Polycystic Ovarian Disease Survival Guide: Insulin overdose. Yes there's too much of a good thing.

I'm continuing my neverending diatribe regarding this overhyped blanketed cure of "sugar" aka. HIGH INSULIN. After the partnership between Sino Pharmaceuticals who has the patent on "Metformin cures PCOS" (which it doesn't because PCOS is caused by high insulin and Metformin raises insulin, reference: the insulin-activin-LH-FSH cascade).

I want to start out by mentioning Leena Wen MD admission to what the doctors were doing to the patients everywhere.

Per the transcript: They told me that I'm a traitor to my own profession, that I should be fired, have my medical license taken away, that I should go back to my own country. My email got hacked. In a discussion forum for other doctors, someone took credit for "Twitter-bombing" my account. Now, I didn't know if this was a good or bad thing, but then came the response: "Too bad it wasn't a real bomb."0:43

I never thought that I would do something that would provoke this level of anger among other doctors...

...Now, imagine being his parents who flew in from Seattle, 2,000 miles away, to find their son in a coma. I mean, you'd want to find out what's going on with him, right? They asked to attend our bedside rounds where we discussed his condition and his plan, which I thought was a reasonable request, and also would give us a chance to show them how much we were trying and how much we cared. The head doctor, though, said no. He gave all kinds of reasons. Maybe they'll get in the nurse's way. Maybe they'll stop students from asking questions. He even said, "What if they see mistakes and sue us?"

What I saw behind every excuse was deep fear, and what I learned was that to become a doctor, we have to put on our white coats, put up a wall, and hide behind it. There's a hidden epidemic in medicine. Of course, patients are scared when they come to the doctor. Imagine you wake up with this terrible bellyache, you go to the hospital, you're lying in this strange place, you're on this hospital gurney, you're wearing this flimsy gown, strangers are coming to poke and prod at you. You don't know what's going to happen. You don't even know if you're going to get the blanket you asked for 30 minutes ago. But it's not just patients who are scared; doctors are scared too.

We're scared of patients finding out who we are and what medicine is all about. And so what do we do? We put on our white coats and we hide behind them. Of course, the more we hide, the more people want to know what it is that we're hiding. The more fear then spirals into mistrust and poor medical care. We don't just have a fear of sickness, we have a sickness of fear.

http://www.ted.com/talks/leana_wen_what_your_doctor_won_t_disclose?language=en

From one of my excessive blogs:

(1) The patient has the right to receive information from physicians and to discuss the benefits, risks, and costs of appropriate treatment alternatives. Patients should receive guidance from their physicians as to the optimal course of action. Patients are also entitled to obtain copies or summaries of their medical records, to have their questions answered, to be advised of potential conflicts of interest that their physicians might have, and to receive independent professional opinions."

http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion1001.shtml

Opinion 9.095 - The Use of Patents and Other Means to Limit Availability of Medical Procedures

Physicians have ethical responsibilities not only to learn from but also, when possible, to contribute to the total store of scientific knowledge. Physicians should strive to advance medical science and make their achievements known through publication or other means of disseminating such information. This encourages physicians to innovate and to share ensuing advances.

The use of patents, trade secrets, confidentiality agreements, or other means to limit the availability of medical procedures places significant limitation on the dissemination of medical knowledge, and is therefore unethical. (V, VII)http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion9095.shtml

"greater safeguards against conflicts of interest are needed to ensure the integrity of the research and to protect the welfare of human subjects."http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion80315.shtml

Unethical conduct that threatens patient care or welfare should be reported to the appropriate authority for a particular clinical service.
http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion9031.shtml

Edward Bernays is rolling in his grave.

