their low protein counterparts (P less than 0.05). The effect of fiber on ammonia concentration depended on the fiber type. In the distal colon, pectin-fed animals had three times the ammonia concentration of the fiber-free animals, and 4-5 times the ammonia concentration of the cellulose-fed animals (P less than 0.001). Blood urea nitrogen values were higher in the high protein than in the low protein groups (P less than 0.05), and highest in the high protein/pectin animals (P less than 0.01). This study clearly demonstrates that luminal ammonia concentration is dependent upon both protein level and fiber type, and that a fermentable fiber (pectin), rather than decreasing colonic ammonia concentrations, actually increases them several-fold.
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Dietary fats protect against anxiety from bacterial fermentation.

Physiol Behav. 1996 Sep;60(3):1039-42.
Short-term consumption of a diet rich in fat decreases anxiety response in adult male rats.
Prasad A, Prasad C.
Short- and long-term changes in the composition of dietary macronutrients [protein (P), carbohydrate (C), and fat (F)] alter neurochemistry and behavior in animals. We examined whether short-term intake of a diet rich in P, C, or F affected their anxiety response (AR). AR of Sprague-Dawley rats was measured in an elevated plus maze. Rats were placed in the black compartment facing the wall opposite the aperture, and the time (max. 360 s) it took to enter the white compartment with all four paws was noted. Rats were fed Purina chow and tap water unless otherwise indicated. On repeated testing (three times on the same day) AR increased and, consequently, most rats spent the entire 360 s in the dark. Whereas most rats exhibited low anxiety response in trial 1, which increased during successive trials (low-high group), some exhibited high initial anxiety that remained unchanged (high-high group). To determine whether macronutrients may alter AR, groups of low-high and high-high rats were tested three times on the same day and then put on a P, C, or F diet for 7 days. On day 8, they were again tested for AR in a single trial and the results compared with those of the third trial of the previous test (preC: 302 +/- 39, post-C: 294 +/- 42, p > 0.05; pre-P: 305 +/- 35, post-P: 297 +/- 43, p > 0.05; pre-F: 321 +/- 17, post-F: 241 +/- 24sec, p = 0.009; n = 30; mean +/- SEM). The results show that a diet rich in F, but not P or C, decreases AR in rats.

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By Team FPS – June 22, 2012

Growth Hormone and Edema

Also see:
W.D. Denckla, A.V. Everitt, Hypophysectomy, & Aging
Removal of the Pituitary: Slows Aging and Hardening of Collagen
“Normal” TSH: Marker for Increased Risk of Fatal Coronary Heart Disease
Inflammatory TSH

“Growth hormone clearly causes edema, and this is probably involved in the pathological processes that it can produce.”-Ray Peat, PhD

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.
Møller J, Jørgensen JO, Møller N, Hansen KW, Pedersen EB, Christiansen JS.
Sodium retention and symptoms and signs of fluid retention are commonly recorded during GH administration in both GH-deficient patients and normal subjects. Most reports have however, been casuistic or uncontrolled. In a randomized double blind placebo-controlled cross-over study we therefore examined the effect of 14-day GH administration (12 IU sc at 2000 h) on plasma volume, extracellular volume (ECV), atrial natriuretic peptide (ANP), arginine vasopressin, and the renin angiotensin system in eight healthy adult men. A significant GH induced increase in serum insulin growth factor I was observed. 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). A significant decrease in plasma ANP (pmol/L) after GH administration was observed: 2.28 +/- 0.54 (GH), 3.16 +/- 0.53 (placebo) P less than 0.01. Plasma aldosterone (pmol/L): 129 +/- 14 (GH), 89 +/- 17 (placebo), P = 0.08, and plasma angiotensin II (pmol/L) levels: 18 +/- 12 (GH), 14 +/- 7 (placebo), P = 0.21, were not significantly elevated. No changes in plasma arginine vasopressin occurred (1.86 +/- 0.05 pmol/L vs. 1.90 +/- 0.05, P = 0.33). Serum sodium and blood pressure remained unaffected. Moderate complaints, which could be ascribed to water retention, were recorded in four subjects [periorbital edema (n = 3), acral paraesthesia (n = 2) and light articular pain (n = 1)]. The symptoms were most pronounced after 2-3 days of treatment and diminished at the end of the period. In summary, 14 days of high dose GH administration caused a significant increase in ECV and a significant suppression of ANP.

