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Saturday, January 13, 2018

Insulin Treatment in Diabetes ~ Why Does It Often Cause Weight Gain?


Diabetes, whether Type 1 or Type 2, is a dysfunctional, wasteful metabolic state.  As a result, an uncontrolled diabetic either uses or loses more energy than their non-diabetic selves would otherwise use.  As such, the untreated diabetic is essentially "underweight" compared with the body weight that the same energy intake would produce were they not diabetic.

There are differences in endogenous insulin production between the two types of diabetes.  In Type 1, there is effectively no insulin production.  In Type 2, there is usually elevated basal insulin production, but a relative deficiency in acute insulin secretion, specifically an impaired early insulin response to glucose (GSIS). 

The absolute or relative insulin deficiency results in the following to a greater or lesser degree:
  1. Excessive lipolysis resulting in an increased cycling of the Triglyceride/Fatty Acid cycle.  
  2. Impaired suppression of glucose production in the liver, specifically an increase in glucose production via gluconeogenesis.
  3. Glycosuria (sometimes called glucosuria) due to impaired re-uptake of glucose in the kidneys and/or hyperglycemia exceeding re-uptake capacity.
All three of these are "Calories Out" in the Calories In - Calories Out (CICO) energy balance model.   Thus to greater or lesser degrees, diabetic individuals have greater energy expenditure.  When insulin therapy corrects these, energy expenditure is reduced.  Thus if the treated diabetic continues to consume their habitual amount of food, they will gain weight accordingly.   This is in contrast to the often postulated model whereby insulin treatment either induces hunger and overeating due to hypoglycemia, or the thoroughly debunked TWICHOO (aka the Carb-Insulin Hypothesis/Model) whereby insulin magically traps fat made from carbs in the fat cells thereby starving the rest of the body and causing hunger and overeating.  

The diabetic state also increases protein turnover rate, but this post focuses on the energetics.  While protein breakdown and synthesis require energy, the difference doesn't seem to be significant compared to total energy expenditure or the contributions of the three processes listed above.

Recently Dr. David Ludwig (Top-Menace-In-Nutrition-Research) tweeted out the following:

Fearing his impending muttering old man status, science "journalist" Gary Taubes dutifully retweeted.  

See what Taubes did there?  There's no serious person who is making the claim that fat mass cannot be altered independently of caloric intake.   That only looks at one side of the energy balance equation, and it is well known that the there are many ways to alter CO = Calories Out without changing CI = Calories In.  Just off the top of my head:  sitting naked in a cold room, DNP, nicotine, running around the block, reading Taubes' drivel and banging your head against the wall repeatedly ...   etc. etc. ...

I retweeted Ludwig's tweet with commentary, because this study -- even if you only read the abstract! -- does not support the fallback version of TWICHOO put forth by Ludwig in his book Always Hungry.   That version of TWICHOO, commonly described as some sort of internal starvation, goes something like this:  Eat carbs, secrete insulin, insulin sweeps calories out of circulation into the fat cells, energy is trapped in fat thereby depriving the other cells of energy, this makes you hungry and eat more.    You can mentally conjure up Gary Taubes droning on:  "you overeat because you're getting fat, you don't get fat because you overeat".  In the end, even TWICHOOBs, including both Taubes himself, and Ludwig, acknowledge the role of overeating in the development of obesity.  


Long-term, intermittent, insulin-induced hypoglycemia produces marked obesity without hyperphagia or insulin resistance: A model for weight gain with intensive insulin therapy
ABSTRACT:  {emphasis mine}
A major side effect of insulin treatment of diabetes is weight gain, which limits patient compliance and may pose additional health risks. Although the mechanisms responsible for this weight gain are poorly understood, it has been suggested that there may be a link to the incidence of recurrent episodes of hypoglycemia. Here we present a rodent model of marked weight gain associated with weekly insulin-induced hypoglycemic episodes in the absence of diabetes. Insulin treatment caused a significant increase in both body weight and fat mass, accompanied by reduced motor activity, lowered thermogenesis in response to a cold challenge, and reduced brown fat uncoupling protein mRNA. However, there was no effect of insulin treatment on total food intake nor on hypothalamic neuropeptide Y or proopiomelanocortin mRNA expression, and insulin-treated animals did not become insulin-resistant. Our results suggest that repeated iatrogenic hypoglycemia leads to weight gain, and that such weight gain is associated with a multifaceted deficit in metabolic regulation rather than to a chronic increase in caloric intake.