Here's a list of doctors who get kickbacks from Big Pharma.

http://projects.propublica.org/docdollars/companies

http://pcossurvivor.blogspot.com/2011/03/reality-stumps-theories-stated-by.html
http://www.moneydrivenmedicine.org/index.php?start=3

http://pcossurvivor.blogspot.com/2011/03/metformin-lie-and-pcos.html

And let's not forget the Hippocratic Oath:

The Oath By Hippocrates
Written 400 B.C.E
Translated by Francis Adams

I SWEAR by Apollo the physician, and Aesculapius, and Health, and All-heal, and all the gods and goddesses, that, according to my ability and judgment, I will keep this Oath and this stipulation- to reckon him who taught me this Art equally dear to me as my parents, to share my substance with him, and relieve his necessities if required; to look upon his offspring in the same footing as my own brothers, and to teach them this art, if they shall wish to learn it, without fee or stipulation; and that by precept, lecture, and every other mode of instruction, I will impart a knowledge of the Art to my own sons, and those of my teachers, and to disciples bound by a stipulation and oath according to the law of medicine, but to none others. I will follow that system of regimen which, according to my ability and judgment, I consider for the benefit of my patients, and abstain from whatever is deleterious and mischievous.

I will give no deadly medicine to any one if asked, nor suggest any such counsel; and in like manner I will not give to a woman a pessary to produce abortion. With purity and with holiness I will pass my life and practice my Art. I will not cut persons laboring under the stone, but will leave this to be done by men who are practitioners of this work. Into whatever houses I enter, I will go into them for the benefit of the sick, and will abstain from every voluntary act of mischief and corruption; and, further from the seduction of females or males, of freemen and slaves.

Whatever, in connection with my professional practice or not, in connection with it, I see or hear, in the life of men, which ought not to be spoken of abroad, I will not divulge, as reckoning that all such should be kept secret.

While I continue to keep this Oath unviolated, may it be granted to me to enjoy life and the practice of the art, respected by all men, in all times! But should I trespass and violate this Oath, may the reverse be my lot!

The Blood Sugar Con Job has been way overdone.

As a runner, my glucose levels have been low. Sometimes my glucose levels have been so low that I get Rhabdomyolysis- from LOW blood sugar. It almost happened to me this morning. Yes I consume dextrose.

An except from "The Blood Sugar Con Job"

When you eat any food, even fat, your insulin level will rise. Higher amounts of refined carbohydrates or simple sugars will raise your insulin faster and in higher amounts. The greater the fiber content of your diet, the slower insulin is raised and the more controlled the process. When you eat a large meal, regardless of the type of calories, it causes a large surge in insulin that is difficult to manage.

Insulin is a taxicab for calories. Its goal is to take blood sugar, as its passenger, to various locations in your body that want it. It helps if you are active, as some of the sugar is more likely to be wanted by cells in your body, including your many muscle cells.

Blood sugar is fuel, like gasoline is to a car. Your brain must have a regular supply or your head conks out. Thus, following a meal your insulin taxi’s are busy transporting sugar through your circulation and out to your cells, hoping to find cells that need some sugar.

In a healthy person, insulin drops off a whopping 60 percent of the sugar at your liver, which acts as a warehouse, converting the blood sugar to glycogen for storage.

Insulin is released by your pancreas in two phases. The first phase is from insulin that is already made and stored in your pancreas, which is just waiting for some food to come along. This is your first wave of taxis coming to pick up the first set of blood sugar passengers. The release of this insulin triggers your pancreas’ beta cells to start making more insulin to deal with the rest of the meal.

As you are eating, some of the insulin transports blood sugar to your white adipose tissue or stored fat. The blood sugar is taken up by fat cells, activating their metabolism, in turn producing the hormone LEPTIN. Leptin now enters your blood and begins traveling up to your brain. The more you eat, the more insulin you make, and the more leptin you make.

When leptin levels get high enough, meaning you have eaten enough, then leptin permeates into your brain and tells your subconscious brain you are full. At the same time, the higher levels of leptin also tell your pancreas that you are full, which turns off the beta cell production of insulin, as no more taxis are needed.

If you ate the right amount of food for your physical activity level, then blood sugar always has some place healthy to go; insulin rises and falls in a controlled manner, as does leptin.

When insulin has too many blood sugar passengers, and cells don’t need any sugar, then insulin stimulates the production of TRIGLYCERIDES, which can become stored fat. This is how you gain weight. Unfortunately, as AS TRIGLYCERIDES ELEVATE IN YOUR BLOOD, THEY GET IN TEH WAY OF LEPTIN GETTING INTO YOUR BRAIN....."

