Yet Another Estrogen Question

[4tuneit1]

Human's are like the only mammal to keep drinking milk into adulthood, and we don't even drink our own species milk...we drink highly modified animal milk.  I gave up milk years ago in my late teens, but by then had already gotten gynecomastia in small but noticeable ways.  I'm not making any correlation to milk for my gyne, but i have noticed how young women are especially blossoming earlier and earlier...and i think further studies should be looked into how all these hormones are filtering down into our childrens health.  My children and I will drink Soy over animal milk until growth hormones and animal steroids are eliminated from the process.

[STILLgotIT]

Human's are like the only mammal to keep drinking milk into adulthood, and we don't even drink our own species milk...we drink highly modified animal milk.  I gave up milk years ago in my late teens, but by then had already gotten gynecomastia in small but noticeable ways.  I'm not making any correlation to milk for my gyne, but i have noticed how young women are especially blossoming earlier and earlier...and i think further studies should be looked into how all these hormones are filtering down into our childrens health.  My children and I will drink Soy over animal milk until growth hormones and animal steroids are eliminated from the process.

I'm with you on this. I've recently given up milk, and all milk products, due to research on the subject.

But, as is obvious from my posts above.. I'm not a fan of soy either. So, I'm going to try rice or almond milk.

Pizza is my one "splurge item" that I'll have every now and then. Otherwise, I don't eat cheese, yogurt, sour cream, cottage cheese, etc.

I read a statistic that the top milk-producing dairy cows of the 1950's produced about 2,000 gallons of milk per year.
Now, with scientific manipulation through hormones, antibiotics, selective breeding, etc. the average "top producing" dairy cow produces upwards of 50,000 gallons per year.

Something ain't right here, folks. We've tinkered with nature and in so doing are tinkering with our own biochemistry seeing as we are ingesting the results of the tinkering... modified foods.

[Hypo-is-here]

Is it not true that if one were to draw up a pie-graph of all present cases of gynecomastia globally (hypothetically speaking), with all the segments/slices/portions of the pie representing causes (proven or speculative) of gyne, then by far the largest segment (hands-down) would be "IDIOPATHIC" .....?

ie. The vast majority of all gyne cases anywhere, would have no pinpoint-able cause. ( and this bracket would also include those who had a temporary pubertal hormone shift that resulted in gyne which remained permanent thereafter. As those now in their 20s.30s.40s,etc would have no way now of proving that their current gyne was in fact the exact result of said pubertal hormonal shift, these cases could all be deemed idiopathic cases of gyne)

It depends what is deemed/termed to be gynecomastia.  

Many people think they have gynecomastia because of the presence of very little tissue at all.  Such people would not be deemed to have gynecomastia by the medical community but BDD.  

On which note there are quite a few people on the board who have BDD, some who probably have a certain amount of gynecomastia others with straightforward BDD as well as those of us who have or have had straightforward gynecomastia.

When referring to medically defined gynecomastia the best research to date calls into question the previously held notion that the vast majority of cases of gynecomastia are down to pubertal imbalances/idiopathic.  

This research by Glen D Braunstein (endocrinologist) showed that while the majority of cases of gynecomastia are of a pubertal/idiopathic nature, a significant minority are due to underlying causes and side-effects of drugs (prescribed and otherwise).

The above research showed;


29% of all those with gynecomastia have an underlying causative condition and 10-20% of all those with gynecomastia typically have the condition because of drug related side effects (medicated or otherwise) that are responsible for causing the condition.

Here are the relative frequencies of causative conditions for gynecomastia in a typical group of 100 men.


Cirrhosis/Liver problems 8%
Primary Hypogonadism 8%
Testicular Tumor 3%
Secondary Hypogondism 2%
Hyperthyroidism 1%
Renal Disease 1%
Others 6% (this is the title as they are many causes that add up to less than 1% each)  

Total 29%


Given then that 29% of gynecomastia suffers (relative frequencies detailed by Glen D Braustein in his 1993 white paper entitled Gynecomastia) have an underlying causative issue, the need/requirement for pathology/endocrine testing is abundantly obvious.

Such testing reveals a whole host of underlying conditions in a significant minority of sufferers some of which if left undiagnosed can lead to SERIOUS consequences.
The figures presented were corroboarated by ismail and Baths 2002 white paper “The Endocrinology of Gynecomastia”.

Pathology/endocrine testing should be routine in ALL instances of gynecomastia in order to confirm/rule out various aetiologies/underlying causes of the condition.

It is standard good practice for a full hormonal evaluation of ALL patients with gynecomastia.


Sorry for hijacking the Herring  

[tonysoprano]

It depends what is deemed/termed to be gynecomastia.  

Many people think they have gynecomastia because of the presence of very little tissue at all.  Such people would not be deemed to have gynecomastia by the medical community but BDD.  

On which note there are quite a few people on the board who have BDD, some who probably have a certain amount of gynecomastia others with straightforward BDD as well as those of us who have or have had straightforward gynecomastia.

When referring to medically defined gynecomastia the best research to date calls into question the previously held notion that the vast majority of cases of gynecomastia are down to pubertal imbalances/idiopathic.  

This research by Glen D Braunstein (endocrinologist) showed that while the majority of cases of gynecomastia are of a pubertal/idiopathic nature, a significant minority are due to underlying causes and side-effects of drugs (prescribed and otherwise).

