Tag Archives: insulin resistance

December 18, 2009 · 4:18 PM

Low-Carb Killing Spree Continues

The choice is clear . . . NOT

Low-fat and low-carb diets produce equal weight loss and improvements in insulin resistance but the low-carb diet may be detrimental to vascular health, according to a new study in Diabetes.

Methodology

Researchers in the the UK studied 24 obese subjects—15 female and 9 male—randomized to eat either a low-fat (20% fat, 60% carbohydrate) or low-carb (20% carb, 60% fat) diet over 8 weeks.  Average age was 39; average body mass index was 33.6.  Most of them had prediabetes.  Food intake was calculated to result in a 500 calorie per day energy deficit (a reasonable reduced-calorie diet, in other words).  Study participants visited a nutritionist every other day, and all food was provided in exact weighed portions. 

Results

Both groups lost the same amount of weight, about 7.3% of initial body weight. 

Triglycerides dropped by a third in the low-carb group; unchanged in the low-fat cohort.  Changes in total cholesterol, LDL cholesterol, and HDL changes were about the same for both groups.

Systolic blood pressure dropped about 10 points in both groups; diastolic fell by 5 in both.

“Aortic augmentation index” fell significantly in the low-fat group and tended to rise in the low-carb group.  According to the researchers, the index is used to estimate systemic arterial stiffness.  [In general, flexible arteries are better for you than stiff ones.  “Hardening-of-the-arteries,” etc.]  The low-fat group started with a AAI of 17, the low-carb group started at 12.  They both ended up in the 13-14 range. 

Peripheral insulin sensitivity improved significantly only in the low-carb group but “there was no significant difference between groups.”  No difference between the groups in hepatic (liver) insulin resistance. 

Fasting insulin levels fell about 20% in the low-fat group and about 40% in the low-carb group, a difference not reaching statistical significance (p=0.17).

The Authors’ Conclusions

This study demonstrates comparable effects on insulin resistance of low-fat and low-carbohydrate diets independent of macronutrient content.  The difference in augmentation index may imply a negative effect of low-carbohydrate diets on vascular risk.

My Comments

Yes, you can indeed lose weight over eight weeks on both low-fat and low-carb diets, if you follow them.  So diets DO work.  No surprise.

Loss of excess body fat by either method lowers your blood pressure.  No surprise.

Once again, concerns about low-carb/high-fat diets adversely affecting common blood lipids—increasing heart disease risk—are not supported.  No surprise

Hyperinsulinemia and insulin resistance are risk factors for development of diabetes and cardiovascular disease.  Results here tend to favor the low-carb diet.  I have to wonder if a study with just twice the number of test subjects would have shown a clear superiority for the low-carb diet.

The authors imply that aortic augmentation index is an important measure in terms of future cardiovascular health.  A major conclusion of this study is that a change in this index with the low-carb diet might adveresly affect heart health.  Yet they don’t bother to discuss this test much at all.  I’m no genius, but neither are the typical readers of Diabetes.  I doubt that they are any more familiar with that index than am I, and I’d never heard of it before. 

[Feel free to educate me regarding aortic augmentation index in the comment section.]

Unfortunately, many readers of this journal article and the associated news releases will come away with the impression, once again, that low-carb diets are bad for your heart. 

I’m not convinced.

Steve Parker, M.D.   

References:

Bradley, Una, et al.  Low-fat versus low-carbohydrate weight reduction diets.  Effects on weight loss, insulin resistance, and cardiovascular risk: A randomized control trial.  Diabetes, 58 (2009): 2,741-2,748.

Nainggolan, Lisa.  Low-carb diets hit the headlines again.  HeartWire, December 11, 2009.

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June 24, 2009 · 2:00 AM

High Protein Ketogenic Diet Beats High Protein/Medium Carb Diet in Men, at Least Short-Term

Low-Carb Steak

Low-Carb Steak

Scottish researchers last year reported greater weight loss and less hunger in obese men on a high-protein ketogenic diet compared to a high-protein, moderate-carbohydrate diet.

