The Myth Of Low SHBG And High Free T (1 Viewer)

[bluefish]

What supplements do you take?

Ah...
5000 D3
Am/pm packs of jigsaw brand supps
(Seems like it’s fair decent at hitting all the general nutrients)
Creatine
Ginkgo biloba
Ciltep
(Just started using gonadin)

 

[Aleeri]

Right... The best way to deal with this is determining why it’s high and adjusting... I’m pretty sure I’m getting enough saturated fats... all the other factors I’m not totally clear on. I can begin to look into each one of those.
I should mention I’ve been doing a ‘slow-carb’ diet ... which, based on Aleeri’s comments on lowering his SHBG... perhaps is part of why mine is as high as it is.

If you include more fructose I am sure it will bring it down, it did on my labs.

Is it the correct way to do it? I don't know, but there is very few things I have found that actually affects SHBG, sugar and tongkat ali seems to be safe bets.

Too Much Sugar Turns Off Gene That Controls Effects Of Sex Steroids

 

[jet9]

If you include more fructose I am sure it will bring it down, it did on my labs.

Is it the correct way to do it? I don't know, but there is very few things I have found that actually affects SHBG, sugar and tongkat ali seems to be safe bets.

Too Much Sugar Turns Off Gene That Controls Effects Of Sex Steroids

Just to clarify you mean that more fructose brought SHBG down on your labs? Correct? What was effect of free T, and in what form was fructose? What fruits/foods?

 

[Aleeri]

Just to clarify you mean that more fructose brought SHBG down on your labs? Correct? What was effect of free T, and in what form was fructose? What fruits/foods?

Yes SHBG down which in turn brought free T up a lot for me.

I used mostly fruit and milk sugars. Tropical fruits and low-fat milk, sometimes sugar/honey added to the milk. I went from low sugar consumption to 200-300g daily. The interesting thing is that it had a very low impact on my blood sugar and triglycerides. I saw zero negative impact, my labs were the best I ever tested.

So after that experiment, I concluded that Peat is right about everything concerning sugar and I now feel comfortable consuming it daily.

 

[baccheion]

Yes SHBG down which in turn brought free T up a lot for me.

I used mostly fruit and milk sugars. Tropical fruits and low-fat milk, sometimes sugar/honey added to the milk. I went from low sugar consumption to 200-300g daily. The interesting thing is that it had a very low impact on my blood sugar and triglycerides. I saw zero negative impact, my labs were the best I ever tested.

So after that experiment, I concluded that Peat is right about everything concerning sugar and I now feel comfortable consuming it daily.

What about AGE?

 

[bluefish]

If you include more fructose I am sure it will bring it down, it did on my labs.

Is it the correct way to do it? I don't know, but there is very few things I have found that actually affects SHBG, sugar and tongkat ali seems to be safe bets.

Too Much Sugar Turns Off Gene That Controls Effects Of Sex Steroids

Can you say where you get your tongkat Ali from? I hear it’s often times hard to find good quality.

 

[Aleeri]

Can you say where you get your tongkat Ali from? I hear it’s often times hard to find good quality.

I source it myself, I run a supplement company and we got some samples I've been using. I think the 200:1 extracts are a waste of time and money. Look for the yellow/orange water extracts, usually labelled 50:1 or 100:1.

One of our competitors Lost Empire Herbs has a good Tongkat Ali extract product. I've tracked it down to a supplier in Malaysia that I've been in touch with and confirm it's the same extract. I've been using this one the most myself, good value for money.

Right now I have a few samples for analysis from Vitajoy in China as well as the strongest one on the market from Javaplant in Indonesia. We'll be testing the levels of active ingredients to pick which supplier we will be using. I can posts results here later if you guys are interested.

 

[Aleeri]

What about AGE?

Are you referring to advanced glycation end-products or my age? haha

Concerning advanced glycation end-products:

Animal-derived foods that are high in fat and protein are generally AGE-rich and are prone to further AGE formation during cooking.[3] However, only low molecular weight AGEs are absorbed through diet, and vegetarians have been found to have higher concentrations of overall AGEs compared to non-vegetarians."

I think if you cook your food properly, as in no frying in anything except stable oils (saturated) and don't burn anything, it's not a problem with sugar.

