June 20, 2013

Major Breakthrough in Using Stem Cells to Cure A Genetic Form of Diabetes

A study just published in the Journal of Clinical Investigation describes what sounds like a very important advance in the treatment of genetically-caused diabetes.

The study is iPSC-derived β cells model diabetes due to glucokinase deficiency.  Haiqing Hua et. al Journal of Clinical Investigation, 2013; DOI: 10.1172/JCI67638

To better understand what was done here, read Science Daily: Researchers Demonstrate Use of Stem Cells to Analyze Causes, Treatment of Diabetes

The particular form of diabetes that was studied here was MODY-2. This is a monogentic genetic form of diabetes, which means you need have only one copy of the gene to experience its symptoms. MODY-2 involves the glucokinase gene (GCK) which is often described as a "glucose thermostat." It affects the control of fasting blood sugar, and when it is broken people have diabetic-level fasting blood sugars that, in theory, can not be lowered.

This it turns out, is not entirely true. I have heard from several people diagnosed via gene tests with MODY-2 who report that cutting carbs does lower their fasting blood sugar, even though they were told it would not. My guess is that while their base fasting blood sugar is higher than normal eating a high carb diet further stresses their blood sugars as it does in people without the defect, so removing the carb-related stress lowers their fasting blood sugar to a level slightly higher than normal, but not nearly as bad as what they experience while eating a high carb diet.

But because their fasting blood sugar is higher than normal from birth, which in most people leads to post-meal blood sugars that are also higher than normal, People with this gene often die of heart attacks at very young ages, which is why, though it doesn't cause the extremely high post meal blood sugars that produce the classic diabetic complications, MODY-2 is still a very serious condition which requires life-long vigilance on the part of those who suffer from it.

What the researchers did in this study was to take skin cells from people with MODY-2 and using the kind of wizardry that stem cell scientists now routinely pull off, use them to create pluripotent stem cells--cells that can become any kind of tissue.

The researchers then, using even more stem cell magic, turned these pluripotent stem cells into beta cells, implanted them into mice, and three months later confirmed that these cells were in fact beta cells that showed the characteristics of MODY-2.

That's already pretty amazing, but the researchers were just getting going. Next the scientists "repaired the GCK mutation using molecular techniques."  After doing this, "cells with two restored copies of GCK responded normally to the glucose stress test. Unlike other reported techniques, the researchers' approach efficiently repaired the GCK mutation without introducing any potentially harmful additional DNA."

In short, what they did was create perfectly normal beta cells that would have been immunologically identical to those of the skin cell donors that had repaired the flaw that gave these people MODY-2 diabetes. If this is really the case, it should eventually be possible to grow a significant number of these new, repaired beta cells and transplant them back into the people with MODY-2  where they would be able to respond like normal beta cells, secreting insulin when exposed to rising glucose levels. Best of all, these transplants shouldnt require the use of any immunosuppressant drugs.

The part about growing enough cells and transplanting them is still in the future. So even if you have MODY-2  it's going to be a while until there is an actual cure your doctor can prescribe for you. But even so, this is, obviously, extremely good news for anyone who has a genetic form of diabetes which involves damaged beta cells.

And though few people with Type 2 realize it, this would include a lot of people with Type 2, as there are a couple of damaged genes affecting insulin secretion that are very commonly found among Europeans with Type 2 diabetes, for example TCF7L2, which is discussed HERE.

There are other commonly damaged beta cell genes that are found in other ethnic populations too. So in the long run this research could lead to effective beta cell transplants for people with Type 2 that could normalize their blood sugars.

Will it really happen? Hard to say. Sadly, all the money in diabetes treatment lies in creating drugs that have to be taken every day for decades and devices that require very expensive consumable parts that have to be replaced frequently. Since the companies that make those drugs are the companies that fund most research--and the ADA and the JDRF and drive the diabetes research agenda, it may be difficult for the scientists who performed this particular miracle to get the kind of funding it would take to turn beta cell implantation for MODY or Type 2 diabetes into a viable treatment covered by insurance.

Still, if you have a genetic form of diabetes, it's good to know that your children might not have to go through what you did, thanks to the advances made in stem cell research today.

NOTE: Don't confuse this research which is in its early stages with the fake claims of the many scammy  "stem cell clinics" you will find on the web that claim to cure diabetes (and anything else that ails you) with transfusions of your own stem cells. These slimy weasels prey on people who don't understand science and cure them only of having healthy bank accounts. Ignore them.

The exciting stem cell research that may pay off for people with diabetes is still, like the study discussed here, in the preliminary lab-bench stage which is very far from being something you could have done to your body to heal it. But someday, if we're lucky . . .

Big Changes in the Drug Patent World Are Good News for People with Diabetes

Several days ago the Supreme Court of the U.S. issued a decision saying that the FDA could sue drug companies that paid off generic drug makers to keep them from releasing generic versions of drugs that had gone off patent.

A second decision that may be just as important for controlling the costs of drugs for people with diabetes occurred on June 18, 2013. A U.S. appeals court found the patent on Novo Nordisk's Prandin diabetes drug Prandimet, a combination of Prandin with metformin to be invalid, paving the way for introduction of a generic version of the medicine.

MedCity Newsletter: Novo Nordisk’s diabetes drug patent ruled invalid, door open for generic version

Drug companies have been creating combination drugs with two off patent drugs claiming they are new drugs that deserve new patents. Then they convince doctors to only prescribe the expensive, patented combination drug rather than the separate generics. ("So much more convenient." "More effective!" Both lies, of course.)

This is good news not only because it makes the combo drug cheaper, but because if upheld it will dissuade drug makers from marketing these combo drugs, which are a very poor choice for consumers because they make it impossible to dose the individual components correctly.

Some people need 1000 mg of metformin a day for it to be effective. Some need 1500, and some need 2000. However, if you put 1000 mg of metformin in the same pill with a full dose of Prandin, an insulin secretion stimulator, you have to double the Prandin to double the metformin dose. Doubling Prandin can cause hypos in people who are sensitive to it. So with a combo pill the person is likely to end up with an optimal dose of only one component of the pill.

Two generic prescriptions should be the same cost or, more commonly, cheaper than one patented pill, except for people who have top tier health  insurance whose co-pays are low enough that this shouldn't be an issue. Most people with diabetes can handle opening two pill containers and taking two pills if that means they are a) paying less and b) getting more effective doses.

The drug companies are likely to lobby and appeal this one to the top, too, since their failure to come up with effective new drugs drives them to more and more tricks, like bribing generic drug makers or creating these combo pills to keep their expiring patent moneymakers profitable.

June 14, 2013

The ADA's "Investigation" of Incretin Drugs is a Gift to the Drug Companies

UPDATE 6/20/2013: Here's an excellent summary of ALL the studies pointing to serious problems with all the incretin drugs. There are a lot of them from many different kinds of research and they make it crystal clear that the American Diabetes Association's claim discussed below that the research about incretin drugs causing pancreatitis and cancers is ambiguous is an industry-sponsored lie.

 Pharmlot: Troubling New Signals? Diabetes Drugs & Adverse Event Reports


You may have heard that the American Diabetes Association (ADA) had called for a review of the incretin drugs--Januvia, Onglyza, Byetta, Victoza, etc.--in response to the recent discovery, which I described HERE, that they cause abnormal patterns of growth within the pancreas of a kind that lead to both pancreatitis and cancer.

The call for review can be read HERE.

Sadly, this call for review has nothing to do with protecting people with diabetes, a group for whom the ADA has never had much concern, save as a source of contributions to pay the inflated salaries of its top executives.

The ADA is heavily funded by drug manufacturers, and this call for review is an attempt to protect the profits of the companies who make the incretin drugs. That this is the case is made crystal clear in the ADA's call.

They state, "A recent case control trial examining autopsy specimens suggested that exposure to sitagliptin or exenatide in a small number of subjects increased neoplastic changes in the pancreas of subjects with type 2 diabetes to a greater extent than that seen in nondiabetes subjects or diabetic patients treated with drugs other than incretins. This analysis has been criticized from a methodologic standpoint and remains unconfirmed. [emphasis mine]"

This last statement is an out and out lie. The only criticism I have been able to find of Dr. Butler's brilliant study came from a PR flack working for one of the drug companies. Dr. Butler's research validated previous findings in animal research, and it was all the more compelling because though it used "a small number of subjects" taking incretin drugs, every single one of them had abnormal cells, cell growth patterns, and neuroendocrine tumors in thier pancreases after years of taking these drugs--and NONE of the normal people or people with diabetes not taking incretin drugs had these changes or tumors in their pancreases.

The "review" the ADA is calling for, is largely an analysis of previously published research which it believes will show no problems with these drugs. As the ADA's call  points out "Administrative database analyses suggest either no effect on pancreatitis or a small risk associated with incretin therapy, but it is less than that due to obesity or alcohol ingestion."

The ADA's specific prescription in the "call" is that, "Independent review of available clinical and pathologic data be conducted. Toward this end, the Association is calling on all pharmaceutical companies with incretin therapies in development or currently marketed to make patient-level data available on all subjects involved in regulatory trials for an independent analysis."

This review is guaranteed to find no problems because, a) the drug company's studies do not include any study of the actual pancreases of the subjects. Remember none of the people autopsied by Dr. Butler's showed ANY symptoms of anything amiss in their pancreases before death. b) The drug company data only covers a brief time period, far too short a period for tumors visible with image technology to develop, or for pancreatitis to occur as a result of abnormal patterns of beta cell growth. c) Drug companies have a long and ugly history of hiding data that might dissuade doctors from prescribing their most profitable drugs, and the incretins are the single most profitable drug category of most of the large drug companies.

So this "review" is guaranteed to find nothing so that the ADA's sponsors can keep selling these highly profitable drugs to every newly diagnosed person with diabetes. But any sense of security the review establishes is delusory, because  the highly abnormal cell growth that Dr. Butler found in the pancreases of all the people taking these drugs, who died with no idea that their pancreases had become abnormal,  betray the kinds of changes that though they do, eventually kill people, kill people slowly.

Pancreatic tumors are completely undetectable until they reach the point where they are almost universally fatal. They do not show up on scans until they are much larger than the tumors Dr. Butler discovered. So it may take ten years for the abnormal cell growth and small tumors found in the pancreases of people taking incretin drugs to grow to the point where they start killing the people now taking these drugs--the oldest of which, Januvia, has only been on the market for 6.5 years.

Professionals who care about the health of their patients should be calling NOT for "reviews" of existing demographic research, or relying on the drug companies to provide evidence about the drugs' safety. They should be asking why, if these drugs massively enlarge the beta cell mass of people who take them, the blood sugar of people taking incretin drugs continues to be much higher than normal, and, in fact, worsens the longer they take the drugs. (A finding documented by research discussed HERE.)

They should be looking at  the glucagon levels in people taking these drugs to see if they are abnormal, which would validate Dr. Butler's finding that the abnormal beta cells grown in response to incretin therapy secrete glucagon not just insulin.

And finally, they should demand that the ADA apologize to Dr. Butler for making completely unsupported attacks on what was a brilliantly conducted, highly technical piece of research.

It won't happen. Instead, this window dressing "review," will find, based on the fact that until now incretins haven't killed enough people to rise to significance, that these drugs are "perfectly safe."

The ADA's press releases will saturate the medical and popular press. Doctors, reassured by the findings of the review will continue to prescribe these drugs to every new patient with diabetes.  In another five or six years, when the patents on these highly profitable drugs have expired, the first wave of pancreatic cancer deaths and the pancreatitis epidemic will begin, and they will continue for years to come.

But few will know that these deaths were caused by the incretin drugs. The ADA will assure the public that this wave of deaths is just a terrible, tragic hitherto not understood complication of diabetes, since it has found all the diabetes drugs to be completely safe.

The drug companies will have booked their profits, so they won't care. The ADA's executives who commissioned the study at the request of the drug companies will be enjoying retirements funded by the huge salaries the ADA pays them, or have moved back to their original jobs as highly paid drug company lobbyists.

But you don't have to be one of the victims. If your doctor suggests you take any one of these very worrisome drugs, point your doctor to Dr. Butler's findings (which you will find HERE) and demand that he think critically about any claims of safety made by the ADA's venal flacks.

If you can't normalize your blood sugar by cutting back on carbs and exercising, stick with the safe drugs: Metformin and insulin (and Prandin for those of you who respond very strongly to beta cell stimulation.)

The drugs to watch out for are: Januvia, Janumet, Onglyza, Combiglyze, Victoza, Trajenta, Jentadueto, Byetta, Bydureon, and Victoza.  There are more in the pipeline. Any drug whose mechanism involves DPP-4 inhibition or which is a GLP-1 analog falls into the incretin family.

June 7, 2013

Phosphate Additives Promote Hardening of the Arteries

Several weeks ago I posted about the disturbing link between blood phosphate levels and heart disease, pointing out that people eating low carb diets have a unique exposure to phosphates because they are added to so many of the meats you buy at the grocery store and order in restaurants. In this post I will explain more about what these phospate additives are and why they are so dangerous to our health.

Phosphates are compounds that contain phosphorous and oxygen. They are essential to the construction of every cell in our body as phosphates make up the backbone of DNA, They form essential components in cell membranes and are essential to the proper growth of plants. Adenoside Triphosphate (ATP) is the molecule every cell uses used to store energy. Without it, we're dead meat.

Therefore we get a dose of phosphates any time we eat any meat or vegetable. These are "organic phosphates" which are deeply bound into the structure of the foods we eat--so much so that only 40-60% of the phosphate we consume is actually bioavailable. The rest goes through us undigested.

But these organic are not the phosphates that pose a threat to health. The problem phosphates are the "inorganic phosphates"--chunks of phosphate containing rock--that are added to our foods. The are commonly used as preservatives, flavor additives, and to keep cream from separating in dairy products. Phosphoric acid, which converts to phosphate in our bodies, is added to soda to keep brown sodas from turning jet black, which would make them unappealing to most people. Phosphates are also frequently used to provide the chalky white pill material that holds the supplements you buy in pill form.

Unlike the organic phosphates these inorganic phosphates are 100% bioavailable. That means if you eat 500 mg of calcium phosphate, disodium phosphate, or any of the many other inorganic phosphates added to processed foods or supplements, the whole 500 mg will be absorbed. When it is, it will go into your bloodstream where where will raise your serum phosphate level.

It has long been known that consuming inorganic phosphates can be very dangerous for  people with severe kidney disease, as failing kidneys can't remove phosphates from teh blood, and these phosphates precipitate out in the kidney, destroying what little function is left.  But while doctors may be aware of this, few of them know that consuming inorganic phosphates also poses a major risk to normal people, because it can promote heart disease.

We know from several well-conducted studies that there is a direct link between serum phosphate level and heart disease. As a recently published review article explains, " Higher serum phosphate levels were independently associated with coronary artery calcification, vascular stiffness, left ventricular hypertrophy, and carotid artery disease, even among individuals with normal kidney function and serum phosphate levels within the normal range."

A study that matched CAC scans to serum phosphate levels verified that rising serum phosphate levels correlated directly to rising Agaston scores in a population who had completely normal kidney function.

The most comprehensive  study to investigate the impact of phosphates on heart disease was a study of the Framingham Offspring. It looked at serum phosphate levels in a group of over 3,000 normal people and then looked to see which of them had developed heart disease sixteen years later. It found that:
... a higher level of serum phosphorus was associated with an increased CVD [cardiovascular disease] risk in a continuous fashion. ... Individuals in the highest serum phosphorus quartile experienced a multivariable-adjusted 1.55-fold CVD risk ... compared with those in the lowest quartile... Serum calcium was not related to CVD risk.
Does Eating Inorganic Phosphates Raise Serum Phosphate Levels? 

After reading this, I could not help but wonder if those high serum phosphate levels that caused heart disease were caused by eating diets high in phosphate or whether people destined to get heart disease migh6 have high serum phosphate levels as a side effect of an undiagnosed preexisting health issue.

Could eating a diet high in phosphates be all it took to raise serum phosphate levels? This question was elegantly answered by a study published back in 1977.

In this study subjects who were allowed to eat only the foods supplied by the researchers were, for four weeks, fed a control diet free of any phosphate additives. Then, for the next four weeks, they were fed a diet that contained the identical amount of calories, protein, fat, and carbohydrate as the control diet but this diet was made up of foods containing inorganic phosphate additives, like American cheese, soda, and processed meats.

The report explains, "The average phosphorus content of the daily menu was 979 mg during the control period and 2124 mg during the test period." After a month of eating the foods with the added phosphates, the study participants blood was tested and it was found that they had experienced a dramatic rise in serum phosphates, accompanied by a decrease in serum calcium.  The addition of the phosphates to their diets also caused digestive distress to many of the participants--in some cases it persisted throughout the whole study.

When their serum phosphate levels were measured, they were found to have "increased from 3.76 ±0.38 mg/100 ml during the control period to 4.43 ±0.30 mg/ 100 ml [mg/dl] during the high-phosphorus period."  This was an 18% rise in serum phosphate level.  So yes, upping dietary consumption of inorganic phosphates will raise serum phosphate a lot, even in completely normal people.

And it is also worth noting that the amount of phosphate being consumed by the subjects in this study is likely to be far less than that consumed by the average person today since they were being fed a controlled diet containing only 2,200 calories.  Higher caloric intakes would result in higher intakes of inorganic phosphates, and higher serum phosphate levels, too. And people eating "healthy diets" who use supplements might be getting even higher amounts, since many chalky pill substrates are made mostly of dicalcium phosphate.

How Damaging Is This Added Phosphate?

The Framingham Offspring study found that in normal participants whose serum phosphate levels were in the top quarter of readings for the whole research group at the beginning of the 16 year study   there was a 55% higher risk of developing cardiovascular disease at the end of the study .  This is a big leap in risk, especially when it is attributed to a factor that is completely ignored by doctors, health authorities, and food companies.

Though we can't be confident in comparing the blood phosphate levels in the 1977 diet study and the Framingham Offspring study, as using different lab techniques will give different reference ranges, it's worth noting that the serum phosphate value representing beginning of the highest quartile in the Framingham Offspring Study--the level at which cardiovascular risk was 55% higher--was only 20% higher than the top of the lowest quartile.

So since we have seen that boosting the phosphate intake of a 2,200 calorie diet can easily achieve an 18% rise in serum phosphate levels,  it seems very likely that dietary consumption of phosphates, alone, is enough to boost serum levels into the range that correlates with a higher risk of heart disease.

Is it the Phosphates Causing Heart Disease or Are They A Lifestyle Marker?

Since inorganic phosphate intakes rise dramatically when people eat diets high in fast food and soda, it would be easy to dismiss the link between serum phosphates and heart disease as being due not to the phosphates themselves, but to the unhealthy diet that results in those high serum phosphate levels. In short, to point to serum phosphates as a marker of a diet rich in junk food.

But there is some other research that contradicts this argument.  The researchers who published the Framingham Offspring Study cite a study that found that  "... higher phosphorus levels increase the propensity of mineral deposition in vascular smooth muscle cells in vitro."  That study found that
HSMCs -[Aortic Smooth Muscle Cells] cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition.
Furthermore,  exposure to high levels of phosphates induces a phenotypic transformation of vascular smooth muscle cells into osteoblast-like cells that express biochemical markers characteristic of the cells that turn into bone.

What this means in plain English  is that in a petri dish, cells from heart arteries were fine when exposed to normal levels of phosphates, but when the levels rose to abnormally high levels the artery cells started to act like bone stem cells and fill up with tiny bits of rock. The higher the amount of phosphate they were exposed to, the more rock.

The Framingham researchers also cite a study showing that "higher serum phosphorus levels increase circulating PTH [parathyroid hormone] levels even in healthy individuals," pointing out that "Higher PTH levels may be proinflammatory" as they raise the level of a substance, IL-6, linked to heart disease.

These findings suggest that the problem is that when you eat too much phosphate-containing rock, that rock ends up floating around your bloodstream until it precipitates out in your heart muscle (and other) cells.

Phosphate, Vitamin D, and Niacin

An interesting side note to the issue of high serum phosphate is the finding that rising serum phosphates will lower Vitamin D production as Vitamin D is one of the regulators of blood phosphate levels.  (Discussed HERE).  If you have abnormally low Vitamin D levels when not supplementing Vitamin D, this could be pointing to the fact that your serum phosphate level is unhealthily high.

In patients with kidney failure, there is some evidence that supplemental niacin lowers the very high serum phosphate levels characteristic of kidney failure, though there is no research to answer the question of whether niacin lowers phosphate levels in people with normal kidneys. But it makes a lot more sense to lower serum phosphate levels by cutting out of your diet as much inorganic phosphate as possible rather than to drive with one foot on your physiological accelerator and one on the brake, which is what you do when you attempt to lower these levels by taking a supplement while consuming the phosphates.

What's Next?

I'll be writing more about the role of inorganic phosphates in our diets and what we can do to achieve normal serum phosphate levels. For now, your homework is to start reading labels for all the foods and supplements you consume, to see how many items you eat each day contain added inorganic phosphate.

Since I started doing this, back when I published my first post about the dangers of high phosphate levels, I've been at first surprised, and then horrified, to see just how much of what I have thought of as "healthy" foods and supplements are full of these dangerous, inorganic phosphate minerals.

June 3, 2013

May Diabetes-Related News Snippets

Here are the diabetes news items posted during May, 2013 that may have some lasting value:


Jenny said...

Finally, some research that really does sound like it might go a long way to controlling Type 1 diabetes in a more physiological way.

Science Daily: Injectible Nano Network Controls Blood Sugar in Diabetics for Days at a Time

A subcutaneous network of nanoparticles releases insulin only when blood sugars rise. And yes, the "Diabetics" in this report turn out to be rodents, but I don't see any reason why the concept would work in people too, since it it the chemistry between blood sugar and the network that controls the release of insulin, not anything particularly rodent-specific.

The only challenge that leaps to mind is that humans use a lot more insulin than tiny mice, so could you inject a large enough network to provide the needed insulin?

Let's hope this isn't one of the many promising research avenues that gets bought up and buried by the drug companies who would lose a lot of money if effective treatments for diabetes were to be created.

OTOH, ten days translates into a lot of treatments, and given the obscene amounts that get charged for any truly lifesaving treatment, this one might end up too expensive to be widely deployed.

It's not clear to me from the little I have read about this whether it would be of use to people with Type 2 who are insulin resistant, probably because the amounts of insulin needed with Type 2 can be as much as 10 times higher than those needed to control Type 1. (Or at times even higher.)

Jenny said...

Yet another contributing cause to the increase in diabetes: Arsenic compounds fed chickens which turn into pure arsenic when the meat is cooked and eaten.

"Arsenic-based drugs have been used in poultry production for decades. Arsenical drugs are approved to make poultry grow faster and improve the pigmentation of the meat. ...the researchers were able to identify residual roxarsone in the meat they studied; in the meat where roxarsone was detected, levels of inorganic arsenic were four times higher than the levels in USDA Organic chicken (in which roxarsone and other arsenicals are prohibited from use)."

The FDA as is so often the case, doesn't care. You should. Besides causing cancer, arsenic has been shown to raise the incidence of diabetes.

Between the high level of phosphates in most chicken sold today which promote heart disease and the high concentration of antibiotics--and arsenic--in the meat, I think we can safely dismiss the idea that chicken is health food.

Science Daily: Poultry Drug Increases Levels of Toxic Arsenic in Chicken Meat

Jenny said...

Doctors may dismiss patient reports that statins damage their ability to think, but the effect is real. A set of studies documents disturbing changes in the neurons following statin use: "unusual swellings within neurons," described as "beads on a string."

This is research on cultured neurons in petri dishes not living people, but it seems significant, given how many people report thinking problems after taking stains.

In the petri dish, removing the statin will reverse the neurological damage. The reports from people are mixed.

Science Daily: Possible Reason for Cholesterol-Drug Side Effects Such as Memory Loss

Jenny said...

Measuring the calories in common restaurant meals shows just how out of control portion size has gotten.

"On average, the meals studied contained 1,327 calories, which significantly exceeds the estimated energy needs of an individual adult at a single meal,"

"Nearly three-quarters (73%) of the meals analyzed contained more than half of the FDA's daily energy recommendation of 2,000 calories,"

"Among the meal categories studied, the Italian (1,755 calories), American (1,494 calories) and Chinese (1,474 calories) meals had the highest average calorie levels. Vietnamese meals had the lowest calorie levels as measured by gross energy, with an average of 922 calories. The Japanese meals had the second lowest calories, with an average of 1,027 calories."

Considering that a middle aged woman of normal size can eat no more than 1800 calories a day without gaining weight, it's not surprising how easily we become. That 2,000 calorie a day intake recommendation only works for YOUNG people. With each decade your caloric needs drop, and you would have to exercise for several hours every day to make up for the change age induces.

Science Daily: Individual and Small-Chain Restaurant Meals Exceed Recommended Daily Calorie Needs

Jenny said...

Yet another well-documented cause of insulin resistance: The kinds of air pollution given off by motor vehicles. A new study documents its effect on children:

"levels of insulin resistance were greater in children with higher exposure to air pollution. Insulin resistance increased by 17% for every 10.6 µg/m3 (2 standard deviations [SDs] from the mean) increase in ambient nitrogen dioxide (NO2) and 19% for every 6 µg/m3 (2 SDs) increase in particulate matter of up to 10 μm in diameter. Proximity to the nearest major road increased insulin resistance by 7% per 500 metres. All the findings were statistically significant."

Air Pollution Increases Risk of Insulin Resistance in Children

Jenny said...

A hormone, aP2, secreted by (mouse) fat cells helps regulate the release of glucose by the liver. Suppressing the secretion of this hormone lowers blood sugar in mice.

Worthy of follow up in people to see if it holds up. Much mouse research doesn't.

Science Daily" Discovery of New Hormone Opens Doors to New Type 2 Diabetes Treatments

Jenny said...

Several recent studies have shed light on why it is blood sugar, not a diagnosis of the underlying condition that causes high blood sugar, that damages the body.

Rising blood glucose, it turns out, raises the level of various inflammatory proteins. Inflammation in turn damages the blood vessels including the arteries causing heart disease and those involved in other diabetic complications.

Lowering blood sugar prevents these changes.

Injecting Insulin also decreases inflammation.

University of Buffalo: Study: Insulin fights inflammation and even small amounts of glucose trigger it in Type 1 diabetics Note: the study also documents these effects in people with Type 2 diabetes.

Science Daily: Protecting the Heart Health of Diabetic Patients

Jenny said...

A careful study casts doubt on the theory that viral infections are what trigger the development of Type 1 diabetes in children.

Diabetes Daily: No Link Found Between Viral Infection and Rapidly Developing Type 1 Diabetes in Young Children

Jenny said...

Marijuana users have better blood sugar control

NHANES data. Is this effect from smoking dope, or do people with normal blood sugar self-select ad habitual users, since they don't get overpowering munchies when they smoke and thus find it more enjoyable?

Jenny said...

Yet another large, long population study finds that taking high potency statins raises the risk of developing Type 2 Diabetes.

Conclusion: "Compared with pravastatin, treatment with higher potency statins, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset diabetes."

22% higher risk with Lipitor (atorvastatin) and 18 percent higher with Crestor (rosuvastatin).

In mainstream press coverage, Drug company shills,, a.k.a. well known cardiologists, bend over backward to ignore this latest confirmation of a phenomenon that has been public knowledge for more than a year.

The reason that statins cause diabetes may have to do with the fact that they impair the operation mitochondria--the part of the cell that burns glucose, which is why you are supposed to take Coenzyme Q10 with them

Risk of incident diabetes among patients treated with statins: population based study BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f2610 (Published 23 May 2013)

In press coverage

Jenny said...

As I have been writing for years, the condition called "Type 2 Diabetes" is actually many different conditions with different genetic causes. Ethnicity plays a huge role in the kind of diabetes a person might have. The degree to which the problem is lack of insulin secretion or high insulin resistance varies greatly too.

Science Daily: Diabetes Genetic Underpinnings Can Vary Based On Ethnic Background.

This points out just how stupid most rodent research is, as the "Type 2 Diabetes" that lab rodents get is caused by completely different genes than the ones that affect humans. Even in the rare cases when they insert a human gene in a rodent, it is one that causes diabetes in only a small subset of humans.

But mouse research is a lot cheaper than research in humans and there are too many people who have built careers and got inside tracks on grant money using rodents for the situation to change.

Bottom line, remember that eating fat does not cause diabetes in anything but rodents selected as "Models" of diabetes because they get diabetes when they eat fat. Humans get diabetes when they eat more carbs than their genetically weak bodies can tolerate.