Studies Shed Light on Falsification and Bias in Medical Studies

First off, I apologize for the drop off in post frequency. One "side effect" of getting a three book contract from a major publisher, as exciting as it is, is that I have to write the two sequels to the first book I sold. That gives me less time to read and report on the diabetes news. I'm still at it, but I'm blogging only about issues that stand out to me as important or those that readers write me email about.

I'm pleased to see that the most recent, extremely poorly designed study intended to prove that low carb diets will give people heart attacks has not raised a furor.

My readers, and most other people who know anything about science, realized that genetically engineering a mouse to be unable to process fat without developing heart disease and then feeding that mouse fat and giving it heart disease proved nothing except that some people will stop at nothing to defend a discredited theory.

Unengineered mice do not get heart disease eating fats. A large number of studies have found that humans do not get more heart disease eating a low carb/high fat diet. You can find links to these studies and to those proving that cutting out fat does not lower heart attack risk in humans HERE.

I also read in another blog that the "high fat" diet these particular mice were fed included a lot of fructose, which we know has a toxic effect on the liver and cardiovascular system.

The way in which these scientists tortured study design to come up with a study that would yield a finding satisfactory to those who share their religious beliefs (eating fat is bad!) along with something else that happened last week, made me think it was time to discuss a study I ran into last year that examined the question of how often scientists consciously misrepresent and skew data. The findings of that study, which got almost no play in the press, were horrifying.

The other thing that brought this to my attention was a visit to a specialist who wanted to prescribe me Celebrex for a foot problem. If you'll recall, Celebrex is a drug very similar to Vioxx--the pain killer that turned out to be a patient killer, thanks to its ability to promote heart attack.

Celebrex is still on the market, thanks to research that appeared to make it look slightly safer than Vioxx, though the official FDA prescribing information includes a warning that it may promote heart attack. What this doctor did not seem to know was that much of the data that had shown Celebrex to be effective turns out to have been faked, as you can read in this March 10, 2009 report published in the Boston Globe:

Springfield doctor accused of fabricating research results.

The specialist who wanted me to take this dangerous drug practices out of the same hospital as the fraudulent researcher. Current prescribing recommendations for Celebrex make it crystal clear it should never be prescribed to anyone with any possible heart disease, which means it should never be given to someone with diabetes. Deleting the fraudulent studies suggests that the very expensive Celebrex is no more effective than Tylenol, too. Nevertheless 2 billion dollars worth of Celebrex is still being prescribed each year. Probably by doctors unaware of the fraudulent research suppporting it's effectiveness.

Which brings me to the study that looked at how common such fraud and other research malfeasance might be. You can read the study in its entirety here:

How Many Scientists Fabricate and Falsify Research? A Systematic Review and Meta-Analysis of Survey Data. Daniele Fanelli. PLos One 4(5): e5738. doi:10.1371/journal.pone.0005738 (May 29, 2009).

This was a metastudy--a study that combined and analyzed data from other, smaller studies. It found,

A pooled weighted average of 1.97% (N = 7, 95%CI: 0.86–4.45) of scientists admitted to have fabricated, falsified or modified data or results at least once –a serious form of misconduct by any standard– and up to 33.7% admitted other questionable research practices. In surveys asking about the behaviour of colleagues, admission rates were 14.12% (N = 12, 95% CI: 9.91–19.72) for falsification, and up to 72% for other questionable research practices.

This is a horrific finding. Almost 2% of the scientists admitted (anonymously) to out right fraud. One third admitted "other questionable research practices" which included doing things like ignoring other previously published studies whose results would cast doubt on their own, nonpublication of results unfavorable to a sponsor like a drug company, and "altering and modifying data “to improve the outcome”".

That is bad enough, but the study also looked at what happened when you asked scientists not to report on their own behavior but about that of their colleagues.

Do that and the incidence of reported fraud (outright falsification and fabrication--making things up) goes up to 14.12--meaning one in seven scientists reports observing such behaviors in peers. The reports of other questionable research practices shoots up to 72%--meaning a whopping majority of these scientists believed they had observed these behaviors.

