@hardasnails1973 591 wrote:

Every since I have been having problems with estrogens related symptoms such as gyno and BPH, labs showed that there were never imbalances within the estrodial.

I know that BPH is mainly due to high e2 in the lab work, but upon further investigation I have seen several males with BPH that had perfect e2 and also DHT levels.

In clinical setting I was seeing a trend and could not identify why. When running the estrogen metabolism test there seem to be a good level of e2 in the urine, but there was a high incident of low ratio of 2/16,4 ohe. It was amazing that a lot of these people also has some kind of thyroid and adrenal imbalances which made it more interesting. They where also complaining of estrogen like symptoms like my self such as having gyno and ED when all their hormones where in balance.

When I first got tested my 2/16 ratio was .50 which was extremely low. When I started DIM and iodoral my levels started to normalized as well did my symptoms.

After clearing of symptoms I did not know where to go from there. Should I have continue the current dosage or go back to maintaince dosage.

I called Dr Zeligs and he told me just to stop DIM and let the system rebalance it self.

In order to get my levels to be some what normal it took me 50 mgs of iodoral and 6-8 pills of time for over 3 months to just reach the healthy level of past 2. This tells me that genetically I could have an imbalance in specific cyp 450 enzyme system for proper detoxification of estrogen metabolites. I even tested deficient in the methyl metabolites as well no matter how much sam-e, b-12, folinic acid.

What the advantages of iodoral over dim? I had to take both of them combined in order to get any clinical response.

As more research comes about I believe that people with BPH are going to have this abnormal 2/16 ratio which is going to go treated by unnecessary drugs when the root cause may be a genetic defect triggered by hormonal imbalances.

It will be curious to see if I also have a defect in the COMT as this would indicate a build up in catecholamines in the blood and low in the urine. If there is a defect then how can one circumvent this? COMT is sam-e driven which could explain my past issues with methylation with defects in MS and also MTHFRR. Witha defect in MTHFRR this could also cause a problem in iodine up take as well which may be affecting my estrogen metabolites (just a thought) .

I have read that several articles that back up the fact that lithium in the hair is a valid test. My lithium levels have been

Since I have a problem up taking folate and b-12 into the cell this may be due to the fact that lithium may be an an important factor in b-12 and folate transport mechanism.

GYNECOMASTIA:

Gynecomastia is an enlargement of the male breast resulting from the growth of the glandular component of the breast. There has to be a palpable firm mass extending away from the nipple. Pseudogynecomastia is the deposition of fat in the breast without an increase in the glandular component.

Gynecomastia is not nipple sensitivity. Gynecomastia is not a hardening of the nipples. The nipples have erectile tissue which can become hard and painful when stimulated – similar to priapism – a painful, hard erection of the penis. Again, in gynecomastia, there is a mass that extends away from and surrounds the nipple. On exam, when one palpates the breast with thumb and forefinger, the fingers are stopped by this ridge of tissue enlargement before even touching the nipples.

Nipple sensitivity or pain or hardness is NOT gynecomastia. From my perspective, testosterone/DHT has more to do with this than estrogen but both interact to have this happen. Some men have better developed nipple tissue than others. Thus this phenomenon may be more prominent in them.

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BENIGN PROSTATIC HYPERTROPHY:

Prostatic growth can occur from the stimulation of DHT (Dihydrotestosterone) and Estrogen. Even with “perfect levels” of these signals/hormones, men can still have prostatic growth depending on the tissue’s sensitivity to these signals/hormones.

Notably, 5-Alpha Reductase inhibitors such as Finesteride, which block DHT production from testosterone (shunting testosterone metabolism toward estrogens) are the primary treatment for BPH. They don’t work all the time to shrink the prostate (perhaps because of the increase in estrogens).

Testosterone, itself, may shrink the prostate, particularly when in high ratio to DHT since testosterone binds to androgen receptors, blocking them from binding DHT.

BPH is not sensitivity in the prostate area. It is actual growth of the prostate, which would be verifiable via rectal exam.

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DIM AND 2-HYDROXY / 16-HYDROXY ESTROGEN METABOLITE RATIO, 4-HYDROXY METABOLITES:

DIM apparently induces enzymes primary to the 2-Hydroxy estrogen pathways, helping shunt estrogen metabolism away from the 16-hydroxy and 4-hydroxy metabolites. I would wonder about its effects on the 4-hydroxymetabolites, however. That isn’t clear to me.

The 16-hydroxy and 4-hydroxy metabolites are estrogens that stimulate growth – more so than the 2-hydroxy metabolites – and are thus considered more of a risk for the development of breast cancer than the 2-hydroxy metabolites.

Interestingly, a build-up of 2-hydroxy metabolites of estrogens would compete with catecholamines for processing via the COMT (Catechol-O-methyl transferase) enzyme. This potentially could increase catecholamine levels.

Stress indicates an increase in norepinephrine, a catecholamine. This would then compete with the 2-hydroxy and 4-hydroxy estrogen metabolites for COMT, thus increasing 4-hydroxy and 2-hydroxy estrogens compared to the 16-hydroxy estrogens (which are processed instead by 15-beta-hydroxy steroid dehydrogenase ).

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IRON

A lot of the enzymes that process testosterone and other androgens to create the estrogens require the presence of adequate iron. Depending on which of the numerous cytochrome enzymes is altered in production, this may alter which of the estrogen metaboltes that are created.

Thus, a person with low ferritin does not have a stable picture of where estrogen is going to go until adequate iron stores are present.

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IODINE:

Iodine, Iodoral, affect multiple other signals, not just estrogens. Thus if improvement occurs, I would wonder about the effects on the other systems – thyroid, adrenals, etc. For example, improvement in adrenal function occurs with optimal iodine intake, as stated to me by Jonathan Wright MD, as an additional rationale for taking Iodoral.