High-Sugar Diet = Less SHBG

Pharma
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Not sure I’d recommend this dietary approach, but apparently conversion of sugar (and carbs in general to some extent) to fatty acids in the liver reduces the output of SHBG by the liver. I’ll probably check the original study to see what the exact changes are, but I’d imagine it wouldn’t be worth it.

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

ScienceDaily (Nov. 21, 2007) �?? Eating too much fructose and glucose can turn off the gene that regulates the levels of active testosterone and estrogen in the body, shows a new study in mice and human cell cultures that�??s published this month in the Journal of Clinical Investigation. This discovery reinforces public health advice to eat complex carbohydrates and avoid sugar. Table sugar is made of glucose and fructose, while fructose is also commonly used in sweetened beverages, syrups, and low-fat food products. Estimates suggest North Americans consume 33 kg of refined sugar and an additional 20 kg of high fructose corn syrup per person per year.

Glucose and fructose are metabolized in the liver. When there�??s too much sugar in the diet, the liver converts it to lipid. Using a mouse model and human liver cell cultures, the scientists discovered that the increased production of lipid shut down a gene called SHBG (sex hormone binding globulin), reducing the amount of SHBG protein in the blood. SHBG protein plays a key role in controlling the amount of testosterone and estrogen that�??s available throughout the body. If there�??s less SHBG protein, then more testosterone and estrogen will be released throughout the body, which is associated with an increased risk of acne, infertility, polycystic ovaries, and uterine cancer in overweight women. Abnormal amounts of SHBG also disturb the delicate balance between estrogen and testosterone, which is associated with the development of cardiovascular disease, especially in women.

�??We discovered that low levels of SHBG in a person�??s blood means the liver�??s metabolic state is out of whack �?? because of inappropriate diet or something that�??s inherently wrong with the liver �?? long before there are any disease symptoms,�?? says Dr. Geoffrey Hammond, the study�??s principal investigator, scientific director of the Child & Family Research Institute in Vancouver, Canada, and professor in the Department of Obstetrics & Gynecology at the University of British Columbia.

�??With this new understanding, we can now use SHBG as a biomarker for monitoring liver function well before symptoms arise,�?? says Dr Hammond, who is a Tier 1 Canada Research Chair in Reproductive Health. �??We can also use it for determining the effectiveness of dietary interventions and drugs aimed at improving the liver�??s metabolic state.�??

Physicians have traditionally measured SHBG in the blood to determine a patient�??s amount of free testosterone, which is key information for diagnosing hormonal disorders. In addition, SHBG levels are used to indicate an individual�??s risk for developing type 2 diabetes and cardiovascular disease.

The discovery dispels the earlier assumption that too much insulin reduces SHBG, a view which arose from the observation that overweight, pre-diabetic individuals have high levels of insulin and low levels of SHBG. This new study proves that insulin is not to blame and that it�??s actually the liver�??s metabolism of sugar that counts.

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Do you have the URL to this?

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Better than eating all that sugar. :wink:

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I always thought insulin lowered SHBG, but mayber this is the mechnism and the insulin is just there. Makes sense that when there is high insulin there will be high glucose,probably too much being converted to fat for storage. I said it before, but could this be why metformin raises SHBG? Oops, I re-read and noticed the last paragraph says what I concluded.

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Fortunately, contrary to what is often said (never with proof, which is why it’s possible for it to be wrong) change in SHBG just does not have the effects stated in the article, which is just hideously wrong on this particular claim:

“If there’s less SHBG protein, then more testosterone and estrogen will be released throughout the body,”

Simply not true. SHBG is a carrier and depot not a generator or producer, let alone a situation in which having less produces more, as the article tries to say.

Some authors have imagined, but without considering the details, that reduction in amount of SHBG would release testosterone as that is happening and that would be significant. However the problem with that theory is that the amount of testosterone actually bound to SHBG is less than a milligram, and so even an instanteous release of all of it would not be at all substantial in effect, and on top of this it would be a one-shot deal rather than an ongoing source.

I can’t even imagine how the author of this article, or really person trying to supply a summary of others’ work – interesting on its main point and I don’t doubt that part of it – got it so far off as to imagine that less SHBG resulted in more effect of testosterone. Actually it helps enable transport of testosterone and has some androgenic biological properties of its own.

Pointing out a problem with the article doesn’t mean not thinking it was a good post or that the main point is off. Great post and interesting main point, just that the author was more than fuzzy on trying to interpret the meaning. That is a problem with the “popular science” magazines: the articles are written by editors who usually are not expert in the given field but are trying to restate things for people, sometimes not correctly.

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Good points Bill. Perhaps the author was simplifying the fact that less SHBG would mean an increase in free testosterone. These summary articles are somewhat dumbed down for the lay population, so I’m sure there was some info lost in translation. I do agree that it can misconstrue the truth.

The large majority of testosterone is bound to SHBG, and a significant portion to albumin as well. So I’d imagine that a significant drop in SHBG, and eventually bound T, would result in a significant anabolic/androgenic effect, albeit until the body restored homeostasis. SHBG is a weird subject and it seems it’s interaction and manipulation seem almost futile in terms of increasing the androgenic/anabolic capacity of what T we do have in our bodies. It seems as though SHBG itself, or many other pathways, balance out our hormonal interactions quite efficiently. I’ve always meant to look into it further, as I see a lot of potential there for increasing the efficacy of small androgen doses, but I just never got around to putting the time in.

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I’d also like to note that your posts are always a welcome addition to this board.