Bulletin Board
Archived Bulletin Board
About John
Latest Ideas
Symptoms
Tests and Drugs
Weight Loss Experiment
Hyperthyroidism
Hypothyroidism
Supplement List
Medical Science
Heredity
Other Diseases
Thyroid Physiology
Deeper Studies
Nutrients and Toxics
Hair Analysis
Book Reports
Glossary
Table of Contents | |
- MILK
Many hypers find that milk increases hyper symptoms. The high
amounts of calcium versus magnesium in milk may be the reason for this
observation but there may be another reason: estrogen.
Estrogen is found in milk and studies have shown that estrogen increases
cadmium absorption. I believe that cadmium is a major promoter of Graves'
disease and TED and the effects of estrogen on cadmium (and possibly other
metal) absorption may be the major factor explaining why women get thyroid
disease at a much higher rate than men.
Following is a study which states that cadmium toxicity causes anemia, a
condition highly associated with thyroid disease. As the
article states, cadmium "absorption is increased by co-administration of milk and in conjunction with
iron deficiency."
Quoting the study, "Hg++ accumulation in the brains of
suckling rats is approx. 10 times higher than in grown animals. Milk increases
the bioavailability of Hg++." Does this "10 times" strike a
bell for you as it does for me? This is the factor by which women (high in
estrogen) are more likely to get hyperthyroidism than men.
The evidence is
clearly pointing to heavy metal toxicity from cadmium and mercury which is
accelerated by estrogen as the causative factor for hyperthyroidism and
hypothyroidism. Milk consumption may be one of the ways that estrogen
levels are increased in the body and cadmium absorption is magnified.
Z Ernahrungswiss 1990 Mar;29(1):54-73 |
|
[The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in
food for infants and small children].
[Article in German]
Schumann K
Walther-Straub-Institut fur Pharmakologie und Toxikologie der Ludwig-Maximilians-Universitat,
Munchen, FRG.
There are differences between young and adult organisms regarding toxokinetic
aspects and clinical manifestations of heavy metal intoxications. Chronically,
toxic Cd intake causes a microcytotic hypochromic anemia in young rats at
lower exposure levels and after shorter exposure periods than in adult
animals. Cd absorption is increased by co-administration of milk and in
conjunction with iron deficiency. After long exposure periods toxic Cd
concentrations accumulate in the kidney cortex; this process starts very early
in life. In 3-year-old children Cd concentrations in the kidney can reach up
to one-third of those found in adults. Hg++ and methyl-Hg can cause Hg
encephalopathia, and frequently cause mental retardation in adults. Correspondingly,
Hg++ accumulation in the brains of suckling rats is approx. 10 times higher
than in grown animals. Milk increases the bioavailability of Hg++. In
suckling rats Hg is bound to a greater extent to ligands in the erythrocytes.
Methyl-Hg concentrations in breast milk reach 5% of those in maternal plasma
and that is a severe hazard for breastfed children of exposed mothers. Toxic
Pb concentrations can lead to Pb encephalopathia. A high percentage of
surviving children have seizures and show signs of mental retardation. Anemia
and reduced intelligence scores were recently observed in children after
exposure to very low levels of Pb. Pb absorption is increased in children
and after co-administration of milk. There are no definite proofs for
carcinogenesis or mutagenesis after oral exposure to Cd, Hg, and Pb in man.
Heavy metal concentrations were found in the same order of magnitude in
commercial infant formulas and in breast milk. When infant formulas are
reconstituted with contaminated tap water, however, Pb and Cd concentrations
can be much higher. The average heavy metal uptake from such diets exceeds the
provisional tolerable weekly intake levels set by the WHO for adults,
calculated on the basis of an average food intake and a downscaled body
weight. These considerations do not even provide for differences in absorption
and distribution or for the increased sensitivity of children to heavy metal
exposure. However, dilution effects for essential heavy metals were observed
in fast-growing young children; this effect might be extrapolated to toxic
metals. These theoretical considerations are compared with epidemiological
evidence. A health statistic from Baltimore shows a decline of Pb
intoxications in infants. This observation correlates with a simultaneous
decline in exposure to Pb which was due, for example, to decreased use of lead
dyes in house paints and the abolition of tin cans for infant food.
Ann N Y Acad Sci 1986;464:75-86 |
|
Hormones in milk.
Schams D, Karg H
Protein hormones (especially prolactin) and steroid hormones (gestagens,
estrogens, corticoids, and androgens) can be detected by bioassay and
radioimmunoassay in milk in a variety of species. In addition, milk contains
vitamin D and beta-casomorphins (opiate-like peptides). It has been assumed
that most of the hormones are transferred into milk by diffusion. However,
evidence is available for active mechanisms like those for progesterone in
goats and prolactin in cows. Most of the hormone profiles in milk are
similar to the ones in blood plasma. Hormone concentrations in milk seem to
be a good estimate of the average hormone content in plasma, especially for
the measurement of longer-lasting secretory activities like progesterone and
estrogen release during the estrous cycle or seasonal changes of prolactin
in ruminants. Determination of progesterone and estrone sulfate in milk
serves as a diagnostic tool in fertility control, especially in cows. Enzyme
immunoassay kits are available for this monitoring purpose. Exogenously
administered hormones are also transferred into milk. Residue studies have
shown that the dilution is so great that it may be assumed that there is no
potential risk for the consumer.