There are some important things to keep in mind with this study:  

  • It was in rodents.  This does not dismiss the results of the study, but it has been demonstrated repeatedly that very small animals expend a far greater proportion of their resting metabolic rate on maintaining body temperature than do larger animals like humans.  Therefore they have a greater capacity to "blow off" excess calories as well as to conserve.  
  • It involved exogenous insulin -- e.g. an artificial addition of the hormone.  This does not mimic hyperinsulinemia in intact rodents or humans.
  • Insulin was given to non-diabetic rats specifically to promote hypoglycemic episodes.  This is not the same as some diabetics miscalculating their insulin needs to combat hyperglycemia thus eliciting a hypoglycemic response.
  • Glucose is always the majority energy substrate in circulation.  Thus artificial hypos in a normal rodent would trigger "low energy state!" alert.  In an diabetic rodent or human, this may do much the same thing, but the "natural" recovery would be much quicker via their own "normal" excessive production of glucose.
Personally, I do not find the results of this study to be all that surprising.  It would be interesting for them to have measured the energy expenditure directly over the course of the study.  Repeated periodic bouts of "energy shortage" intuitively would cause a reduction in activity and/or whatever metabolic adaptations are available to the organism to conserve energy (e.g. the reduced thermogenesis seen).  

Take Aways:
  • This study upholds the energy balance model for weight gain and the development of obesity.
  • In non-diabetic rodents, periodic hypoglycemic episodes created with exogenous insulin injections resulted in a reduction in calories out.
  • The reduction in calories out was not compensated for by reducing intake, so the rodents gained weight.  
  • This study does not support the insulin-induced internal starvation model promoted by Ludwig and Taubes, despite the mountain of scientific evidence (including Ludwig's own research) to the contrary.

But wait, there's more!

Over the years, I've come across a few studies in humans with diabetes (T1 and T2) that have looked into the cause of the weight gain often accompanying the initiation of insulin therapy.   This Ludwig tweet provided me with the impetus to collect them in one place and share them with you.  Indeed this line in the Abstract of that (2013) study is not entirely true:
"Although the mechanisms responsible for this weight gain are poorly understood ..."
The bioenergetics of metabolism and some basics of physiology provide numerous possible mechanisms that, as it turns out, have been studied in human diabetics.

It is very important to keep in mind that the diabetic state is one of metabolic dysfunction.  This is an energetically wasteful state.  

It is both predicted, and has been shown in human studies that uncontrolled diabetics have elevated resting metabolic rates (REE, RMR, BMR), and that this increase occurs before overt diabetes in the case of Type 2.  See for example:

Increased energy expenditure in poorly controlled Type 1(insulin-dependent) diabetic patients  (1984)
Metabolic Factors Contributing to Increased Resting Metabolic Rate and Decreased Insulin-Induced Thermogenesis During the Development of Type 2 Diabetes (1999)

Substrate Cycling in Health and Disease:

Before discussing the above and other studies, I want to briefly discuss some of what goes into our basal or resting metabolic rate or energy expenditure.  This can be considered to be analogous to the gasoline usage of an idling car, but there is an additional component in animals that is not accounted for in this analogy.   In your car,  gasoline is added directly to the storage tank where it sits until you start the car.  Then it is delivered to the engine where it is burned to keep it running.  It's a one way trip, and for all intents and purposes, almost no energy is required to fill the tank or deliver the gas to the engine.   

In animals, we do not have this sometimes-static, one way system, rather there is continual substrate cycling (and recycling).  Additionally, fuel substrates are continuously circulated to all corners and curves of the body, even in a comatose state, whether or not a particular cell or organ takes up the fuel or lets it pass on by.   In addition to this cycling, another key difference is that the oxidative substrates are of different chemical form than the storage molecules.  For the two most important substrates of glucose and free fatty acids (FFA or NEFA), the respective storage forms are glycogen and triglycerides.  The "gas" fed into our cellular engines is of a different form than that stored in our "tanks".   Because of this:
Some energy is expended to store energy, and some more energy is expended to liberate "burnable" fuels from storage.  
This happens continually in what are often referred to as futile cycles.  While there are also some re-cycling paths, the basic cycles are:

Glucose:  Once glucose is absorbed into the body, some may be used immediately for fuel and excesses are converted to glycogen in the liver and muscles.  When circulating glucose is high (like after a carby meal), glycogen synthesis is stimulated to save excesses.  When circulating levels fall, glycogenolysis (breakdown) is stimulated to liberate glucose.  Both of these processes require some energy.  There's an added "twist" to this cycle in that when both glucose and glycogen stores are low, various other molecules (glycerol, lactate and some other SCFA, certain amino acids) are converted into glucose.  This gluconeogenesis is more energy expensive than glycogen breakdown.