This should give you pause, because these statistics, as the authors point out, require people to admit to malfeasance, which we know many will not. The actual incidence of intentional research fraud is therefore likely to be much higher.

Another study on a similar topic analyzed impact that drug company sponsorship or the existence of financial ties between researchers and drug companies on the design and findings of studies of Actos and Avandia, the TZD drugs.

You can read this research, in full here:

Factors Associated with Results and Conclusions of Trials of Thiazolidinediones Gail Rattinger1, Lisa Bero. PLoS ONE 4(6): e5826. doi:10.1371/journal.pone.0005826. June 8, 2009.

The researchers here examined

61 published RCTs [random controlled trials] comparing a thiazolidinedione [Avandia or Actos] to another anti-diabetic drug or placebo for treatment of type 2 diabetes. Data on study design characteristics, funding source, author’s financial ties, results for primary outcomes, and author conclusions were extracted.

They found that trials that reported favorable glycemic control results for the glitazone were four times more likely to have a corresponding author with financial ties to the glitazone manufacturer (OR (95% CI) = 4.12 (1.05, 19.53); p = 0.04)."

In addition, "trials with conclusions favoring the glitazone were less likely to be funded by a comparator drug company than a glitazone company." Studies showing favorable results for Avandia and Actos also were "less likely to be published in journals with higher impact factors," i.e. the journals that apply more rigorous peer review to articles before accepting them for publication.

The authors note one factor that makes it likely that the real impact of drug company money on study results is much higher: Though 59% (36/61) of the trials studying Actos and Avandia were funded by industry, "39% (24/61) did not disclose any funding" This makes it very likely that many more of these studies were supported by and skewed by researcher financial ties with the drug companies.

Put the results of these two studies together and what emerges is not pretty. For every doctor whose fraudulent research, delivered in response to the marketing needs of his drug company paymasters, is exposed--as happened to Scott S. Reuben, MD of Baystate Medical Center in Springfield, MA, whose work impelled other doctors to prescribe the questionable drug Celebrex, dozens or perhaps even hundreds go undetected.

The fact that at least 59% of all studies of Actos and Avandia were sponsored by drug companies with a stake in proving them effective, or comparing them unfavorably with their own drugs, and that we don't know the sponsorship of another 39%, makes it crystal clear how little research about the effects of the drugs we take is untainted.

Scientists who are in the pay of drug companies face a lot of pressure to deliver the results their masters demand. The tools at their disposal include outright fraud, or the more subtle techniques described by Ms. Fanelli in the first study above: Neglecting to cite studies casting doubt on the desired result. "Tweaking" statistics, not publishing studies with results showing poor outcomes with the drug, designing studies with flawed methodologies intended to produce the desired result. Etc. etc.

All this should explain to you the reason I look with such skepticism on the drug and food studies that get such play in the press and why I analyze their methodology looking for signs that the study was designed to produce a certain result. In many cases the bias is obvious to anyone who hasn't drunken the drug company Kool-Aid, though apparently not to the peer reviewers.

By the same token, what these studies have not looked at, but what would also result in some useful information, is the extent to which drug company funding raises the likelihood that a study will be reported in the print and TV media outlets that are so dependent on drug company income for their revenue.

Very few of the studies I see that were done by scientists not affiliated with drug companies or other powerful interests make it into the health news headlines--especially not those studies that contradict the findings of the drug company supported research.

As readers of my blog know, I reported years before these topics hit the headlines about the link between Avandia and Actos and heart failure, macular edema (a cause of blindness) and osteoporosis. These studies were ignored by the mainstream press. The mainstream press has yet to publish a word about the problems with the DPP-4 inhibitors, though a considerable body of research suggests they may be promoting cancers. When Avandia was finally revealed for the questionable drug it is, the media jumped on the bandwagon suggesting Actos was a safe alternative, though the data connecting Actos to heart failure and broken bones is identical to that involving Avandia.