The above research showed;


29% of all those with gynecomastia have an underlying causative condition and 10-20% of all those with gynecomastia typically have the condition because of drug related side effects (medicated or otherwise) that are responsible for causing the condition.

Here are the relative frequencies of causative conditions for gynecomastia in a typical group of 100 men.


Cirrhosis/Liver problems 8%
Primary Hypogonadism 8%
Testicular Tumor 3%
Secondary Hypogondism 2%
Hyperthyroidism 1%
Renal Disease 1%
Others 6% (this is the title as they are many causes that add up to less than 1% each)  

Total 29%


Given then that 29% of gynecomastia suffers (relative frequencies detailed by Glen D Braustein in his 1993 white paper entitled Gynecomastia) have an underlying causative issue, the need/requirement for pathology/endocrine testing is abundantly obvious.

Such testing reveals a whole host of underlying conditions in a significant minority of sufferers some of which if left undiagnosed can lead to SERIOUS consequences.
The figures presented were corroboarated by ismail and Baths 2002 white paper “The Endocrinology of Gynecomastia”.

Pathology/endocrine testing should be routine in ALL instances of gynecomastia in order to confirm/rule out various aetiologies/underlying causes of the condition.

It is standard good practice for a full hormonal evaluation of ALL patients with gynecomastia.


Sorry for hijacking the Herring  

thanks for the clarification.

what is the difference between primary and secondary hypogonadism?

and where would one (a layman in Australia) be ABLE To view ismail and Baths 2002 white paper “The Endocrinology of Gynecomastia”? if possible?

[tonysoprano]

Human's are like the only mammal to keep drinking milk into adulthood, and we don't even drink our own species milk...we drink highly modified animal milk.  I gave up milk years ago in my late teens, but by then had already gotten gynecomastia in small but noticeable ways.  I'm not making any correlation to milk for my gyne, but i have noticed how young women are especially blossoming earlier and earlier...and i think further studies should be looked into how all these hormones are filtering down into our childrens health.  My children and I will drink Soy over animal milk until growth hormones and animal steroids are eliminated from the process.

Im not disputing or discrediting anything you are saying.
If anything I generally lean towards your school of thought.
But... one has to wonder , as I estimate well over 90% of men/women/children in the west (north america,uk,europe,aus) it seems would be drinking cows milk and associated by-products (most likely daily too), yet the very vast majority of all these people would be of average/normal health status and the majority of the males would NOT have any form of gyne.

Just makes you wonder. I also think that there is something inherently sinister in the dairy industry and in the nature of the scenario you have outlined ( though most people wouldnt think twice about it), but the fact remains that I barely know anyone who doesnt drink milk or eat dairy basically daily, yet I know very few males that do have gynecomastia.

[tonysoprano]

bump^

[Hypo-is-here]

thanks for the clarification.

what is the difference between primary and secondary hypogonadism?

and where would one (a layman in Australia) be ABLE To view ismail and Baths 2002 white paper “The Endocrinology of Gynecomastia”? if possible?

On a very basic level;

Primary hypogonadism is a failure of the testicles to produce testosterone despite there being adequate instruction to do so by the pituitary (one such genetic example is Klinefelters Syndrome).

Conversely;

Secondary hypogonadism is a failure of the pituitary to adequately send enough instruction to the testicles in order for them to produce testosterone.

But it is far less simple than that in reality.  Deficiency of both types can occur both pre and post puberty; it can occur because of genetic factors, illness, trauma, the result of treatments such as chemotherapy/radiotherapy, age related delecine or be idiopathic (of unknown origin).

If deficiency occurs pre-puberty then skeletal formation is greatly affected as are the size of the testes and the penis (if TRT is not instigated at the time of puberty).

If secondary hypogonadism occurs pre puberty this often results in a failure of the testes to mature and this itself means that the testes cannot function (as demonstrated in Kallmans Syndrome) even if the correct function from the pituitary is restored.  This is  something that is radically different in secondary hypogonadism post puberty where testicles can and will return to a functional level if the pituitary stimulus is restored.

There is then the situation that relates to metabolic hypogonadism of varying types.  This can occur when androgen to testosterone ratios are poor and elevated estradiol suppresses the hypothalamus/pituitary from correctly functioning.  This can also occur due to high SHBG either singularly or in conjunction with high estradiol.

Many men have combinations of problems such as a failure of the testicles and pituitary, otherwise known as central hypogonadism, or metabolic hypogondism coupled with partial testicular failure.

Then you have dihydrotestosterone deficiency otherwise known as alpha 5 reductase deficiency and various testosterone insensitivity syndromes which are part of the genetic/chromomal conditions that I barely mentioned.

On the illness front many conditions cause temporary and permant problems at either the pituitary, testicular or metabolic level.  Most obvious of all are pituitary tumors such as prolactinomas, testicular and breast cancer, hemochromatosis (iron overload), autoimmune syndromes, Mumps, sleep apnea.

The above is not exhaustative information- just what I wrote as it came to mind from my laymans knowledge.


Ismail and Barth’s white paper was in pdf format on the internet but has since been removed as all old links are broken.  This is unfortunate to say the least as it was and still is the most authoritative  article on the subject to date.  If anyone knows how to locate the said paper and can do so for the benefit of members of the site I am sure we would all be grateful.

I do have a hardcopy of Glen D Braunsteins original white paper from which the statistics that Ismail and Barths paper originate (thanks to the New England Journal of Medicine) and am willing to photocopy and send it to those that wish to view it.