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 ratio of left atrial to aortic diameter measured by echocardiography was only minimally increased (1.29 +/- 0.04), indicating that in constrictive pericarditis the atria are prevented from expanding. The studies repeated after pericardiectomy in the eight patients showed that all measurements returned toward normal.
CONCLUSIONS:
The restricted distensibility of the atria, in constrictive pericarditis, limits the secretion of atrial natriuretic factor and, thus, reduces its natriuretic and diuretic effects. This results in retention of water and sodium greater than that occurring in patients with edema from myocardial disease. The arterial pressure is maintained more by the expansion of the blood volume than by an increase in the peripheral vascular resistance.

Circulation. 1989 Aug;80(2):299-305.
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. Eight patients were studied; two had ischemic cardiac disease, and six had dilated cardiomyopathy. Mean hemodynamic measurements at rest were as follows: cardiac index, 1.8 l/min/m2; pulmonary wedge pressure, 30 mm Hg; right atrial pressure, 15 mm Hg. 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.

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.”

J Endocrinol Invest. 1999;22(5 Suppl):106-9.
Growth hormone and body composition in athletes.
Frisch H.
The anabolic properties of growth hormone (GH) have been investigated extensively. The effects of GH on normal, hypertrophied and atrophied muscles have been studied previously in animal experiments that demonstrated an increase in muscle weight and size, but no comparable increase in performance or tension. In adults with GH deficiency, the changes in body composition can be corrected by GH treatment; lean body mass and strength increase within a few months. In children with GH deficiency, Turner’s syndrome or intrauterine growth retardation, an increase in muscle tissue is seen after treatment with GH. In acromegalics with long-standing GH hypersecretion, the muscle volume is increased, but muscle strength and performance are not improved. These observations gave rise to the interest shown by healthy subjects and athletes in using GH to increase their muscle mass and strength. The improvements in muscle strength obtained by resistance exercise training in healthy older men or young men were not enhanced by additional administration of GH. The larger increases in fat-free mass observed in the GH-treated groups were obviously not due to accretion of contractile protein, but rather to fluid retention or accumulation of connective tissue. In experienced weightlifters, the incorporation of amino acids into skeletal muscle protein was not increased and the rate of whole body protein breakdown was not decreased by short-term administration of GH. The results of a study in power athletes confirm the results of these investigations. The study used GH treatment in power athletes compared with a placebo-control group, and the results indicated no increase in maximal strength during concentric contraction of the biceps and quadriceps muscles, although levels of insulin-like growth factor-I were doubled. In highly trained power athletes with low fat mass and high lean body mass, no additional effect of GH treatment on strength is to be expected.

Trends Endocrinol Metab. 2011 May;22(5):171-8. doi: 10.1016/j.tem.2011.02.005. Epub 2011 Mar 17.
Growth hormone and physical performance.
Birzniece V, Nelson AE, Ho KK.
There has been limited research and evidence that GH enhances physical performance in healthy adults or in trained athletes. Even so, human growth hormone (GH) is widely abused by athletes. In healthy adults, GH increases lean body mass, although it is possible that fluid retention contributes to this effect. The most recent data indicate that GH does not enhance muscle strength, power, or aerobic exercise capacity, but improves anaerobic exercise capacity. In fact, there are adverse effects of long-term GH excess such that sustained abuse of GH can lead to a state mimicking acromegaly, a condition with increased morbidity and mortality. This review will examine GH effects on body composition and physical performance in health and disease.

Endocrinol Metab Clin North Am. 2010 Mar;39(1):11-23, vii. doi: 10.1016/j.ecl.2009.10.007.
Growth hormone administration: is it safe and effective for athletic performance.
Birzniece V, Nelson AE, Ho KK.
Human growth hormone (GH) is widely abused by athletes; however, there is little evidence that GH improves physical performance. Replacement of GH in GH deficiency improves some aspects of exercise capacity. There is evidence for a protein anabolic effect of GH in healthy adults and for increased lean body mass following GH, although fluid retention likely contributes to this increase. The evidence suggests that muscle strength, power, and aerobic exercise capacity are not enhanced by GH administration, however GH may improve anaerobic exercise capacity. There are risks of adverse effects of long-term abuse of GH. Sustained abuse of GH may lead to a state mimicking acromegaly, a condition with increased morbidity and mortality.

