Avoid this cooking method! You might be damaging your lungs

Avoid this cooking method! You might be damaging your lungs

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Anyone making food in their kitchen needs to aware of this dangerous, asthma-causing activity…

——Important Message—–

“Why is your T so high?”

The doctor crossed out the chemicals Ron was taking with a big line…

Ron knew why his testosterone got so high…

And it wasn’t from any injection or Big Pharma chemical.

The 29-year-old doc shrugged: “I’ve never seen a man your age with so much testosterone. Your levels are higher than mine!”

Ron’s testosterone shot higher, thanks to a strange natural brew he’s been drinking in the mornings.

Ron wasn’t even in good shape…nope…his newly discovered manliness was all because of this strange natural brew…

Ron told his 29-year-old doc about this brew and warned him: “It’s a bit bitter, son.”

Here’s what Ron had to say about this strange natural brew:

Here’s the strange brew that made Ron’s testosterone skyrocket…

—————–

Avoid this cooking method! You might be damaging your lungs

There are many things associated with asthma, but they all eventually meet and then channel down one biochemical pathway.

Asthma can be initiated by many inhalants…

Chitin is a polysaccharide characteristic of fungi. It induces a powerful immune response.

Inhaled bird dust will do the same in people cross-sensitized to alpha-livetin, an egg yolk protein.

But in every case of allergic asthma (whatever the cause may be, )the cytokines interleukin-5 and interleukin-13 are released.

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Interleukin-5 induces the multiplication of eosinophils – immune cells that are always found to be increased in asthmatic airways.

These observations are so consistent that asthma is unheard of without eosinophils in the lung.

This is also the very reason why glucocorticoids are often prescribed.

Cytokine interleukin-13 induces the enzyme lipoxygenase, which is highly expressed in the lungs.

Its function is to transform linoleic acid into the more active 13-HODE (13-hydroxyoctadecadienoic acid) metabolite:

This toxic metabolite is what ultimately accounts for the majority of asthma symptoms and breathing difficulties in general.

Besides the characteristic presence of eosinophils, the presence of this lipid is the most consistent finding found in asthma:

Linoleic acid can be eliminated completely…simply by choosing the right foods.

It’s not that hard to do.

It’s fairly easy to stick to the saturated fatty acids found in dairy, beef, chocolate, and coconuts.

Frying food with vegetable oils produces volatilized linoleic acid and its peroxidation products… And we often inhale these directly while cooking!

This process completely bypasses a few of the steps necessary for allergic asthma and induces it directly instead.

Female restaurant cooks have a 410% higher rate of breathing difficulties…

And that is probably an underestimation since only compliant restaurants – those with good ventilation – chose to participate in the study.

“During frying at high temperatures, fat will enter the atmosphere as an aerosol. The lung-damaging potential of aerosols from vegetable and animal fats is supposed to be dependent on the content of free fatty acids in the fat.”

So, whether a person has been diagnosed with asthma or not, this one fatty acid can contribute to breathing difficulty.

AND this has all been proven.

The best science always shows us what needs to be done to prevent, treat, and eventually even eliminate nearly every condition.

And we have that going on with asthma now too:

This study examined the effects of 13-HODE (13-hydroxyoctadecadienoic acid) and the enzyme that makes it – and the receptor it acts on: vanilloid receptor type 1.

Up to this point, previous studies led researchers to discount this pathway due to the minimal effects noted.

But more recent evidence had shown this was simply because the researchers had used an unusual strain of mice:

They showed that 13-HODE (13-hydroxyoctadecadienoic acid) causes characteristic asthma symptoms in nearly every way imaginable.

They did this by:

(1) Lowering 13-HODE levels by blocking its enzyme, lipoxygenase, with a drug

(2) Using interfering RNA to lower lipoxygenase expression

(3) Using antibodies to bind and incapacitate 13-HODE itself

(4) Directly through the inhalation of 13-HODE

The results were consistent in every way they tested them.

Since 13-HODE works on the vanilloid receptor, this also explains why asthma patients are often reported to cough more in response to capsaicin than other people.

Capsaicin works on the vanilloid receptor quite strongly.

If the asthmatic response in BALB/c mice (see the graph two pictures above here) are to be extrapolated to humans, this would mean there are more vanilloid receptors in asthmatics…

And that would explain the capsaicin hypersensitivity.   

Blocking this receptor with capsazepine has been shown effective… But simply lowering linoleic acid intake would be a better idea.

(Capsazepine is a synthetic antagonist of capsaicin.)

But this advice is not generally given to patients…

Besides being less known among the older doctor crowd, most profits are geared towards glucocorticoid and Albuterol™ prescriptions.

But there are much safer options than glucocorticoids, which indiscriminately shift the entire immune system towards a Th2-dominant state.

(Th2 dominant is one type of immune system imbalance.)

For this reason, glucocorticoids very often lead to invasive fungal infections such as aspergillosis and candidiasis.

Nitric-oxide-stimulating Th1 cytokines such as interferon gamma are needed to destroy fungi…

But glucocorticoids inhibit those Th1 cytokines.

And 13-HODE can also explain the eosinophils that are always found in asthmatic lungs.

Experiments have shown that eosinophil cells actually are attracted to 13-HODE in particular.