In short, it's a jungle out there, and your doctor is much too busy to do the detective work it takes to protect you from the dangerous drugs, whose utility is supported by fraudulent research.

Another Cause of Diabetes? Weed Killer in Many Water Supplies Damages Mitochondria and Produces IR

An investigative journalist has learned that the EPA has failed to pass on to the public the information that drinking water in four states and more than 40 municipal water systems contains levels of atrazine, a commonly used herbicide, that violate federal safety standards.

Huffington Post: EPA Fails To Inform Public About Weed-Killer In Drinking Water

Why should you care? Because researchers have found "There is an apparent overlap between areas in the USA where the herbicide, atrazine (ATZ), is heavily used and obesity-prevalence maps of people with a BMI over 30."

Authors of a study that looked closely at this relationship explain,

Given that herbicides act on photosystem II of the thylakoid membrane of chloroplasts, which have a functional structure similar to mitochondria, we investigated whether chronic exposure to low concentrations of ATZ might cause obesity or insulin resistance by damaging mitochondrial function.

They conducted a rat experiment to see exactly what happened to mitochondria in mammals exposed to this herbicide. You can read the full study here:

Chronic Exposure to the Herbicide, Atrazine, Causes Mitochondrial Dysfunction and Insulin Resistance. Lim S, et al. PLoS ONE 4(4): e5186. doi:10.1371/journal.pone.0005186

This study found "Chronic administration of ATZ [atrazine] decreased basal metabolic rate, and increased body weight, intra-abdominal fat and insulin resistance without changing food intake or physical activity level".

The effect was worsened in rats fed a "high fat diet" (which we will look at more closely further on in this post.)

When the researchers looked at the mitochondria of the rats exposed to atrazine, they found

Mitochondria in skeletal muscle and liver of ATZ-treated rats were swollen with disrupted cristae. ATZ blocked the activities of oxidative phosphorylation complexes I and III, resulting in decreased oxygen consumption. It also suppressed the insulin-mediated phosphorylation of Akt [emphasis mine].

These results suggest that long-term exposure to the herbicide ATZ might contribute to the development of insulin resistance and obesity, particularly where a high-fat diet is prevalent.

The "high fat diet" fed the rats--which worsened the effect of this herbicide on obesity--is worth a look. This "high fat" diet was made up of

33.0% shortening, 7.0% corn oil, 10.0% sucrose, 13.2% dextrose, 5.0% cornstarch, 5.0% cellulose and 20.0% casein (by weight).

So it was in fact a high transfat and Omega 6 oil diet that was very rich in sugar. This is a very unhealthy diet quite apart from the fat percentage.

The HuffPost article reports that water customers in some Midwestern cities were sent reports of atrazine levels in their water that underreported actual levels by a factor of 10. According to the article:

based on the quarterly tests, residents of Mt. Olive, Ill., were told that the highest level of atrazine in their drinking water last year was 2 ppb. However, the EPA data shows a spike in June of 16.47 ppb. The same year, residents of McClure, Ohio, were told that the highest level of atrazine in their drinking water was 3.4 ppb. The EPA data shows a spike in June 2008 of more than ten times that amount -- 33.83 ppb.

The states where the highest levels have been reported are Illinois, Indiana, Ohio, and Kansas.

The EPA insists that atrazine poses no public health threat, though male frogs exposed to this herbicide have been known to produce eggs.

Perhaps, the levels of this herbicide might be safe, were they the only persistent organic pollutants (POPs) the public was exposed. But this chemical is only one of the POPs mixing in our blood streams. It joins detectable levels of bisphenol-a, the fertility-impairing organic fluorine compounds that leach from nonstick pans, the birth control pill hormones and pharmaceutical drugs that have leaked into public water supplies, and the pesticide residues that we get from the foods we import from all over the world.

These pollutants in our blood stream probably work synergistically. So the combined effect of all these chemicals may be far more destructive than that of each chemical in isolation.