Background

Dietary protein seems to be more satiating – able to satisfy hunger, that is – than carbohydrate and fat. 

The typical Western (especially American) diet derives about 55-60% of total calories from carbohydrates.  When carbohydrate intake is very low, under 20-30 grams per day for example, fat stores are utilized as a source of energy to replace carb calories, resulting in fat breakdown waste products called ketone bodies.  These are ketogenic diets.  In them, carbs are replaced usually by both extra fat and extra protein. 

Methodology

Each of 17 obese men, 20 to 65 years old, were placed on two separate diets for four weeks each time.  Average weight was 111 kg.  Average body mass index was 35.  This was a residential program, but the subjects were allowed to leave and go to work.

  • Diet 1:  high-protein, low-carbohydrate, ketogenic.  30%, 4%, and 66% of energy (calories) as protein, carbohydrate, and fat, respectively.
  • Diet 2:  high-protein, medium-carbohydrate, nonketogenic.  30%, 35%, and 35% of calories as protein, carb, and fat, respectively.

Actually 20 men signed up, but three dropped out for personal reasons after starting. 

They could eat as much as they wanted. 

Results

Subjects had no overall preference for either diet.  No differences in the diets for desire to eat, preoccupation with food, or fullness.  Weight loss was greater for the low-carb diet tahn with the medium-carb diet: 6.34 kg vs 4.35 (P < 0.001).  Subjects lost more weight on their first diet than on their second.  Fasting glucose and HOMA-IR (a test of insulin resistance) was lower than baseline for the low-carb diet but not the other.  Total and LDL cholesterol were tended to fall in response to both diets, but to a statistically significantly great degree only on the medium-carb diet.  When eating the low-carb diet, subjects ate 300 calories per day less than on the medium-carb diet.  [ketones were measures?]

Discussion

We have to assume that study subjects were of Scottish descent.  Applicability of these results to other ethnic groups is not assured.  Similarly, results don’t necessarily apply to women.

I’m surprised the medium-carb dieters, eating all they wanted, lost weight at all.  Must be a result of the high protein content or lower-than usual carbohydrate content of the study diet.  Study authors cite others who found that doubling protein intake from 15 to 30% of calories reduces food intake, which should lead to weight loss. 

Since protein content was the same on both diets, the greater weight loss seen on the low-carb ketogenic diet was the result of lower caloric intake, in turn due to less hunger.  The reduced energy intake could be due to lower carb or higher fat intake, or both.  The researchers cite one study finding no satiating effect of fat.  Some say that ketone bodies reduce appetite. 

Although the medium-carb diet showed greater improvements in total and LDL cholesterol, the low-carb diet changes trended in the “right” direction (down).

On the low-carb ketogenic diet, lower glucose levels and insulin resistance would tend to help people with (or prone to) type 2 diabetes, prediabetes, and some cases of metabolic syndrome. 

Steve Parker, M.D.

 References: 

Johnstone, Alexandra, et al.  Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum.  American Journal of Clinical Nutrition, 87 (2008): 44-55.

Weigle, D.S., et al.  A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations.  American Journal of Clinical Nutrition, 82 (2005): 41-48.

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April 26, 2009 · 7:08 PM

Lipid Overload as the Cause of Type 2 Diabetes

An up-and-coming theory to explain type 2 diabetes suggests that abnormal lipid metabolism, not glucose/sugar metabolism, is the primary metabolic defect.  Roger H. Unger, M.D., writes about this in the March 12, 2008, issue of the Journal of the American Medical Association.

Early in the writing of this blog entry, I realized it is much too technical for many readers.  I’m writing this to solidify my own understanding of a new theory.  If you are not interested in physiology, you can quit reading now. 

Still with me? 

Definitions and Physiology

Diabetes is defined by high blood glucose (sugar) levels. 