Prog Food Nutr Sci 1990;14(1):1-43 |
|
A review of the hormone prolactin during lactation.
Ostrom KM
Department of Nutritional Sciences, University of Connecticut, Storrs.
The principal lactogenic hormone, prolactin, secreted by the anterior pituitary
is critical to the establishment of lactation, milk macronutrient content and
milk production. The concentration of circulating prolactin increases during
pregnancy so that by the end of gestation, levels are 10 to 20 times over normal
amounts. However, prolactin is prevented from exerting its effect on milk
secretion by elevated levels of progesterone. Following clearance of
progesterone and estrogen at parturition, copious milk secretion begins. The
minimal hormonal requirements for normal lactation to occur are prolactin,
insulin and hydrocortisone. Prolactin stabilizes and promotes transcription of
casein mRNA; may stimulate synthesis of alpha-lactalbumin, the regulatory
protein of the lactose synthetase enzyme system; and increases lipoprotein
lipase activity in the mammary gland. Prolactin levels decrease as lactation is
established but nursing stimulates prolactin release from the pituitary which
promotes continued milk production. Prolactin is secreted into milk at levels
representative of the average circulating concentration. The physiological
significance of milk prolactin to the infant is uncertain. Prolactin exists in
three heterogenic forms which possess varying biological activity. The monomer
with a molecular weight of 23 kDa is found in greatest quantity and is the
principal biologically active form. The pattern of heterogeneity changes during
pregnancy to favor even more monomer in proportion to the dimer. However, during
lactation, the proportion of the monomer in circulation decreases in response to
selective uptake of the monomer by the mammary gland. Over 90 percent of the
prolactin in milk is present as the monomer. Prolactin may exert some of its
biological effect by a shift in the ratio of active to less active forms of the
molecule.
-
Med Hypotheses 1997 Jun;48(6):453-61 |
t |
Dairy products and breast cancer: the IGF-I, estrogen, and bGH hypothesis.
Outwater JL, Nicholson A, Barnard N
A. B. Princeton University 1996, Physicians Committee For Responsible
Medicine, Washington, DC 20016, USA.
Research on the role of dietary factors in breast cancer causation has
focused predominantly on fat intake. While some studies have examined
associations between breast cancer rates and consumption of whole milk,
there has been less attention given to dairy products in general. Dairy
products contain both hormones and growth factors, in addition to fat and
various chemical contaminants, that have been implicated in the
proliferation of human breast cancer cells. This literature review evaluates
the epidemiological and mechanistic evidence linking dairy consumption with
breast cancer risk.
In a message dated 11/3/00 8:59:09 AM Pacific Standard Time, getdawnrose@hotmail.com writes:
<< Several studies have reported a seasonal variation in the presentation of
patients with Graves' disease. This was observed in European studies dating
back to the 1920s as well as more recent studies from the United States, the
United Kingdom, and New Zealand . These studies suggest that cases tend to
present in the spring and early summer months both in the Northern and the
Southern hemisphere. The most obvious explanation of this trend is that
higher summer causes the symptoms of hyperthyroidism to be less well
tolerated so that patients are more likely to seek medical attention.
However, there are other possible explanations. In a study in the UK it
appeared that the onset as well as the the presentation of the disease was
seasonal with a peak period of onset from January to June. It was
suggested that a winter increase in the iodine content of the diet could
have triggered the disease in some patients. The winter increase in
dietary iodine intake is well recognized in Northern European countries and is due
to the practice of supplementing cattle feed with iodine during the winter
months.">>
Hi Dawn,
There are probably some very logical explanations of why hyperT increases in the late winter to the summer. I was unaware that iodine supplementation for cattle was increased during the winter, but this would probably mean higher iodine content in milk. We know that milk is a real negative for hypers and I know of three reasons: (1) Milk cans at the dairy are cleaned with iodine and there is always some retained in the can, (2) The milk cans are galvanized which means that zinc and cadmium get into the milk from the can and both these metals are copper antagonists, and (3) Milk is extremely low in copper.
Humans drink milk for vitamin D and vitamin D status declines to a minimum in February. Since it is an oil vitamin, it is stored in the body from the prior fall, but people run very low by Jan-March. Increased milk and dairy consumption to get vitamin D increases the hyper promoting effects of milk
consumption
Also, in spring and summer, people start eating more fruit. Fruit is another negative for hypers because it is copper depleting. It may deplete copper because of the high iron to copper ratio of most fruits.
There could easily be other dietary factors that affect the seasonal variation in hyperT symptoms. John
|