The prostaglandin leukotriene B₄ had actually been discovered because of its ability to attract certain white blood cells.

Polymorphonuclear leukocytes respond to leukotriene B₄ – neutrophils, basophils, and eosinophils are all members of this subclass.

These migrating cells respond to leukotriene B₄ by releasing themselves from the blood vessel wall at higher concentrations.

These cells then reattach, or “replant” themselves once they reach an area of even higher concentration.

This biphasic release–attach mechanism is how they move.

“It was found that 9-HODE and 13-HODE induced a chemotactic response of both human and bovine PMNs in vitro.”

Among the lipids tested, leukotriene B₄ will attract white blood cells the most, without a doubt.

But some 1991 research discovered that 13-HODE was nearly just as effective:

This is ~75% as strong as the strongest lipid chemoattractant.

And 13-HODE exists in far higher concentrations than leukotriene B₄, especially in the lungs where 15-lipoxygenase is highly expressed.

Moreover, leukotriene B₄ itself is derived from the same omega-6 fatty acids.

This eicosanoid can only be made from either gamma-linolenic or linoleic acid.

So being cognizant of exactly what fatty acids are in our foods can radically reduce eosinophil migration to the lungs.

Although 13-HODE is most likely responsible for the general increase of airway resistance, it is the eosinophil specifically that is responsible for the “asthma attack.”

The eosinophils cause this as they “degranulate.”

Degranulation is a term derived from the microscopic appearance of the exploded cell after its stored internal contents are released.

When mast cells degranulate they release histamine…

When eosinophils degranulate, they release eosinophil basic protein.

This eosinophil protein is a powerful ligand (a molecule that binds) for an acetylcholine receptor called M₂.

The eosinophil binds onto the M₂ and helps to induce muscle spasms along with mast cell histamine.

Even though 13-HODE will attract a subclass of white blood cells, this is really most characteristic of the eosinophil only:

A group of Dutch biochemists separated all the different types of white blood cells from human blood, added linoleic acid to a dish of each type, and then measured the results.

They found that eosinophil produced far more 13-HODE than did neutrophils, basophils, monocytes, and lymphocytes combined:

Eosinophil both uniquely produces and is attracted to the same fatty acid that’s been shown to cause breathing difficulties in asthma.

These pulmonary effects of 13-HODE were first noted by these same Dutch researchers over 30 years ago.

“We demonstrate that the eosinophil preferentially produces 13-HODE, whereas the other cell types produce equal amounts of 9-HODE and 13-HODE.”

So this 13-hydroxylated linoleic acid is more characteristic of eosinophils than any other human immune cell…or any other human cell at all…

And 13-HODE is also the most asthmatic fatty acid.

The presence of eosinophils can be explained by their honing properties towards 13-HODE in the lungs…

And the increased concentrations of 13-HODE in the lungs can be partially explained by the eosinophils which make that happen.

It’s a chicken-and-egg vicious circle.

Which comes first? Eosinophils or 13-HODE?

Do eosinophils and 13-HODE amplify each other in a positive-feedback way?

Regardless of the answer to those questions, reducing omega-6 fatty acids is certain to increase lung capacity in everyone.  

Many linoleic acid products are highly involved in the breathing difficulties of asthma…

They are much more powerful at this than their more natural omega fatty acid counterparts.

“First, eosinophils have markedly higher levels of 15-lipoxygenase activity than other cell types, which would be in agreement with our observation that eosinophils produce more 13-HODE than the other cell types investigated.”

—-Important Message—-

The Montana Miracle is reversing diabetes!

The darker the state, the more diabetes will develop. Notice where all the diabetes is developing?

It’s developing in the southern United States. And in some parts of the Midwest.

You can really see that certain states are very dark, such as Georgia and Florida.

But look at Montana – it remains white, with very little diabetes!

What’s so special in Montana?

Well, they call it the “Montana miracle” – as you can see, it is working.

Also, you don’t have to live in Montana to reverse your diabetes this way!

Please watch this important quick video where I show you the “Montana miracle” that fixes diabetes…

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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.
Henricks, P. "13-Hydroxy-linoleic acid induces airway hyperreactivity to histamine in guinea-pigs." European journal of pharmacology (1991) https://www.ncbi.nlm.nih.gov/pubmed/7622761Mabalirajan, U. "Linoleic acid metabolite drives severe asthma by causing airway epithelial injury." Scientific reports (2013) https://pdfs.semanticscholar.org/a7e4/f015c8e845f093a858c3e28b939beed0cd63.pdfHenricks, P. "9-and 13-hydroxy-linoleic acid posses chemotactic activity for bovine and human polymorphonuclear leukocytes." Prostaglandins (1991) https://www.sciencedirect.com/science/article/pii/009069809190101KEngels, F. "Preferential formation of 13-hydroxylinoleic acid by human peripheral blood eosinophils." Prostaglandins (1996) https://www.sciencedirect.com/science/article/pii/0090698096000573Millqvist, E. "Cough provocation with capsaicin is an objective way to test sensory hyperreactivity in patients with asthma‐like symptoms." Allergy (2000) http://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2000.all2513.x/fullSvendsen, K. "Respiratory symptoms in kitchen workers." American journal of industrial medicine (2003) http://onlinelibrary.wiley.com/doi/10.1002/ajim.10197/full

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