The lipid family includes triglycerides (fats and oils), sterols (e.g., cholesterol), and phospholipids (e.g., lecithin, a major cell membrane component).  Fats are almost entirely composed of trigylcerides.  When fats are broken down, fatty acids are produced.  On the other hand, fatty acids can be joined together, along with glycerol, to form triglycerides. 

Glycogen is a storage form of glucose in liver and muscle tissue. 

Insulin is a protein hormone produced by pancreatic beta cells.  Insulin:

  1. lowers blood glucose levels by driving glucose into cells 
  2.  inhibits breakdown of glycogen into glucose
  3. inhibits formation of new glucose molecules by the body
  4. stimulates glycogen formation
  5. promotes storage of triglycerides in fat cells (i.e., lipogenesis, fat accumulation)
  6. promotes formation of fatty acids (triglyceride building blocks) by the liver
  7. inhibits breakdown of stored triglycerides
  8. supports protein synthesis. 

Fatty acids in muscle tissue block the uptake of glucose from the bloodstream by muscle cells.  Fatty acids in liver tissue impair the ability of insulin to suppress breakdown of glycogen into glucose, and impair the ability of insulin to suppress production of new glucose molecules.  In other words, an “excessive fatty acid” environment in liver and muscle tissue promotes elevated glucose levels.

Got that?  [This is very difficult material.]  Now on to . . .

 The Lipocentric Theory of Type 2 Diabetes

Type 2 diabetes may be caused by:

  1. Eating too many calories, leading to…
  2. High insulin levels, leading to…
  3. Stimulation of fat production, leading to…
  4. Increased body fat, leading to…
  5. Deposition of lipids in cells where they don’t belong (that is, not in fat cells), leading to…
  6. Resistance to insulin’s effects on glucose metabolism, leading to…
  7. Lipid accumulation in pancreatic beta cells, damaging them, leading to…
  8. Elevated blood glucose levels, i.e., diabetes.

Perhaps the key to understanding this is to know that “insulin resistance” refers to insulin having less ability to suppress glucose production by the liver, or less ability of various tissues to soak up circulating glucose.  Insulin resistance thereby leads to elevated glucose levels.  But insulin’s effect of “producing fats” (lipogenesis) continues unabated.  Excessive fats, actually fatty acids, accumulate not only in fat cells, but also in liver cells, muscle cells, pancreatic beta cells, and others.  This lipid overload can damage those cells.

If This Theory Is Correct, So What?

Steps #1 and 2 of the lipocentric theory involve excessive caloric intake and high circulating insulin levels, leading to problems down the road.  So overweight people should restrict calories and try to lose at least a modest amount of weight.  Particularly if already having type 2 diabetes or prone to it.

And what about people with type 2 diabetes who have insulin resistance and have poorly controlled glucose levels?  Most of these have high insulin levels already, contributing to a fat-producing state.  Adding more insulin, by injection, would not seem to make much sense.  The extra insulin would bring glucose levels down, but might also cause lipid overload with associated cellular damage.  Effective clinical strategies according to Dr. Unger would include 1) caloric restriction, which helps reduce weight, high insulin levels, and fat production, and 2) if #1 fails, add anti-diabetic drugs that reduce caloric intake (exenatide?), that reduce lipid overload (which drug?), or that do both.  Dr. Unger suggests consideration of bariatric surgery, for caloric restriction and cure of diabetes.

Compared with dietary fats and proteins, carbohydrates generally cause higher circulating insulin levels.  And type 2 diabetics taking insulin shots need higher doses for higher intakes of carbohydrate. So it makes sense to me to consider preferential reduction of carbohydrate intake if someone is going to reduce caloric intake.

Dr. Unger and I agree that reduction of excessive food intake and excess body fat is critically important for overweight people with type 2 diabetes.

Steve Parker, M.D.

References: Unger, Roger H.  Reinventing Type 2 Diabetes: Pathogenesis, Treatment, and Prevention.  Journal of the American Medical Association, 299 (2008): 1185-1187.

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