 

[baccheion]

Are you referring to advanced glycation end-products or my age? haha

Concerning advanced glycation end-products:

Animal-derived foods that are high in fat and protein are generally AGE-rich and are prone to further AGE formation during cooking.[3] However, only low molecular weight AGEs are absorbed through diet, and vegetarians have been found to have higher concentrations of overall AGEs compared to non-vegetarians."

I think if you cook your food properly, as in no frying in anything except stable oils (saturated) and don't burn anything, it's not a problem with sugar.

Isn't sugar prone to forming AGE in the body? Binding to collagen?

 

[Aleeri]

Isn't sugar prone to forming AGE in the body? Binding to collagen?

It makes little sense to me. I feel it is too reductionist to think this way.

First, I think it is important to compare your blood sugar levels on a diet high in sugar vs a diet high in starch vs a diet low in carbs and then judge what potential effects it might have.

If I have normal blood sugar levels on a diet high in sugar as well as normal levels on a diet low in sugar, what does it tell me? Probably that it makes no real difference for my unique body. There is likely an ideal level for all of us that is strictly individual.

Remember that many things are converted into simple sugars such as glucose in the body, for example protein. The body uses simple sugars for fuel, that's a fact.

If you take the stance that all sugar is bad then you are basically restricting yourself to living of fat, aka ketosis and I think that is far from ideal if at all possible.

I also think consuming your sugar in the form of refined sugar consistently is bad, short term it is ok but you're deriving yourself of nutrients if that is your only source.

The ideal would be sugars from whole foods such as fruits or milk that also contains antioxidants and other phytochemicals that seems to balance things such as AGEs.

My only real concern is like I said cooking methods such as frying and overprocessed animal foods that seems to increase AGE levels beyond what is naturally there.

Here are some links that I think add to this well:

Fructose, Glycation and AGE formation
Citrus fruit extracts reduce advanced glycation end products (AGEs)- and H₂O₂-induced oxidative stress in human adipocytes. - PubMed - NCBI
Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet
Advanced Glycation End Products (AGEs): A Complete Overview

 

[baccheion]

It makes little sense to me. I feel it is too reductionist to think this way.

First, I think it is important to compare your blood sugar levels on a diet high in sugar vs a diet high in starch vs a diet low in carbs and then judge what potential effects it might have.

If I have normal blood sugar levels on a diet high in sugar as well as normal levels on a diet low in sugar, what does it tell me? Probably that it makes no real difference for my unique body. There is likely an ideal level for all of us that is strictly individual.

Remember that many things are converted into simple sugars such as glucose in the body, for example protein. The body uses simple sugars for fuel, that's a fact.

If you take the stance that all sugar is bad then you are basically restricting yourself to living of fat, aka ketosis and I think that is far from ideal if at all possible.

I also think consuming your sugar in the form of refined sugar consistently is bad, short term it is ok but you're deriving yourself of nutrients if that is your only source.

The ideal would be sugars from whole foods such as fruits or milk that also contains antioxidants and other phytochemicals that seems to balance things such as AGEs.

My only real concern is like I said cooking methods such as frying and overprocessed animal foods that seems to increase AGE levels beyond what is naturally there.

Here are some links that I think add to this well:

Fructose, Glycation and AGE formation
Citrus fruit extracts reduce advanced glycation end products (AGEs)- and H₂O₂-induced oxidative stress in human adipocytes. - PubMed - NCBI
Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet
Advanced Glycation End Products (AGEs): A Complete Overview

I'm not saying sugar is bad, but it certainly seems easy for it to end up down that path. I was more wondering about some of the negative effects associated with consumption. Would calcium also be required to buffer against bone loss to keep serum alkaline?

 

[bluefish]

I source it myself, I run a supplement company and we got some samples I've been using. I think the 200:1 extracts are a waste of time and money. Look for the yellow/orange water extracts, usually labelled 50:1 or 100:1.

One of our competitors Lost Empire Herbs has a good Tongkat Ali extract product. I've tracked it down to a supplier in Malaysia that I've been in touch with and confirm it's the same extract. I've been using this one the most myself, good value for money.

Right now I have a few samples for analysis from Vitajoy in China as well as the strongest one on the market from Javaplant in Indonesia. We'll be testing the levels of active ingredients to pick which supplier we will be using. I can posts results here later if you guys are interested.

I’d love to hear more. Please let me know what comes of it. And thanks for the info.