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By Team FPS – June 22, 2012

Glycolysis Inhibited by Palmitate

Also see:
Aldosterone, Sodium Deficiency, and Insulin Resistance
Diabetes: Conversion of Alpha-cells into Beta-cells
Free Fatty Acid Suppress Cellular Respiration
Women, Estrogen, and Circulating DHA
Insulin Inhibits Lipolysis
The Randle Cycle
Comparison: Carbon Dioxide v. Lactic Acid
Carbon Dioxide Basics
Carbon Dioxide as an Antioxidant
Comparison: Oxidative Metabolism v. Glycolytic Metabolic
Promoters of Efficient v. Inefficient Metabolism
Trauma & Resuscitation: Toxicity of Lactated Ringer’s Solution
Enzyme to Know: Pyruvate Dehydrogenase
Insulin Inhibits Lipolysis
Lactic Acidosis and Diabetes

“Therapeutically, even powerful toxins that block the glycolytic enzymes can improve functions in a variety of organic disturbances “associated with” (caused by) excessive production of lactic acid…But several nontoxic therapies can do the same things: Palmitate (formed from sugar under the influence of thyroid hormone, and found in coconut oil), vitamin B1, biotin, lipoic acid, carbon dioxide, thyroid, naloxone, acetazolamide, for example.” -Ray Peat, PhD

“Thyroid hormone, palmitic acid, and light activate a crucial respiratory enzyme, suppressing the formation of lactic acid. Palmitic acid occurs in coconut oil, and is formed naturally in animal tissues. Unsaturated oils have the opposite effect.” -Ray Peat, PhD

Am J Physiol. 1997 Nov;273(5 Pt 1):C1732-8.
Glycolysis inhibition by palmitate in renal cells cultured in a two-chamber system.
Bolon C, Gauthier C, Simonnet H.
A major shortcoming of renal proximal tubular cells (RPTC) in culture is the gradual modification of their energy metabolism from the oxidative type to the glycolytic type. To test the possible reduction of glycolysis by naturally occurring long-chain fatty acids, RPTC were cultured in a two-chamber system, with albumin-bound palmitate (0.4 mM) added to the basolateral chamber after confluency. Twenty-four hours of contact with palmitate decreased glycolysis by 38% provided that carnitine was present; lactate production was decreased by 38%, and the decrease in glycolysis resulted from a similar decrease of basolateral and apical net uptake of glucose. In contrast to the previously described effect of the nonphysiological oxidative substrate heptanoate, palmitate promoted a long-term decrease in lactate production and sustained excellent cellular growth. After 4 days of contact, decreased glycolysis was maintained even in the absence of carnitine and resulted from a decrease of basolateral uptake only, suggestive of long-term regulation different from the earlier effects. Thus, although cultured RPTC lost their oxidative phenotype, they exhibited a type of regulation (Randle effect) that is found in the oxidative-type but not in the glycolytic-type tissues, therefore unmasking a regulative capacity barely detectable in fresh RPTC. Low PO2 (50 mmHg in the apical chamber) could be a major cause of elevated glycolysis and could hinder the effects of palmitate.

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By Team FPS – June 22, 2012

Growth Hormone Unncessary for Normal Height

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). A 37-year-old man was devoid of secondary sexual characteristics, but manifested tall stature with a eunuchoidal feature. Serum levels of GH, insulin-like growth factor-I, gonadotropins and testosterone were all below normal. GH secretion was not enhanced by any provocative stimulus. Adrenocorticotropic hormone increased after administration of corticotropin releasing hormone, but not after insulin-induced hypoglycemia. Thyrotropin increased in response to thyrotropin releasing hormone, but both free T3 and T4 did not rise. Magnetic resonance imaging disclosed a transected pituitary stalk. The present patient had hypopituitarism due to perinatal problems but had grown with the aid of non-GH growth-promoting factors, which suggests that man may be able to achieve statural growth even without GH.

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By Team FPS – June 22, 2012