TRIGLYCERIDES BLOCK LEPTIN. TRIGLYCERIDES FROM INSULIN.

HIGH FRUCTOSE CORN SYRUP RAISES TRIGLYCERIDES. XENOHORMONES LIKE ESTROGEN RAISES TRIGLYCERIDES!!!

Back to the article:

This keeps you eating more than you need to because you don’t yet have a full signal, a problem called leptin resistance. This encourages even further insulin driven triglyceride formation, making it more likely you will gain weight.http://www.wellnessresources.com/tips/articles/insulin_leptin_and_blood_sugar_why_diabetic_medication_fails/

The Blood Sugar Con Job"

When you eat any food, even fat, your insulin level will rise. Higher amounts of refined carbohydrates or simple sugars will raise your insulin faster and in higher amounts. The greater the fiber content of your diet, the slower insulin is raised and the more controlled the process. When you eat a large meal, regardless of the type of calories, it causes a large surge in insulin that is difficult to manage.

Insulin is a taxicab for calories. Its goal is to take blood sugar, as its passenger, to various locations in your body that want it. It helps if you are active, as some of the sugar is more likely to be wanted by cells in your body, including your many muscle cells.

Blood sugar is fuel, like gasoline is to a car. Your brain must have a regular supply or your head conks out. Thus, following a meal your insulin taxi’s are busy transporting sugar through your circulation and out to your cells, hoping to find cells that need some sugar.

In a healthy person, insulin drops off a whopping 60 percent of the sugar at your liver, which acts as a warehouse, converting the blood sugar to glycogen for storage.

Insulin is released by your pancreas in two phases. The first phase is from insulin that is already made and stored in your pancreas, which is just waiting for some food to come along. This is your first wave of taxis coming to pick up the first set of blood sugar passengers. The release of this insulin triggers your pancreas’ beta cells to start making more insulin to deal with the rest of the meal.

As you are eating, some of the insulin transports blood sugar to your white adipose tissue or stored fat. The blood sugar is taken up by fat cells, activating their metabolism, in turn producing the hormone LEPTIN. Leptin now enters your blood and begins traveling up to your brain. The more you eat, the more insulin you make, and the more leptin you make.

When leptin levels get high enough, meaning you have eaten enough, then leptin permeates into your brain and tells your subconscious brain you are full. At the same time, the higher levels of leptin also tell your pancreas that you are full, which turns off the beta cell production of insulin, as no more taxis are needed.

If you ate the right amount of food for your physical activity level, then blood sugar always has some place healthy to go; insulin rises and falls in a controlled manner, as does leptin.

When insulin has too many blood sugar passengers, and cells don’t need any sugar, then insulin stimulates the production of TRIGLYCERIDES, which can become stored fat. This is how you gain weight. Unfortunately, as AS TRIGLYCERIDES ELEVATE IN YOUR BLOOD, THEY GET IN TEH WAY OF LEPTIN GETTING INTO YOUR BRAIN....."

TRIGLYCERIDES BLOCK LEPTIN. TRIGLYCERIDES FROM INSULIN.

HIGH FRUCTOSE CORN SYRUP RAISES TRIGLYCERIDES. XENOHORMONES LIKE ESTROGEN RAISES TRIGLYCERIDES!!!

Back to the article:

This keeps you eating more than you need to because you don’t yet have a full signal, a problem called leptin resistance. This encourages even further insulin driven triglyceride formation, making it more likely you will gain weight.http://www.wellnessresources.com/tips/articles/insulin_leptin_and_blood_sugar_why_diabetic_medication_fails/

WNT=leptin

1. Hypothalamic WNT signalling is impaired during obesity ... Hypothalamic WNT signalling is impaired during obesity and reinstated byleptin treatment in male mice. Benzler J(1), Andrews ZB, Pracht C, ...

1. Epigenetics in Human Disease - Google Books Resulthttps://books.google.com/books?isbn=0123884160

MESODERM SPECIFIC TRANSCRIPT aka. “Mest”/Peg1 inhibits Wnt signalling through regulation of LRP6 glycosylation. ... Effects ofmiR-335-5p in modulating osteogenic differentiation by specifically ...http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574032/

(WNT tells the mesenchymal stem cells to make or break down bones)...