 

[Sulcuscentralis]

Damn, I just realized, this low SHBG could be why estrogen works against hairloss in men coz estrogens induce SHBG. You see, Dht and estradiol have the same action when binded to SHBG which has a receptor also in hair follicles. Then it is plausible that the DHT found in balding scalp is not being bound in the case of having low SHBG and so E2 and DHT end up doing uncontrolled inhibition and damage then. hehe

Lets check for studies in balding men with low SHBG

...and here we have:
Hormonal Profile in Indian Men with Premature Androgenetic Alopecia
Decreased levels of SHBG with high free androgen index were found in cases when compared with the controls.

[edit]more relevant stuff Update Low Sex Hormone Binding Globulin a Marker for MPB

I have almost twice the norm SHBG and MPB with upper range total T and low free T, normal estradiol.

 

[Vanset]

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[Vanset]

Associations of Sex-Hormone-Binding Globulin (SHBG) with Non-SHBG-Bound Levels of Testosterone and Estradiol in Independently Living Men

Abstract. Results of in vitro experiments indicate that with increasing concentrations of SHBG, testosterone (T) is preferentially bound to SHBG in compari

academic.oup.com

Abstract:
Results of in vitro experiments indicate that with increasing concentrations of SHBG, testosterone (T) is preferentially bound to SHBG in comparison with estradiol (E2). In these studies, the ratio of non-SHBG-bound E2 (non-SHBG-E2) to non-SHBG-T increased with increasing levels of SHBG. SHBG has consequently been regarded as an estrogen amplifier. In this cross-sectional study in 399 men aged between 40 and 80 yr we tested whether higher levels of SHBG are associated with a higher estrogen/androgen ratio in vivo. The mean T level of these men was in the eugonadal range [536 ± 152 ng/dl (18.6 ± 5.26 nmol/liter), mean ± SD]. With increasing SHBG levels the non-SHBG-bound fraction of T decreased from 80 to 36% and that of E2 from 89 to 53%. Higher levels of SHBG were associated with higher levels of both total T [regression coefficient (β) after adjustment for age and body mass index, 286 ± 15.8; P < 0.001] and total E2 (β = 4.47 ± 0.90; P < 0.001). However, SHBG levels were negatively related with levels of non-SHBG-E2 (β = −1.78 ± 0.69; P < 0.001), whereas there was a positive association between levels of SHBG and non-SHBG-T (β = 32.0 ± 9.78; P = 0.001). Furthermore, we observed a negative relationship between SHBG levels and the E2/T ratio of either total (β = −0.016 ± 0.002; P < 0.001) or non-SHBG-bound (β = −0.011 ± 0.002; P < 0.001) hormone. Therefore, we conclude that in eugonadal men, higher SHBG levels are associated with lower levels of non-SHBG-E2 but slightly higher levels of non-SHBG-T. This means that SHBG cannot be regarded as an estrogen amplifier in eugonadal men.

 

[Vanset]

The higher the SHBG the better the t/e2 ratio and non-shbg t/non-shbg e2 ratio.

 

[Vanset]

In this study, the relationship between SHBG levels and the E2/T ratio was studied in eugonadal healthy men. The concept of SHBG as an estrogen amplifier (6) is based on the observation that with stable T and E2 levels, an increase of SHBG will decrease unbound T more than unbound E2, resulting in an increase of the non-SHBG-E2/non-SHBG-T ratio. However, in eugonadal men, this theory does not apply because the hypothalamo-pituitary-gonadal (HPG) axis will respond to a decreasing level of non-SHBG-T with an increase in LH and T, assuming that non-SHBG-T is driving the feedback inhibition of the male HPG axis. The validity of this hypothesis is supported by our observation that increased levels of SHBG are associated with increased levels of total T but are barely associated with the level of non-SHBG-T.

Levels of SHBG show only a modest positive association with total levels of E2 but are negatively related with those of non-SHBG-E2. As a result, a high concentration of SHBG is associated with a lower (non-SHBG-bound) estrogen/androgen ratio and vice versa. Endogenous E2 can also have an effect on LH release by the pituitary (20, 21). However, in contrast to T, E2 levels are not directly regulated by HPG axis activity. When bioavailable E2 levels decrease, this might lead to increased LH release by the pituitary with a resulting increase in testicular T production. Total E2 levels will be increased only if T is subsequently aromatized, the extent of which is influenced by parameters such as age and BMI. The regulation of peripheral E2 levels by the HPG axis is indirect and therefore probably not as tight compared with T levels.

The fact that an intact HPG axis appears to prevent the non-SHBG-T concentration to fall with increasing SHBG levels makes the in vivo situation in eugonadal men totally different from the in vitro situation where changes in hormone binding to SHBG do not evoke adaptations in the HPG axis. This lack of similarity between in vivo and in vitro conditions was already alluded to by Rosner (22) but, to our knowledge, was never formally tested.

Our findings in healthy men seem to conflict with conditions associated with high SHBG levels in men such as advanced age, liver disease, hyperthyroidism, and estrogen administration (22). These conditions are associated with increased estrogen/androgen ratios and gynecomastia (23, 24), and they seem to confirm the concept of SHBG as an estrogen amplifier. However, besides the altered SHBG levels, these conditions are also associated with altered gonadal function. Hypogonadism is frequently observed in liver cirrhosis patients (25, 26). In hyperthyroid men, lower levels of non-SHBG-T are frequently (7–9) but not always (27, 28) reported, which suggests that the HPG axis in these men is not always able to fully compensate for the rise in SHBG concentration. Moreover, the increased estrogen/androgen ratio in hyperthyroid subjects might be caused by increased androgen aromatization (10, 29). The age-associated increase in SHBG is not associated with an increase in T levels (30), which suggests that the HPG axis of older men is not capable of responding to a fall in T levels. Therefore, it is likely that the relative hypogonadism and not the increased SHBG per se may explain the high estrogen/androgen ratio in these men.

The question of the clinical relevance of our observation arises. In the pathogenesis of gynecomastia, a high estrogen/androgen balance seems to be of importance (23, 24). According to our results, men with low levels of SHBG and a resulting high estrogen/androgen ratio would have a higher risk of developing gynecomastia, although this association has not been reported in the literature. Probably the changes in the estrogen/androgen ratio brought about by SHBG in eugonadal men are too subtle to cause gynecomastia.

Our results show that high levels of SHBG are associated with lower levels of non-SHBG-E2 but normal or even slightly higher levels of non-SHBG-T. The decreased feedback inhibition of non-SHBG-E2 on the release of LH by the pituitary probably explains the slightly positive relationship between levels of non-SHBG-T and SHBG.

It is well known that lower levels of non-SHBG-E2 in men are associated with lower bone mineral density (31, 32). Apparently, even in eugonadal men, elevated SHBG levels might contribute to estrogen deficiency and to conditions such as osteoporosis.

One might speculate that while passing through capillaries, a proportion of the bound hormone dissociates from SHBG and in fact becomes bioavailable. In that case, the amount of bioavailable hormone might be underestimated when using the described equations for the calculation of the bioavailable fractions. Consequently, the amount of bioavailable E2 would be underestimated more in comparison with the amount of bioavailable T because of the weaker binding of E2 to SHBG. However, the validity of this hypothesis remains to be determined.

For the calculation of the levels of non-SHBG-E2 and non-SHBG-T we used the equations as described by Sodergard et al. (Table 1) (17) in which the association constants for the binding of T (kt) and E2 (ke) to SHBG are 5.97 × 108 and 3.14 × 108, respectively. In the literature, alternative estimates for these binding affinities are reported (2, 6, 18). Use of a higher association constant in the equation will tilt the slope of the regression lines shown in Figs. 2 and 33 (right panels) slightly down and vice versa. Theoretically, combining a high kt with a low ke in the equations of Table 1 can result in a positive relation between SHBG and the non-SHBG-E2/non-SHBG-T ratio. However, when the combination of values as reported by Dunn et al. (2) and Burke and Anderson (6) were used, this was not the case.

Although the subjects we studied were prone to health selection bias, this does not undermine the conclusions of this study. In fact, it contributed to the uniformity of the analyses because there were only a few hypogonadal subjects (based on T and non-SHBG-T levels) in this group of men. On the other hand, it prevented us from doing separate analyses on data from eugonadal and hypogonadal men.

The conclusion of our study is that in eugonadal men, higher SHBG levels are associated with lower levels of non-SHBG-E2 but unaltered or even slightly higher levels of non-SHBG-T. This means that SHBG cannot be regarded as an estrogen amplifier in eugonadal men.