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—-Important Message for Men Looking to Increase Size—-

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———-

The new miracle treatment called Phlorizin

Doctors have been treating diabetes with phlorizin for over 100 years.

Originally tested against malaria on account of its bitter nature, the results instead revealed anti‑diabetic effects.

“Its unique pharmacologic properties, record of safe administration to humans, and constituent of the human diet make phlorizin a potential ‘natural remedy’ awaiting application.”

This was confirmed innumerable times over the following decades, eventually leading to the characterization of its molecular target being SGLT1.

Moreover, phlorizin has recently been discovered to exert a separate anti‑diabetic effect through a distinct receptor found inside the cell – the nuclear receptor PPAR-gamma.

This dual activity of phlorizin makes it surprisingly potent, analogous to naringenin’s ability to activate both PPAR-alpha and PPAR-gamma.

This property makes these molecules outclass any drug, natural or pharmaceutical, that can correct diabetes only in one way.

These biological effects also make phlorizin a powerful weight‑loss agent, and you’ll soon see why.

The earliest (1988) reliable observation following phlorizin administration was glycosuria (an increase in urinary glucose.

Because of this, they initially thought that phlorizin produced diabetes.

Yet, since plasma concentrations of glucose remained constant, they realized that phlorizin was enhancing its elimination.

According to Leif Poulsson in 1930:

“Under these conditions, the quantity of sugar found in the urine exactly corresponds to the extra amount removed from the blood after addition of phlorizin.”

As science progressed, the studies got more detailed.

Eventually scientists discovered a membrane protein called the sodium∶glucose cotransporter (SGLT1)…

This was originally known as the “phlorizin receptor” due to its strong affinity for phlorizin.

The inhibition of glucose resorption may sound dangerous, but the kidneys and intestines have other glucose transporters…

…including SGLT2, GLUT1, GLUT2…

So inhibiting this one alone does not produce extreme hypoglycemia.

Moreover, glucose can also diffuse through certain cell membranes depending on their specific lipid profile.

And maybe that’s why omega−6 fatty acids tend towards type 2 diabetes.

Reportedly, phlorizin is safe at two gm per day for 30 days, and also at a massive dose of 15 gm taken at once.

A researcher wrote in 1933:

“…one gram in the morning and one gram in the evening, for a period of thirty days. Benedict and Lewis gave 2 grams daily in 10 cc. of sterile olive oil subcutaneously over a period of days. In no instance was permanent injury described.”

So should a person have elevated blood glucose, phlorizin is a safe and effective way to eliminate it naturally.

And since SGLT1 is also found in the intestines, it’s no surprise that phlorizin has predictably been shown to delay glucose absorption there.

These observations make phlorizin the perfect antidote for high-glycemic foods, both delaying the absorption of glucose and then clearing any excessive amounts.

Phlorizin could be part of the reason why apples have a low glycemic index despite their appreciable sugar content…

The other possible reason is their relatively high fructose to glucose ratio (about 3∶2) because fructose does not release insulin.

In fact, phlorizin has such specificity for SGLT1 that its questionable it would’ve been discovered without it.

Phlorizin was instrumental in the recognition, isolation, and initial purification of SGLT1.

Phlorizin binding had routinely been used to infer the presence of SGLT1, to separate it using affinity chromatography.

And also to both photo‑ and radio‑label it for identification via Western blot test.

To put its importance into perspective, the first article in which SGLT1 was unambiguously characterized mentions phlorizin 144 times (1984).

Phlorizin was also useful in earlier physiological studies towards discovering how the kidneys work.

The kidneys were initially though impermeable to glucose on account of urine having less of it than plasma.

But, with the help of phlorizin, the true re‑uptake mechanism was finally established.

Poulsson again (1930):

“The important results of Wearn’s and Clark’s work are that the glomerular fluid probably always contains glucose, and the non-appearance of this substance in the urine must be due to a quantitative reabsorption of sugar by the renal tubule cells.”

Until around 1955, the experiments were relatively crude, and they relied primarily on plasma and urine glucose concentrations.

But the next decade brought more accurate metabolic measurements to demonstrate glucose uptake.

For example, the reduction of lactic acid (a product of glucose) was used to demonstrate the ability of phlorizin to inhibit intestinal glucose absorption…

And this begins to occur even at the lowest concentrations tested.

B.J. Parsons (1958):

Similar effects were described one year later by measuring radioactive carbon dioxide, a product of radioactive glucose.

And then seven years after that using the enzyme glucose oxidase.

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Effective concentrations are even less than what’s found in apples and apple cider.

But all phlorizin is effectively absorbed before it reaches the last section of the small intestine.

So you still have about 1/2 the length of the digestive tract left to absorb glucose at full efficiency.

Thus, phlorizin only has only the effect of delaying intestinal glucose absorption, not ultimately inhibiting it.

Meanwhile, similar effects of phlorizin on the kidneys were being described but at greater potency – because the kidneys also contain the high‑capacity SGLT2.