Obviously, those who will show the strongest impacts from this exposure fall into two groups. The people with the greatest exposure: those who work with these chemicals or live in the most polluted neighborhoods, and those who have genes that already make them prone to insulin resistance and mitochondrial dysfunction. This latter group includes many people with family histories of Type 2 Diabetes.

We know that young, slim relatives of people with Type 2 diabetes often already have signs of mitochondrial dysfunction and higher than normal insulin resistance. (Details, HERE). When these people drink water that contains additional damaging factors like this herbicide they are likely to experience an escalation in insulin resistance,and as we know, as insulin resistance rises, so does post-meal blood sugar, hunger levels, and eventually, weight.

Read the HuffPost article, and if you live in one of the regions discuss, demand that your municipal authorities tell citizens the truth and let the EPA know that you do not want yourself or your children drinking water with detectable levels of a herbicide known to promote insulin resistance and obesity.

UPDATE: September 2, 2009: More insight on how the manufacturer of atrazine herbicide has used its influence to get the EPA to declare atrazine safe despite the evidence here:

HuffPost: Syngenta, Maker Of Weed-Killer Atrazine, Wants Lobbying Documents Excluded From Class-Action Lawsuit

 

Antidepressants NOT Depression Associated with Obesity

There is a major contributor to the so-called "obesity epidemic" which never gets cited in the press--the antidepressant drugs which are the most frequently prescribed class of drugs in the pharmacopoeia.

Now a study that analyzes data from the Canadian National Population Health Survey (NPHS), a longitudinal study of a representative cohort of household residents in Canada, finds a strong correlation between the use of SSRIs, Effexor, and the development obesity. Lest you think that this is because depression makes people fat, this same study found no correlation between a history of a major depressive episode and the development of obesity.

It's the drugs, folks.

Here's the study:

Major Depression, Antidepressant Medication and the Risk of Obesity
Scott B. Patten et al. Psychother Psychosom 2009;78:182-186 (DOI: 10.1159/000209349) Vol. 78, No. 3, 2009

How widespread use of these antidepressant drugs is, is very hard to pin down. Anecdotally, it sometimes seems like everyone who has good health insurance is on them.

A report published in 2005 that analyzed Canadian data reported that "...one in five women (19%) in the province over the age of thirty received at least one prescription for SSRIs in the period between August 1, 2002 and July 30, 2003."

Canada's public health system controls access to prescriptions in the way the US system does not. The data for the US is 7 years old and at that time the CDC reported that 1 in 10 American Women were taking antidepressants which were the single most highly prescribed class of drugs in the US. That 2002 report also reported that antidepressant use had tripled over the previous decade, which makes it likely that antidepressant use has risen significantly in the 7 years since those statistics were analyzed.

The Canadian report also points out that

Prior to the introduction of SSRIs, depression was considered to affect only 100 people per million. Since the introduction of SSRIs, prevalence rates for depression are now considered to be in the range of 50,000 to 100,000 cases per million (a 500 to 1,000 fold increase).

One reason for this huge spike in prescriptions is, of course, the heavy marketing by pharmaceutical companies of these drugs--especially to family doctors not trained in psychiatry who are the doctors most likely to prescribe them.

It has long been known to psychiatrists that fully 1/3 of all people who experience episodes of depression recover naturally without any treatment. This is close to the rate of recovery experienced with the antidepressant drugs, however, the drug companies suppressed publication of the studies that would have made it evident that their drugs were often not any more effective than placebo.

You can read one study documenting the impact of drug company suppression of unfavorable research evidence HERE.

In addition, drug marketers deceptively promoted the factoid that that repeated episodes of depression are likely to lead to a form of permanent brain damage resulting in permanent depression. This is a twisted rendering of data that applies only to extremely severe depression of the kind that results in people being institutionalized because they cannot function at all. That kind of depression does not result from negative life experiences but appears to be a brain syndrome like schizophrenia. It is a very different kind of psychiatric condition from the bouts of sadness most people experience at some point of their lives when they suffer a serious loss or find themselves trapped in a situation, like a bad marriage or dead end career.

But this idea that one depressive episode, if not treated, will condemn a person to a life of worsening depression, has been used to scare family doctors into treating the normal periods of sadness characteristic of young people, who are facing the emotional challenges of growing up, as if they were medical emergencies.

People experiencing the normal struggles of adolescence and young adulthood are told that if they don't take the antidepressant drugs they'll end up permanently depressed. When they start feeling better after a month or two on the drugs--as they would without drugs--they are convinced that the drug saved them and are terrified to stop taking it.

Anyone who went through adolescence in the pre-antidepressant days knows it is not true that the periods of depression so common in early life invariably turn into severe psychiatric disease. Most of us grew out of the miseries of adolescence and have normal happy lives no matter how miserable we were when we broke up with our first serious boyfriend.

For many of us, depression was a signal that we needed to get help to learn why we made bad choices or to take the steps needed to get ourselves out of the dead end situations we had become trapped in. Sometimes therapists were helpful in giving us tools that made it possible to do this. Medicating the bad feelings away may prevented us taking those steps or making those changes which improved our lives and eliminated the causes of our depression.

But for the past decade any teen (or adult woman, for that matter) who experiences overwhelming sadness after breaking up with a boyfriend--or after failing to find an exciting career after earning a college degree in English--is very likely to be put on a powerful, mind altering SSRI drug that numbs their emotions--a drug, moreover, that can be extremely hard to stop since it causes withdrawal symptoms. Any teen with insurance, that is, since these drugs can be very costly.

And once people are, essentially, addicted to these mind-altering drugs, they do what all people who are dependent on mood-altering drugs do--defend their need to take the drugs very strongly and often with anger at any one who would take them away from them.

Because people who take these drugs have not learned that depression can be healed without drugs, and have not been taught the psychologically proven strategies that could help them cope with depressive episodes on their own, they are very frightened of what would happen if they stopped the drugs. Since the withdrawal symptoms when they do stop the drugs can be extremely unpleasant and long lasting, they may interpret this as proof that they need these drugs.

The common analogy--promoted heavily by the drug merchants, is that people with depression need SSRIs the way people with diabetes need insulin. This makes it sound like these drugs supply some essential, missing hormone.

In fact, this is completely untrue. The drugs don't supplement serotonin. It is not even clear if they actually raise serotonin levels long term. As the Canadian report point out, "there have been no studies that assess the effects of blocking serotonin over months or years. Most of the forty-two clinical trials for Prozac, Paxil, Zoloft, Celexa, Serzone and Effexor lasted only six weeks." Studies of other impacts of altering Serotonin levels in the gut suggest that long term use of SSRIs may actually lower Serotonin levels.

Some recent research suggests that these drugs actually work by remodeling the neurons in the hippocampus.You can read about what SSRIs really turn out to do, long term HERE.

Other drugs that affect Serotonin levels include Ritalin, Cocaine and Ecstasy. We know these drugs are addicting, but somehow the drug companies have been able to convince doctors that their mood-altering drugs are "habit forming" but not "addicting" though doctors also warn patients that it is dangerous to suddenly stop these drugs,just as it is with addicting drugs.

What all makes this relevant to diabetes is this: There has always been evidence that the SSRI drugs make people gain weight. Now this latest analysis of the Canadian health survey data makes it clear that the weight gain is almost certainly a side effect of the drugs, not of the depression that might have led to the prescription of the drug.

Obesity raises insulin resistance even in people with normal genes. For those of us who have the genes that lead to diabetes--genes that mean that even when we are thin our beta cells are barely keeping up with our insulin needs--the increase in insulin resistance obesity can push us into full fledged diabetes and by the time that diabetes is diagnosed, the high blood sugars we have lived with for years may have killed off so many of our beta cells we don't have a chance of regaining a normal blood sugar metabolism through weight loss.

