Men who lower their prolactin receive these sexual benefits

Men who lower their prolactin receive these sexual benefits

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Most men don’t realize how badly prolactin is damaging their manliness. Even if these men have high testosterone – they can’t perform because of prolactin!

—-Important Message—-

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——

Men who lower their prolactin receive these sexual benefits…

Prolactin is generally considered to be a female hormone.

As the name indicates, it was named after its ability to increase milk production.

At least, that was the first of its effects that science discovered.

Although the name is appropriate, it is also misleading… The name itself promotes a rather narrow view of prolactin.

That’s because the name obscures other important functions of prolactin…

Prolactin works on many other cell types as well.

Scientists have found receptors for prolactin nearly everywhere in the body that they look for them.

“Prolactin receptors are also present in a wide range of peripheral organs like the pituitary gland, heart, lung, thymus, spleen, liver, pancreas, kidney, adrenal gland, uterus, skeletal muscle, and skin.”

That’s a lot of places.

Prolactin normally spikes under the influence of estrogen during pregnancy – for milk production.

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But men make prolactin too.

We produce prolactin primarily in the pituitary gland, where its release is actually inhibited.

Early studies showed a massive increase in prolactin synthesis in the pituitary upon removal.

With further experimentation, scientists finally discovered the inhibiting factor.

“The impulse to secrete prolactin spontaneously is held firmly in check by the action of hypothalamic prolactin inhibiting factor(s) reaching the pituitary… In brief, spontaneous prolactin secretion is inhibited by dopamine acting in small amounts…”

So why is inhibiting prolactin important?

You might think that men – because they never produce milk – wouldn’t have a need for it anyway.

Well, they don’t. Not really.

But men produce prolactin (in lesser amounts) for other reasons.

It is very similar to growth hormone, which is produced nearby by in the pituitary.

Scientists think that prolactin and growth hormone used to be encoded by the same gene – but that prolactin split off during evolution for a more specialized function.

“The divergence of the prolactin and growth hormone lineages occurred  about 400 million years ago.”

First and foremost, prolactin regulates the calcium balance inside cells.

Actually, it powerfully disturbs calcium balance.

The growth-stimulating properties are mostly just the result of this effect.

Generally, prolactin levels increase with age, and it is a bit higher in females…

Prolactin is actually what best explains osteoporosis.

Even teenagers with high prolactin are constantly found to have both low bone density and man boobs.

“…and gynecomastia in eight males (Table 1)…”

(Gynecomastia = man boobs)

A group of Italian researchers found these two effects in one same.

Bone loss is a common finding. And people talk about it a lot.

For this reason, the researchers decided to test 20 of their male patients who had high prolactin.

They used X-rays to measure their bone density.

They found decreased bone density levels in the high-prolactin participants.

A score of −2.4 might not sound too bad, but it actually is…

Because a score of −2.5 indicates osteoporosis.

“Patients were considered osteopenic when T score was −1/−2·5 and were considered osteoporotic when T score was lower than −2·5.”

And to lower prolactin levels in the patients, they reached for a logical solution.

They gave them a pro-dopamine drug: bromocriptine.

Before-and-after bone scans revealed a considerable improvement… Bone density increased after inhibiting prolactin…

They even checked other blood parameters such as growth hormone – just to make sure nothing else was changing to cause this effect.

And the only change was the amount of prolactin… Getting rid of prolactin improved bone density.

And pro-dopamine drugs can lower prolactin.

These stopped accelerated bone turnover and increased mineralization by inhibiting prolactin.

The statistics they applied showed a good correlation between high prolactin, low bone density, and high crosslinked collagen remnants – all of these are markers for bone turnover (that’s a good thing).

To be clear: The higher the original prolactin levels were, the lower the bone density measurements were.

The researchers also found a negative correlation with osteocalcin…

Osteocalcin is a protein that binds to the bone matrix, binds calcium, and initiates bone mineralization.

To be clear (again), when we’re talking about bone health, osteocalcin is on the good side.

So, a pro-dopamine drug reversed all negative trends.

Bone density increased, as did osteocalcin.

This demonstrates the degree of control dopamine has over prolactin release.

And scientists now understand in better detail how prolactin affects calcium on the cellular level.

Bruno Sorin and friends worked all of this out in a series of experiments started around the year 2000.

The 2002 study was the most spectacular. And it confirmed previous findings.

They used human cells in this study. And they found a way to image calcium so they could both see and measure changes inside the cell in real time.

They used the indicator Indol-1. This is a fluorescent molecule that strongly binds calcium.

It actually changes color when it does this.

And they found that small amounts of prolactin, in the nanomolar range, greatly increased the calcium content of the cell.

The concentrations that could do this were tiny, and well within the range found in people.

More prolactin always caused more calcium to enter the cell – there was no cut-off point.

As one of the larger peptide hormones, prolactin is too big to enter the cell.

It binds to a receptor on the outer membrane where it initiates a sharp influx in calcium.

The fluorescent microscope that the researchers used, with an in-line high-speed camera, recorded this event.

They have frames every 40 milliseconds.

The hotter colors indicate more calcium, where the Indol-1 molecule is changing its fluorescence by binding calcium.

You can see the calcium wave flowing through the cell.

This increased cellular calcium is taken from the blood.

This isn’t good – and it causes the parathyroid gland to release the parathyroid hormone.