Fatty Acids:  By far the main storage fuel for the body is fatty acids and let's pick up this cycle in the fat cell where surplus and "savings" are stored.  Fatty acids are cycled between the "free" form and triglycerides formed from three fatty acids joined by a glycerol backbone.  I've blogged many times about this Triglyceride/FFA cycle, here is one post.   Indeed there are many such cycles.  There is one within the fat cells where the majority of fatty acids liberated are immediately re-esterified (converted back to trigs), there is a whole body cycle where the liver packages up excess FFA in lipoproteins, and fatty acids are cycled inside other cells as well.   In the fat cells (and likely others), the glycerol liberated in lipolysis cannot be used to re-esterify FFAs.  The source of that activated glycerol (glycerol-3-P) is either glucose or synthesized in the cell by glyceroneogenesis, and there is evidence that the latter is the major source for the basal cycling within the fat cells.  Like gluconeogenesis, this is an energy requiring synthesis.  

In addition to the energy cycles, there is protein turnover in the body at all times with a balance between breakdown of proteins and protein synthesis.  These are also energy requiring and factors into REE and turnover (both breakdown and synthesis) is increased in untreated diabetes.  However the difference is apparently too small a portion of the total to make a difference.

Insulin Regulates It All:

Insulin stimulates storage and synthesis and inhibits release from storage and breakdown.  It is unfortunate that these actions have become so demonized by the likes of Gary Taubes.   Clearly insulin is not required for the various cycles to churn on.  If it were, then before the advent of exogenous insulin, Type 1 diabetics would have died more immediately.  Yet clearly insulin is required to sustain life and the body, as without it, Type 1 diabetes was a fatal diagnosis.  The lead up to and manner of death was often quite brutal.   Lots of information HERE (check out the bibliography too).

If you haven't already read this article, please do:  Insulin: understanding its action in health and disease

Diabetes is a Disease of Insulin Deficiency

Whether we are talking Type 1 diabetes and its absolute insulin deficiency, or Type 2 diabetes that (when untreated) progresses through various stages of relative insulin deficiency, diabetes is ultimately about not enough insulin.  This is difficult for those I can only describe as ideologues,  focusing on (reactive, largely basal) hyperinsulinemia in Type 2s, to acknowledge.   The weight of decades of scientific evidence, however, supports this assertion.  See, for example, this post.  There is also ample evidence that the basal hyperinsulinemia in Type 2s is an adaptive response to fat accumulation that exceeds an individual's capacity for safe storage in smaller fat cells.   For the remainder of this post, I would like to refocus the discussion on the impact of the deficiency (absolute or relative) of insulin on the substrate cycles.   The concept of "loss of action" of insulin (insulin resistance) is something that I strongly believe needs to be revisited and overhauled, but even if current thinking in this regard holds up, we are still talking about a deficiency in insulin action that's effectively the same as a deficiency in the amount of insulin.  

Insulin Deficiency and Energy Substrate Cycling

Insulin clearly has additional roles in the body, but for this post I want to focus on what insulin's role is in the substrate cycles, and its purpose.    In this role, insulin's purpose is to maintain circulating substrate levels within certain levels.    Insulin doesn't know or care what storage levels of glycogen and triglycerides are.  Ultimately it just wants to keep circulating blood glucose and NEFA/FFA levels within normal levels so there is always ample supply to every cell in the body if and when those cells need energy.

When insulin is deficient, these cycles are disrupted leading to elevated circulating levels and/or substrate flux.

Bathtub Analogy:  
  • Fill a bathtub up to a line.  If the drain is closed, the level stays the same.
  • If the drain does not close fully, water constantly trickles out of the drain.  If we turn on the faucet just enough to compensate, the water level remains the same, but the water molecules in the tub are exchanged (flux = flow).  
  • Open the faucet to full flow, but also open the drain more fully.  If the rates are equal, again the level in the tub remains unchanged, but the exchange of water molecules has increased dramatically.   
The three cases above are indistinguishable if you are just looking at the water level in the tub.  If we extend this analogy to include the temperature of the bath water.  
  • Fill the tub with hot water and let it sit, it stays hot for a while but eventually cools off.
  • Trickle in hot water and balance the level by opening the drain a bit and the water either stays hot.
  • Open the hot water faucet all the way and open the drain to keep the level the same, and again the water stays hot.  It's easy to envision how your energy bill will go up rather quickly!!
The analogies here are as follows:  
  • Water in the tub is level of substrate in circulation
  • Faucet is endogenous and/or exogenous (dietary) source
  • Drain is cells of the body that take up substrate


Using the bathtub analogy, normal function always involves a constant cycling akin to  the trickling faucet and drain.  When carbs are ingested, this is like dumping some pails of water into the tub, and the water level rises.  When functioning normally, the drain is temporarily opened a bit.  This is done by insulin stimulating glucose uptake into cells and glycogen synthesis in the liver and muscle.   But the more important action of insulin is to shut down the trickling faucet until the level in the tub has receded back to normal.  While it is still popular to look at hyperglycemia (overfilled tub) as a failure to drain the periodic influxes (clogged drain), it has been demonstrated by radiolabel tracers that it's the failure to shut down the faucet -- in the form of unchecked gluconeogenesis -- that is the ultimate cause of hyperglycemia.   The kidneys act like that overflow drain most bathtubs have, so that when the level gets too high, excesses are excreted in the urine -- glycosuria.  (Indeed the newer glucose re-uptake inhibitors work by essentially positioning the overflow outlet lower in the tub.)    

In uncontrolled diabetes, the faucet is on at a higher than normal rate (gluconeogenesis), it is not shut off when pails of water are dumped into the tub, and when the level gets too high, glucose spills over into the urine.   This is energetically expensive in two ways.  First, energy is expended to create glucose that is not "needed" via gluconeogenesis.  While the body still burns that glucose for energy, when hyperglycemia reaches a certain threshold, some of those expensive glucose calories are lost in the urine.  (Indeed this is the mechanism by which glucose re-uptake inhibitors "may help you lose a little weight".)   As the studies I'm about to present demonstrate, the increased energy expenditure in uncontrolled diabetes due to glucose can be in the hundreds of calories per day.

Fatty Acids

The bathtub analogy is a bit different for fatty acids.  There are essentially two Trig/FFA cycles to consider -- one internal to the fat cell, and one between the fat cell and the liver .  The latter fits the bathtub analogy.  Circulating free fatty acid (NEFA or FFA) levels, like glucose, are normally kept within a fairly narrow range.  Unlike glucose, however, basal levels rise with fasting and are suppressed in the fed state when glucose is highly available.  The level is normally controlled by release from fat tissue and repackaging into lipoproteins (VLDL) in the liver.  Insulin "famously" regulates this at the level of the fat cell by inhibiting lipolysis.  However it is a bit more complicated than that as breakdown of triglycerides in the fat cell is NOT a one way ticket out into circulation, and a majority of FFA are usually re-esterified inside said fat cell.    So we have a constant cycling going on inside the fat cell from which insulin regulates the release into circulation to supply other cells with this energy source.  Still, we can envision the fat cell as the faucet of FFA delivery to circulation, and all other cells as the drain.  In a sense, the liver is more of the overflow drain here as it basically repackages excesses and returns to sender.  Unlike glucose, there is no significant overflow drain leading to loss of FFA from the body.

In unchecked diabetes, the faucet is again on at a higher than normal rate.  Keeping this discussion focused on just the energy aspects, any time there is simply conversion of fat molecules from free to esterified (trig) or esterified to free fatty acid form, energy is required.  Like the hot water part of the bathtub analogy, even if the level in the tub is only slightly elevated, it is more the flux -- or increased cycling -- that is energetically wasteful.


You guessed it (?)  

Insulin therapy in diabetes corrects the insulin deficiency.  In doing so, it restores the body from a pathologically energetically wasteful state to a normal energetically efficient one.  Thus, energy expenditure -- otherwise known as "calories out" -- is returned to normal levels when insulin deficiency is corrected.  If intake is not adjusted to reflect this new norm, in other words if the person continues to eat at habitual levels, they will gain weight when their diabetes is brought under control.

And now, those studies ...

Increased energy expenditure in poorly controlled Type 1(insulin-dependent) diabetic patients

In this study of 10 Type 1 diabetics, when untreated with insulin the subjects had an average REE of ~2040 kcal/day.  This was significantly greater than their predicted (~1775 kcal/day) REE.  When treated with insulin, their REE changed to ~1730 kcal/day, similar to predicted.
This study speculates but didn't quantify the contributors to the altered REE. 
The change in REE with insulin treatment was roughly 300 kcal/day, a rather significant reduction of about 15% from baseline REE.

Metabolic Factors Contributing to Increased Resting Metabolic Rate and Decreased Insulin-Induced Thermogenesis During the Development of Type 2 Diabetes

The sleeping metabolic rate of 560 Pima Indians was measured using a respiratory chamber.  It was found that RMR was 4.9% higher in diabetics, and also 2.7% higher in those with impaired glucose tolerance compared to normal glucose tolerance controls.
For 17 subjects, glucose tolerance deteriorated from normal to diabetes over an average of 5 years.  Their RMR was measured (ventilated hood) progressively.    As glucose tolerance went from NGT to IGT, RMR increased 4.2%.  RMR increased another 2.6% as IGT progressed to diabetes.   Insulin-induced thermogenesis (IIT) would raise total energy expenditure but was found to decrease from 11.7% in NGT to 7.3% in IGT to 6.5% in diabetes.  
"In 151 subjects, basal endogenous glucose output (3-3H-glucose), fasting insulin and free fatty acid concentrations, and glucose disposal (hyperinsulinemic clamp) were significant determinants of RMR, independent of body composition, age, and sex." 
"These findings indicate that increases in RMR and decreases in IIT occur early in the development of type 2 diabetes, and that both changes are related to the progressive metabolic abnormalities that occur during the development of the disease."
Three references from this study looking at energy expenditure in diabetes:

  1. Twenty-four-hour energy expenditure in Pima Indians with type 2 (non-insulin dependent) diabetes mellitus. (1992)    A 2.9% increase in sleeping metabolic rate was observed in diabetics compared with NGT.  This correlated with hepatic endogenous glucose production.
  2. Increased resting metabolic rates in obese subjects with non-insulin dependentdiabetes mellitus and the effect of sulfonylurea therapy. (1986)  A 5% increase in RMR was observed in diabetics vs. NGT.   In subjects undergoing 6 weeks TZD treatment, RMR decreased 5.3% while weight remained stable through caloric restriction to compensate.
  3. Effect of impaired glucose tolerance and type2 diabetes on resting metabolic rate and thermic response to a glucose mealin obese women.  (1986 )  This study compared groups of 5 obese women with NGT, IGT and diabetes with 5 lean NGT.  In the obese women, the NGT had RMRs similar to predicted while RMR was 11.7% higher than predicted in IGT or T2D.  
"Obese patients with diabetes and impaired glucose tolerance require more kcal/LBM (lean body mass) to maintain their body weight than the control subjects. "

Intensive Insulin Therapy and Weight Gain in IDDM

This study involved six Type 1 diabetics who were switched from conventional insulin therapy to an intensive insulin therapy regime.  Body weight, composition, energy expenditure, glycosuria and substrate kinetics were measured.
 "intensive insulin therapy causes an increase in body fat as a result of the elimination of glycosuria and reduction in 24-h energy expenditure. The elimination of glycosuria contributed 70% to the positive energy balance during intensive insulin therapy, and the reduction in 24-h energy expenditure contributed the remainder. The reduction in 24-h energy expenditure was the result of the decrease in triglyceride/free fatty acid cycling and nonoxidative glucose and protein metabolism."

Causes of weight gain during insulin therapy with and without metformin in patients with Type II diabetes mellitus


This study looked at resting energy expenditure, energy intake and glycosuria in 26 people with Type 2 diabetes.  Half were treated with insulin therapy alone, and half with insulin therapy and metformin.  The study lasted one year.    The metformin group gained less weight than the insulin-only group.
"Improved glycaemia promotes weight gain by decreasing both basal metabolic rate and glucosuria. Use of metformin decreases weight gain by reducing energy intake and is therefore a useful adjunct to insulin therapy in patients with Type II diabetes." 

Concluding Remarks

The above collection of human studies is certainly not a comprehensive review of the literature, but a clear pattern is emerging:

  • Insulin deficiency -- whether relative or absolute -- is accompanied by an increase in basal energy expenditure.  This may or may not be attenuated by reduced thermogenesis in 24 hour energy expenditure (total daily energy expenditure, TDEE), but TDEE remains increased vs. non-diabetics.
  • The increased resting energy expenditure seems most tightly correlated to increased endogenous glucose production (gluconeogenesis), and increased fatty acid cycling is postulated to make up the difference.
  • A greater "calorie drain" component contributing to increased TDEE is glycosuria in untreated diabetes.  This factor seems to make up the majority of the difference.
  • Insulin treatment corrects this dysregulated state and returns TDEE to *normal* levels.
  • Weight (mostly fat) gain occurs when intake is not reduced to reflect the lower energy needs of the treated diabetic.
What becomes obvious, is that not only is the weight gain "no mystery", but it is about as cut-and-dried an energy balance phenomenon as you will find.

Modern humans are SO FAR from being homeostatic human beings.  Even those boasting of ad libitum intake and maintaining weight are subject to some external cues (clothing fit, getting weighed at the doctor's office even if you don't weigh regularly, societal pressures), and ad libitum intake of a restrictive diet is somewhat of an oxymoron.

When diabetics initiate glucose re-uptake inhibitor therapy and immediately begin peeing out some 300 cal/day of glucose, most spontaneously lose weight.  We are creatures of both habit and consequences.  Initially they'll go on eating the same way as before (habit), but most don't lose all the weight the increased calories out would predict.  While this is interpreted by some as an appetite driven increase in intake, this was not demonstrated and is conjecture.  It's far more "human" to envision the person enjoying a little more dietary freedom once they realize they can do so, keep their HbA1c in check and have slightly looser clothes (consequences).    We see the opposite with many athletes when they are laid up by injury or retire.  Many will gain weight because they are no longer expending calories in training yet continue to eat in similar fashion (habit).  There may be some reduction in appetite as they no longer need to fuel high activity levels, but this rarely is a spontaneous, complete adjustment.  Habit prevails until consequences, e.g. their clothing gets too tight, will prompt some to deliberately cut intake.

The typical obese Type 2 diabetic does not gain the weight and develop the disease overnight.  We are talking a lifetime or at least a decade or so of "bad" eating habits and weight gain before the ultimate consequence.  Furthermore, as the one study showed, there is a slight expenditure "bonus" as glucose tolerance deteriorates.  This person is not only used to eating an amount to sustain their XYZ pound body, but perhaps somewhere in the neighborhood of 5% more.  That may not sound like a lot, but that's 100 cal/day for someone consuming 2000 cal/day ... and that is roughly equivalent to a pound a month.  In other words, if they didn't become diabetic, they would probably weigh 10, 20 or even more pounds than they currently do.    If this person is very diabetic (e.g. T1 or T2 with regular and/or lengthy glucose excursions above 200 mg/dL) they are used to consuming up to around 300 more "free" calories per day -- calories that are spilled over into the urine until insulin and/or tighter glycemic control prevents the spillage.   Like the athlete, when this "bonus expenditure" is erased, habits prevail keeping intake the same.  The consequence is weight gain.

I am not sure how much comfort -- if any at all -- the information in this post is for diabetics.  Especially your obese T2 who is already struggling with their weight and likely has been hearing "lose weight" for seemingly forever, I imagine this is daunting.   However many athletes do not succumb to weight gain when sidelined/retired because they are proactive and deliberately cut back on their intake to match their lower activity and energy expenditures.   There is no reason that this approach cannot be an integral part of insulin therapy, and the patient be provided with tools to help them do so.  I'm no fan of weight loss drugs, but metformin is one diabetes drug known to help with weight loss (it prevented some of the weight gain when used with insulin in one study above), and this may be the appropriate time for that "leg up" of some appetite suppressants.  

It's high time that the scope of the research gets translated from the researchers to the medical profession and patients.  We actually DO know a lot more about why insulin treatment often results in weight gain, and it has nothing to do with the lies the likes of Dr. David $. Ludwig continue to perpetuate.  If the goal is to truly help people take an active interest in their health, they deserve to be told the truth.    At the very least it is time to stop demonizing insulin as the "fattening hormone" that is activated every time a carbohydrate passes through one's lips.  

This focus on insulin = fattening, and a very vocal virtual mob who considers "covering carbs with insulin" to be damaging to health -- has resulted in many avoiding insulin treatment when it is indicated.  If a person is unable to reverse their disease, then there is no shame in actually treating it to improve their health outcomes.  In a way, the weight gain of insulin treatment may well be the best evidence that the treatment is effective.   That may be small consolation, but ultimately a 5-10% reduction in intake should be doable for just about everyone.  Avoiding insulin because that minor adjustment is too much?  I'll admit,  I don't get that.

The cold-hard-bottom line for most of us (the majority of Americans, diabetic or not, are overweight or obese) is that we eat too much.    The focus needs to be brought back to this fact.  Let's all work together to help each other figure this out!

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