Indeed, it is not irrational to wonder if the fact that these drugs are the single most frequently prescribed class of drugs in the US may have something to do with the development of the so-called "Obesity epidemic." SSRIs began to be prescribed in the late 80s. The "obesity epidemic" started catching the public's attention a decade later.

Yes, there are many other contributing factors to the obesity epidemic, including a huge growth in portion size. But when you mess with the brain chemistry involved in the pleasure response, one of the things you also do is mess with the in-built brain mechanisms that control satiety--the feeling that you've eaten enough.

A person with an intact brain satiety function is not likely to be able to eat a whole 10.5 ounce cinnamon roll at once. If they do, they will experience unpleasant emotional responses that are the body's way of teaching them that this is NOT something they should do again. Block those emotions, and they will do it again.

If you have become inadvertently addicted to mood altering drugs and believe that they are contributing to your weight problem and worsening your blood sugar control, you will probably need some help to get off them. A therapist who can help you deal with the emotions you will feel when you stop anesthetizing your feelings can be essential. A doctor who knows how to help you deal with the withdrawal symptoms in a way that does not involve putting you on another addictive drug is also essential.

Unfortunately, doctors have been prescribing antidepressants to pregnant women for the past decade too, which may have something to do with the concomitant epidemic of toddler obesity. How is it possible doctors have not considered the long term physiological consequences of exposing fetuses to a drug that remodels the neurons in their brain that control essential brain structures, while the brain is forming?

One reason is that few doctors have the time to read the research about the drugs they prescribe and so they don't understand what SSRIs really do, since they get all their information about these drugs from the drug company reps and the "education" the drug companies sponsor.

But thinking people cannot help but realize that thanks to aggressive drug company marketing a huge sector of the population--much of it young and female--and their babies--have been the subject of a decades long experiment to find out what it is that these drugs really do. The signal that is emerging out of the the very small amount of research NOT funded by the makers of these powerful, profitable drugs, is that they make people obese.

Note: In the comments that respond to this post, I'm asking you to limit your comments to discussion of the relationship between antidepressants, obesity and diabetes and the research connecting these topics. I am not going to make public the fervid and often hostile personal testimonials that are always provoked by any attempt to discuss the research that examines the true impact of these drugs. So don't waste your energy or mine posting them here.

Lots of Interesting New Diabetes News

There have been quite a few bits of recent diabetes news that don't, individually, rate a blog post, but are well worth your attention. You can find them on my other blog, the one that tracks updates to my main diabetes web site Blood Sugar 101.

This widget will give you the links:


Also, check out this exciting bit of news which Scott Strumello has just brought my attention to:

Exsulin Corporation Announces Publication Of Phase 2 Trial Results For Novel Islet Regeneration Treatment In Type 1 & Type 2 Diabetes

I've been hearing about INGAP almost as long as I have been following diabetes. This INGAP trial (the drug has been renamed) involves a peptide that appears to actually regenerate islet cells in both Type 1 and Type 2 diabetes. Most importantly, the increased C-peptide values remained "after washout" i.e. after the drug was discontinued.

The company behind INGAP has had a lot of trouble getting funding over the years, probably because a cure would rob big pharma of its chronic disease cash cows.

Let's pray that the next stage of testing of this drug finds it to be safe and that some company that cares more about your health than its profits will get behind it.

 

Can Type 2 Diabetes Be "Reversed?"

This is a question a lot of my readers ask me. Their doctors may tell them that if they lost weight they'd reverse their diabetes and there are books on the market that claim the same thing.

Unfortunately, the concept of "reversing" diabetes doesn't hold up well to scrutiny.

The media version is that Type 2 Diabetes is caused by gluttony and sloth and can be prevented or cured by diet and exercise, but the truth is quite different. The research makes it it very clear that overeating doesn't cause diabetes. You can read the documentation for this HERE.

This should help you stop blaming yourself for your condition if you have Type 2 diabetes, but it also implies that if you have the underlying condition, which manifests clear clinical indicators when people with diabetic heritages are young and thin, you aren't going to cure the underlying condition with simple interventions.