Parathyroid hormone is always released when blood calcium levels drop – and then calcium is drawn from the bones to maintain balance.

So, chronically high prolactin levels can lead to bone dissolution by creating unnecessary spikes in parathyroid hormone.

Dopamine is constantly suppressing prolactin release in the pituitary.

In this way, dopamine protects against both osteoporosis and gynecomastia.

Prolactin also increased cell growth in this experiment.

These weren’t even breast cells… As I said above, more cell types are responsive to prolactin than you might think.

Scientists think that the calcium uptake itself initiated this growth.

Calcium in the body normally stays outside of cells, where it mineralizes bone.

Only very small amounts are normally found inside the cell.

The cell’s interior always has higher levels of potassium and magnesium than calcium.

Prolactin seems designed mainly to do this, to increase intracellular calcium and growth – especially during milk production.

Created right next to growth hormone, it is the only thing capable of pulling calcium into the cell and out of the bones in such low amounts.

“The amplitude of prolactin-induced Ca2 increases may be sufficient to provoke several physiological responses, such as stimulating proliferation.”

(Ca2 is carbonic anhydrase II – defects in this enzyme are associated with osteopetrosis.)

Even though prolactin receptors are found nearly everywhere, breast tissues – even in men – usually have the highest levels.

This is why they grow more than any other place in response to prolactin.

So how to combat prolactin? And all the crap that comes of prolactin?

Bromocriptine is a standard way to increase dopamine activity.

But simply eating the direct dopamine precursor, levodopa, is just as effective.

Levodopa is essentially dopamine. It only has to be decarboxylated to become dopamine.

This happens in the brain and elsewhere.

Levodopa was found to lower prolactin as far back as 1971:

(The typesetting of some journals was a bit cruder back then.)

The researchers were motivated by findings that some of their psychiatric medications raised prolactin, apparently by blocking dopamine receptors.

So they injected chlorpromazine and monitored prolactin levels every thirty minutes.

As expected, there was a prolactin spike.

But when given with L-dopa, this effect was prevented.

“Prolactin was undetectable when L-dopa pre-treatment was employed.”

And 500 milligrams of L-dopa by itself, without chlorpromazine, strongly lowered blood prolactin levels.

…with reductions of 65.0%, 73.8%, 87.3%, and 87.6%.

The effects began after half an hour, peaked at the one-hour mark, and persisted for at least another hour.

This is theoretically what you would expect as a precursor to dopamine… But this is experimental confirmation.

And it had no effect on growth hormone, meaning that it’s selective for prolactin.

For the most part, growth hormone is under the control of serotonin.

Serotonin raises growth hormone and dopamine inhibits prolactin.

Other studies have confirmed this effect.

And it happens like clockwork.

It even happens in people with hyperactive pituitary hormones.

It seems that moderate doses are fine for most people.

This is also an all-natural amino acid that cannot be patented. It exists in some foods and can be purchased cheaply.

People use it in gram amounts with no real side effects.

Besides bromocriptine, and a low-wheat diet, levodopa can also lower prolactin.

These three approaches work in different ways, so the effect of using all three would be additive.

——Important Message——

WOW, you have to try this…

My sex life is amazing now that I have figured out how to lower my prolactin.

This trick promotes testosterone and oxytocin, and it results in long-lasting “towel hanger” erections. At least it has for me!

My wife can’t get enough and I can go to round two and even round three… just like I did as a young man.

Most importantly – it’s natural and not that artificial stuff they inject, rub on, or make you drink.

Here’s what I’m doing that has made a huge difference in my erections and my sex life

————–

 

 

 


Matt Cook is editor-in-chief of Daily Medical Discoveries. Matt has been a full time health researcher for 26 years. ABC News interviewed Matt on sexual health issues not long ago. Matt is widely quoted on over 1,000,000 websites. He has over 300,000 daily newsletter readers. Daily Medical Discoveries finds hidden, buried or ignored medical studies through the lens of 100 years of proven science. Matt heads up the editorial team of scientists and health researchers. Each discovery is based upon primary studies from peer reviewed science sources following the Daily Medical Discoveries 7 Step Process to ensure accuracy.
Leong, Denis A. "Neuroendocrine control of prolactin secretion." Annual review of physiology 45.1 (1983): 109-127. 
http://www.annualreviews.org/doi/pdf/10.1146/annurev.ph.45.030183.000545 

Freeman, Marc E., et al. "Prolactin: structure, function, and regulation of secretion." Physiological reviews 80.4 (2000): 1523-1631. 
http://physrev.physiology.org/content/80/4/1523.short 

Ducret, Thomas; Bruno Sorin. "Effects of prolactin on intracellular calcium concentration and cell proliferation in human glioma cells." Glia 38.3 (2002): 200-214. 
http://onlinelibrary.wiley.com/doi/10.1002/glia.10056/full 

Kleinberg, David L., Gordon L. Noel, and Andrew G. Frantz. "Chlorpromazine stimulation and L-dopa suppression of plasma prolactin in man." The Journal of Clinical Endocrinology & Metabolism 33.5 (1971): 873-876. 
http://press.endocrine.org/doi/abs/10.1210/jcem-33-5-873 

Jacobs, Laurence S., William H. Daughaday. "Levodopa suppression of prolactin in nonpuerperal galactorrhea." New England Journal of Medicine 285.21 (1971): 1160-1163. 
http://www.nejm.org/doi/full/10.1056/NEJM197111182852102 

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