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—-Important Message—-

This new foreplay is 100 times more powerful than the old kind of foreplay

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I’m going to show you why massages and jazz music and candlelit dinners are nothing compared to what this 1 simple method can do…

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How to copy these mice who have mutant-like memories

Bacteria is an ever present threat to all other life forms.

This is particularly true of longer living mammals like humans.

Over time, bacteria which live in our gut find ways to infiltrate all the different parts of the body.

These out of place bacteria cause inflammation, disease and aging.

Much of these negative effects are mediated through the immune system.

One aspect of the immune system, a cell receptor called TLR4, has been called the bacterial endotoxin receptor.

This receptor is activated by these common gut bacteria.

And researchers discovered that mice which were bred to be genetically devoid of this cell receptor…

Had much better memory and mental function in older age.

It proves yet again that these bacteria are the major cause of aging and disease.

If we can avoid bacterial overloading of the TLR4 receptor we can slow aging and neurodegeneration.

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The animal experiments were performed at the Department of Neurosurgery of Xijing Hospital in China. The paper was published in Neuroscience.

“Toll-like receptor-4 (TLR4), a member of the TLR family, plays a key role in inflammation-related diseases of the nervous system.”

The researchers carried out their experiments on mutant mice.

These knockout mice are devoid of the genes which code for the TLR4 receptor.

These mice don’t have the endotoxin detecting receptor and they have been the subject of a lot of research into neurological diseases like dementia.

“TLR4 knockout mice are widely used in various neurological disease studies, and there is a clear correlation between inflammation and behavior.”

In this series of experiments the researchers looked at normal mice compared to mice without TLR4 at different ages.

“Male TLR4 knockout and wild-type normal mice of different ages (4, 8, and 16 months) were used for behavioral experiments.”

They looked at the physiological characteristics of the brain as well as proteins, blood flow and inflammation.

All of which determine how the brain ages and how well our mind works over time.

“Synaptic spine, blood-brain barrier integrity, memory regulatory proteins, cortical blood flow, and inflammatory factor examinations were also conducted to explore the possible mechanism by which TLR4 works.”

Mice without the endotoxin receptor had better brain function as they age. They were able to learn and remember like younger mice

“Here, we found that compared with 16-m-old normal mice, age-matched TLR4 knockout mice had better learning and memory abilities.”

This inside the brain, the biochemistry was different too.

The brains of the older mice without the TLR4 receptor were again more similar to that of young mice.

“… increased expression of neuronal synaptic spines, and increased memory-related regulatory proteins in the hippocampus.”

Remember, this is a bacterial endotoxin receptor, it senses the bacteria which leak in the case of “leaky gut syndrome”.

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Fear and anxiety are also common things associated with deteriorating brain function and dementia associated with age.

The researchers found that the mutant mice showed far less signs of fear and anxiety.

“TLR4 knockout significantly attenuated the fear response in 16-m-old mice.”

It seems that the brain was better protected too.

The blood-brain barrier was stronger and the tight junction proteins which make up that barrier were more dense.

“The TLR4 knockout mice also had better blood-brain barrier integrity, increased expression of tight junction-associated proteins.”

Blood flow was improved and inflammation was reduced.

“TLR4 knockout mice had increased cerebral cortical blood flow and reduced proinflammatory cytokine expression in the cortex and cerebrospinal fluid.”

The research shows that genetic modification to remove the endotoxin sensor gene could help to prevent brain aging, age associated cognitive deficits, and dementia.

But more practically it shows that protecting ourselves from activating this receptor by decreasing exposure to endotoxin bacteria can help to slow and prevent aging and dementia too.

“Our results suggest that TLR4 deletion ameliorates significant neurobehavioral dysfunction during the aging stage.”

There are many things which we can do to decrease the endotoxin load inside the body…

And if the endotoxin load is decreased then there will be less activation of TLR4.

Psychological stress, high-fat meals, and certain fibers are some of the ways that people commonly increase gut permeability…

Exposing themselves to high levels of endotoxin these days.

There are also many protective things we can do to fight off endotoxin infiltration of the body.

—-Important Message About Clearing Out Endotoxins—-

Patching up a leaky gut this way restores good rockiness

When the gut is leaking out endotoxins all over the body… eventually these toxins get to the penis…

And when they get to the penis, they poison the blood vessels and hurt rockiness.

Fortunately, if you can patch up a leaky gut, you can get the toxins out of the penis and restore erections again pretty quickly.

But how do you patch up a leaky gut?

Here’s how I’m doing it — try this tonight

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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.
TLR4 Deletion Improves Cognitive Brain Function and Structure in Aged Micehttps://pubmed.ncbi.nlm.nih.gov/35405301/