But what about the studies where interventions "prevent" diabetes? Well, a lot of them turn out to be studies where a group of people with marginal blood sugars--for example an average fasting blood sugar of 123 mg/dl (6.8 mmol/L)-- do something that keeps their blood sugar at 123 mg/dl compared to another group who start out the same but end up with a blood sugar of 126 mg/dl (7 mmol/L). Because diabetes is diagnosed with strict cutoffs, and the fasting cutoff for diagnosing diabetes is 125 mg/dl (7 mmol/L), the first group "prevents diabetes" and the second develop it. The actual difference between the two groups is minuscule and they both have the same likelihood of developing diabetic complications.

This is what happened in the DPP trial that supposedly found metformin "prevented" people with pre-diabetes from developing diabetes. As soon as the study was over, when the people taking metformin stopped taking it their blood sugar rose the couple of points that put them into the diabetic range. Had they prevented diabetes? Of course not. They had controlled their marginal blood sugars a bit, which is something else entirely.

Weight loss can make blood sugar control easier, and there are studies of people who have pre-diabetic blood sugars that make it look like losing weight can "prevent diabetes." But it is worth remembering that the vast majority of the obese who have pre-diabetic blood sugars will never develop diabetes. So interventions where people with pre-diabetes lose weight and with it the insulin resistance caused by overweight may make it look like they "prevented diabetes" but the intervention may have only been effective in those people whose marginal blood sugars were caused by factors other than the genetic damage that leads to diabetes--people, in short, who would never have developed diabetes.

It is also possible that the diet "prevented" diabetes by cutting hundreds of grams of carbs out of the diet--this happens when you cut way down on food. So blood sugar did drop--while the diet was in force, but will come right back up once the diet is abandoned, as most diets are.

This appears to be the main reason that gastric bypass appears to "reverse diabetes." As I blogged earlier, the long term data do not support this claim and over time people whose blood sugars improved with WLS see them deteriorate again.

Indeed, over my eleven years of interacting with the diabetes community online I have met a lot of people with diabetes who have lost enough weight to make it into the normal BMI range who have maintained their weight loss. I did that myself. I have never met anyone with diabetes whose blood sugars became truly normal after losing weight.

Now before I get a load of email from those of you who have cut the carbs, lost a lot of weight, and now have A1cs of 5.0 and fasting blood sugars of 83 mg/dl I want to take a moment to discuss what I mean by "truly normal".

True normal to me means you can eat anything and end up with a blood sugar under 100 at 90 minutes past mealtime. My son can do that. My 93 year old mother can do that. They don't have diabetes genes and they can metabolize any amount of carbohydrate. That's what I consider true normal. Roughly one third of the population appears to have that kind of blood sugar control.

Normal people are the ones who can go on a low fat diet and drop weight without feeling hungry--and who insist we people with diabetes should be able to do the same thing. Because they really can eat bananas on their oatmeal and see completely normal blood sugars, normal people have no clue what we people with diabetes are up against. And sadly, many doctors and nutritionists appear to have normal blood sugars which is one reason they give such flawed advice to the rest of us.

But those of us who have damaged glucose regulation systems are never going to be normal by that definition. If we think we will, because that's what the doctors tell us, and deny our selves food, overwork ourselves at the gym, because of that belief, only to learn we still can't eat a single bagel at coffee break without seeing our blood sugars soar, we may end up very disappointed indeed.

I believe one reason so many people with diabetes give up after a few years of pursuing diet and exercise is because they don't see the promised "reverse" no matter how hard they work--especially if they use the low fat strategies that too many dietitians and doctors still promote.

But this is a shame, becuase while we can't reverse our diabetes we can control that diabetes.

"Control" means doing whatever it takes to give ourselves normal blood sugars. The people in the metformin study were controlling their blood sugars, not reversing their pre-diabetes. People who cut way back on their carbohydrate intake are controlling their diabetes. People who take a brisk walk after dinner to lower their blood sugar are controlling their blood sugar.

Control is different from reversal in that as soon as you stop using the tools and techniques of control your blood sugars will start climbing right back up.

It may take a couple weeks for the deterioration to set in. I often hear from people who report that have been eating low carb diets for months and have lost weight who say that when they eat carbs now they get much better blood sugars. They probably do, but if they keep eating carbs they will see those blood sugars start rise again and they'll also start gaining weight because the rising blood sugars will trigger the secondary insulin resistance which causes weight gain.

Once you have established good control, you can take the occasional day off without harm. But when the occasional turns into the daily, you will quickly learn the difference between control and cure.

You may have been told some drugs can "rejuvenate beta cells" and that they can reverse your diabetes. This claim has been made (and debunked) for Avandia, and is now being made, very loudly for Byetta and Januvia, though without compelling proof.

In fact, I have never yet seen a single study where the blood sugar improvements produced by a drug lasted for any significant time after the drug was discontinued. With one sole exception: people with Type 2 diabetes who are given insulin for a few weeks at diagnosis appear to have much better blood sugars years later. Details HERE. Unfortunately, very few people are given insulin at diagnosis. Instead they are given oral drugs, and none of them produce lasting effects when discontinued.

Someday science may find ways to truly reverse diabetes. But for now we have to be grateful we have learned how to achieve effective control. Because control works. If you keep your blood sugars normal you can avoid diabetic complications. The best way to do this is to follow the advice you'll find on HERE.

But when you find a method of control that works, don't expect your diabetes to go away. Because your diabetes wasn't caused by overeating or lack of exercise, it can't be cured by those tools either. Your diabetes can be managed, superbly, and we have to be grateful for that. But I'd like to see a cure and for me a cure would mean that I could stop counting carbs, stop testing blood sugar and have the same rock solid normal blood sugars a normal person would have.

The drug companies are not working on cures, because if you were cured you wouldn't need to buy $400 dollars worth of their drugs every month. Their drugs provide only control, and not very good control at that. Until we start funding research that is not undertaking to fatten someone's bottom line things are going to stay that way. Why kill the golden goose?

Drug companies sell doctors (and the public) the idea that their drugs do reverse diabetes. The media tell the public people with diabetes could prevent their condition and save the public a ton of money with a few "simple lifestyle changes."
Don't be taken in. We need cures and true reversal of diabetes and the first step to get there is for society to get out of denial.

The only way we will prevent diabetes is to eliminate the toxic pesticides and other pollutants that flow through our blood streams and modify the brains and pancreases of our fetuses. We need to stop prescribing SSRI drugs that modify blood sugar metabolism to every teenager who breaks up with their boyfriend. We need to realize that plastics are bioactive and get them out of our food supply--and our blood streams. We need to demand that fast food outlets take the MSG, transfat and high fructose corn syrup out of their offerings.

Once people have diabetes, we need to stop blaming them for it, and put some public money into looking for interventions that will really cure them, not just control them.

Will any of this happen? Not likely. Too many people make money from poisoning our environment and selling us bio-destructive products. But that is what we need.

UPDATE August 19, 2009: A day after I published this post, Scott Strumello drew my attention to this incredibly exciting piece of news:

Exsulin Corporation Announces Publication Of Phase 2 Trial Results For Novel Islet Regeneration Treatment In Type 1 & Type 2 Diabetes

I've been hearing about INGAP almost as long as I have been following diabetes. This INGAP trial (the drug has been renamed) involves a peptide that appears to actually regenerate islet cells in both Type 1 and Type 2 diabetes. Most importantly, the increased C-peptide values remained "after washout" i.e. after the drug was discontinued.

The company behind INGAP has had a lot of trouble getting funding over the years, probably because a cure would rob big pharma of its chronic disease cash cows.

Let's pray that the next stage of testing of this drug finds it is safe and that some company that cares more about your health than its profits will get behind it.