These experiments show that leptin-LRb signaling in articular chondrocytes modulates expression of canonical Wnt signaling receptors and suggests that direct cross-talk between these pathways is important in determining chondrocyte homeostasis. http://www.ncbi.nlm.nih.gov/pubmed/20868760

In addition to its expression patterns under nutritional manipulations and during development, a role for MEST in fat mass expansion comes from its molecular characteristics. Foremost, MEST is localized to the ER, a site where the VLDL receptor and diacylglyceride acyl transferase 1 (DGAT1) function, together with lipoprotein lipase in the vascular endothelium, to take up fatty acids from the circulation and repackage them into triglycerides (TGs) for assembly into the lipid droplet. These functions of the ER in lipid storage suggest that the function of MEST in the ER may be similarly related to TG storage. Secondarily, the enzymatic role for MEST in the ER to facilitate storage of fat is suggested from putative enzymatic functions of α/β fold hydrolase proteins and, indeed, the presence of the catalytic triad at serine 145-histidine 146-aspartate 147 of MEST strongly suggest an enzymatic function for MEST as a lipase or acyltransferase (15 , 47). Such an enzymatic function could, accordingly, supplement the capacity of DGAT1 or other lipase activities associated with TG metabolism in the ER to efficiently store excess calories in adipose tissue during a positive energy balance.

It is indicative of the potential importance of the α/β fold hydrolase family of proteins in lipid metabolism that the α/β fold CGI-58 protein has recently been found to an integral component of the lipid droplet where it mediates the accessibility of hormone-sensitive lipase (HSL) to the lipid droplet (48). Not only does CGI-58 regulate HSL, but also its binding affinity to adipose tissue triglyceride lipase (ATGL) is essential for the enzymatic activity of ATGL. However, unlike MEST, which has the active site structure necessary for an enzymatically functional protein, CGI-58 lacks the essential serine in the catalytic triad and therefore functions as an accessory/carrier protein.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574032/

MEST = LEPTIN RESISTANCE

MEST is blocked by Metallothioneins; http://www.fasebj.org/content/24/7/2375.full.pdf
Metallothioneins are upregulated with Zinc.

When the bone releases calcium from the bones, it also releases zinc, magnesium and phosphate. That Zinc binds with metallothioneins and moves to the liver as Zinc Metallothioneins aka. Zn-MT.

Therefore there is no more Metallothioneins to block MEST so the body gains weight very rapidly on a high fat diet.

Now back to the horrors of insulin hoax. Manfred J. Sakel is the first coming of Satan.

http://psychrights.org/stories/insulinshock-a-survivor-account.pdf

Insulin is a very powerful stimulant of the endocrine and the neuroendocrine systems, as is the coma produced by it. It is probable that insulin coma's benefits may have been achieved by redressing hormonal imbalances, in a fashion similar to that of ECT. (During the ICT era, we did not have the knowledge of neuroendocrine interactions nor the methods of study that we have today.) Such actions would also explain the benefits achieved when ECT was added to ICT.http://www.pbs.org/wgbh/amex/nash/filmmore/ps_ict.html

The SIDE EFFECTS were of course WEIGHT GAIN! Yup.

Then HYPOGLYCEMIA.
It's heartbreaking to know what the medical community is pulling and watching otherwise nice and normal people- overweight women walk out of Target and Trader Joes with carts of high fat baked goods. Hypoglycemia, or hyperinsulinemia has to be the culprit.

Then EPILEPSY!!! HIGH INSULIN CAUSES EPILEPSY? Will ketogenic diets cure epilepsy? Of course, there are very few epileptics that are schizo? Right?

High insulin causes high LDL:

Exposing 3T3-L1 adipocytes to physiologically relevant doses of hyperinsulinemia (250pM-5000pM) induced a dose-dependent gain in the mRNA/protein levels of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGR). These elevations were associated with elevated plasma membrane cholesterol.

http://www.ncbi.nlm.nih.gov/pubmed/23315940

NOW. BACK TO PCOS.

Did the chicken or the egg come first (insulin or igf-1)---is the almighty causation riddle: