Weird stealth attraction discovery that’s going viral

Watch this controversial video here before it’s banned

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—-Important Message From Richard La Ruina—-

This “stealth attraction” discovery gets her in your bed — no legwork required

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I’ll admit it, I’m spoiled with my new stealth discovery.

Now I don’t have to lift a finger and the girls just keep coming.

But I don’t want to brag…

All I will say is that for any guy using stealth attraction, he has his pick of the litter.

Younger girls, attractive girls, knockout girls…

I put my method into this short little tutorial — watch only if you are sick of rejection and want to get laid like crazy


Blocking the cortisol receptor and naturally raising T

We need cortisol for a number of necessary functions in the body.

This includes breaking down muscle and fat for fuel, and blocking excessive inflammation.

Cortisol is essential – but excess cortisol is a problem of massive proportions.

Cortisol is elevated by many types of stress – poor sleep, inadequate diet, psychological and emotional stress…

…these all lead to chronically elevated cortisol.

This chronically elevated cortisol suppresses beneficial sex hormones like testosterone and DHEA.

Chronically elevated cortisol dissolves bone and muscle.

Chronically elevated cortisol also plays a major role in obesity and type II diabetes.

It does this in part by releasing lots of fats into the blood (free fatty acids).

Elevated free fatty acids block the cellular uptake of sugar – leading to elevated blood sugar.

This is one reason why cortisol causes metabolic issues.

But animal research indicates that there are other mechanisms by which cortisol can cause diabetes.

Researchers found that blocking the cortisol receptor improved symptoms in obese and diabetic mice.

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The animal experiments were performed at the Medical University of South Carolina in Charleston. The paper was published in The International Journal of Obesity and Related Metabolic Disorders.

The researchers were investigating cell signaling in fat cells of obese mice.

This type of cell signaling is compromised in diabetes and obesity – though the precise mechanisms are not yet fully understood.

They were investigating the role of high levels of cortisol-like stress hormones in abnormal cell signaling in these animals.

“We investigated the role of hypercorticism in the development of compromised beta-adrenergic signaling in fat cells of obese mice.”

Hypercorticism means high cortisol in humans – the equivalent is high corticosterone in animals.

The researchers carried out their experiments in different groups of mice.

Some of these male mice were obese, others were lean.

They were given a treatment which blocks the glucocorticoid receptor.

“Mature male obese mice and their lean littermates were treated with a vehicle or the specific glucocorticoid receptor antagonist, RU-486 for 21 days.”

RU-486 blocks the glucocorticoid receptor. In animals this blocks the effects of corticosterone.

In humans RU-486 blocks the stress hormone cortisol.

Cortisol is elevated by fasting, psychological stress, poor sleep, and dietary factors like low carb intake or high protein consumption.

Blocking the cortisol receptor led to normalizing blood sugar levels in the obese mice.

“RU-486 reduced blood glucose levels in obese mice to levels that were not different from lean mice.”

Blocking the effects of corticosterone/cortisol also reduced insulin in the animals.

The researchers did not test free fatty acids…

…but it’s likely that the body needs less insulin because there are fewer free fatty acids in the blood to compete with blood sugar.

“RU-486 also reduced serum insulin by approximately 50% in obese mice.”

The study shows that in rodents, just as in humans, the primary stress hormones corticosterone/cortisol play a major role in diabetes.

The authors found that there were some changes in the cell signaling mechanisms that they were investigating.

This may explain some of the anti-diabetic effects of blocking cortisol.

But it’s likely that most of the anti-diabetic effects are due to decreased free fatty acid production from lower cortisol/corticosterone activity.

“Glucocorticoid antagonism ameliorates diabetic symptoms of the mature obese mouse, but does fully reverse deficient expression and function of components of the fat cell beta-adrenergic signaling.”

The research tells us a little bit more about diabetes promoting the effects of cortisol.

But it doesn’t change the underlying message – chronically elevated cortisol is a trigger for type II diabetes and obesity.

It’s a solvable problem too – there are many, many ways to lower chronically elevated cortisol.

For many people simply getting a little more sleep and eating a little more regularly can have massive effects on cortisol.

—-Important Message—-

1 bite raises T while lowering cortisol

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When men have chronically high cortisol levels, they usually suffer from low libido and erections problems too.

This is because cortisol inhibits testosterone production in men.

So the more cortisol you have, the less T you have.

And that ups your risk of heart disease by a lot… not good…

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But here’s the good news…

If you can naturally raise T, you can naturally lower cortisol…

Because when testosterone is being made in the body, stress hormones automatically go down — including cortisol.

And the easiest way to naturally raise testosterone is to pop this in your mouth


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.
RU-486 (Mifepristone) ameliorates diabetes but does not correct deficient beta-adrenergic signaling in adipocytes from mature C57BL/6J-ob/ob mice