This doesn’t represent a danger from phlorizin either because only about 6% is excreted in the urine.

But it does explain how milligram‑sized doses can normalize blood sugar.

In other words, it can partially explain this study here:

In this study, they used five groups of rats:

1. Control group
2. A group made diabetic through pancreatomy
3. Another group made diabetic but also given phlorizin
4. The fourth was another control group given phlorizin
5. This group was diabetic rats initially given phlorizin and then taken off

This study showed that phlorizin, perhaps not unexpectedly, completely normalized the blood sugar spike seen in the diabetic groups:

The plasma glucose concentration in the fed state was 295 mg/dl diabetic rats.

But this went to 171 mg/dl in diabetic rats given phlorizin. This represents a 42% improvement.

What was actually surprising, however, was the reluctance of phlorizin to affect non‑diabetic rats in any way…

Normal rats given phlorizin had normal blood sugar insulin response and only trace amounts of glucose in their urine.

“Phlorizin administration to sham-operated animals had no effect on the plasma glucose and insulin responses during the MTT…”

“Only trace amounts of glucose were detected in the urine from sham-operated phlorizin-treated rats.”

(Sham surgery is a lab technique.)

On the other side of the coin, comparing the same parameters between phlorizin‑treated diabetic rats and diabetic rats reveals a stunning normalization of the condition…

Blood sugar (171 vs 295 mg/dl), insulin response (33.1 vs 24.8mg/kg/min), and glucose in their urine (8 vs .8 g/dl).

Plasma glucose was thus normalized by increased urinary elimination…

… the classic effect of phlorizin first noted over 100 years ago.

Yet one effect that defied explanation in 1987 was the increased insulin sensitivity:

“Phlorizin treatment of diabetic rats completely restored tissue sensitivity to normal.”

Not knowing any better, the author explained this in a ridiculous way, essentially stating that high plasma glucose per se actually induces insulin resistance.

Yet, exactly 30 years later, phlorizin was shown to potently activate PPAR-gamma and release adiponectin…

This effect could easily account for this increased insulin sensitivity:

This study showed that treating cells with phloretin increased adiponectin secretion, adiponectin RNA, and the RNA of numerous other PPAR-gamma target genes.

Phloretin is the aglycone of phlorizin – it is the core molecule after the bound glucose has been removed.

The phlorizin‑to‑phloretin conversion occurs upon intestinal absorption.

Yet most phloretin is then re‑conjugated with the similar glucuronic acid at the very same position – the №2 carbon on the A‑ring.

This is why phlorizin can have effects on renal SGLT1 and SGLT2 despite being initially converted to phloretin…

It is subsequently reconverted into an essentially identical molecule.

Most notable is phloretin’s ability to express and secrete adiponectin.

That’s a hormone created by adipose cells that is well‑known to enhance insulin sensitivity (Yamaguchi, 2001):

The nuclear receptor PPAR-gamma is also the target of thiazolidinediones, a popular class of antidiabetic drugs.

Thiazolidinediones also increase insulin sensitivity.

A 10 μM concentration of troglitazone had produced the same effect as a 50 μM concentration of phloretin…

Yet this level of phloretin can be achieved safely with dedicated supplementation.

“Note that plasma concentrations of phloretin from phloretin‑supplemented rats reach 55 to 65 μmol/l after 10 hours. This implies that the concentration of phloretin used in our study can be achieved in plasma after supplementation.”

So, shortly after phlorizin delays glucose absorption in the intestines, and before it increases its elimination by the kidneys, it can become phloretin.

And then:

(1) Activate the PPAR-gamma nuclear receptor

(2) Create adiponectin RNA

(3) Secrete adiponectin hormone

(4) Consequently increase insulin sensitivity throughout the body

So phlorizin controls diabetes in three ways, any one of which would make it useful.

These facts makes phlorizin the ideal antidiabetic treatment, notwithstanding its impeccable safety record.

Phloridzin and phloretin are both available over the counter and can be bought at a fraction of the price as the prescription thiazolidinediones…

That’s a drug class that can only activate PPAR-gamma.

And, of course, Phlorizin should lower the body weight of just about anyone in America…

Especially those who routinely eat high-glycemic foods (almost everyone).

“Here we show that phloretin is able to stimulate PPAR-gamma-induced transactivation of human adiponectin promoter. From a physiological point of view, an increase in adiponectin secretion would have favorable effects against insulin resistance…”

—-Important Message for Men with Diabetes or Prediabetes—-

This “forgotten” cure for diabetes can reverse symptoms in 2 weeks

Diabetes was not a huge problem in the old days.

Because they were using this forgotten cure…

But soon they STOPPED using this forgotten cure… And now diabetes is skyrocketing.

Big Pharma started intensively selling its so-called “treatments” – and this forgotten cure is no longer being offered to men.

“It isn’t profitable,” they say. It’s shameful.

Fortunately, you can use the forgotten cure right now, at home, to reverse your diabetes in as little as two weeks.

———-

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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.