Tag Archives: lipogenesis

December 7, 2009 · 2:00 AM

Are Fructose and High Fructose Corn Syrup Bad for Us?

Table sugar (sucrose) is a combination of glucose and fructose

Darya Pino earlier this month posted at her Summer Tomato blog a video regarding high fructose corn syrup.  The speaker in the video is pediatric endocrinologist Robert Lustig, M.D., of the University of California—San Francisco.
In the U.S. between 1970 and 1990, consumption of high fructose corn syrup increased over 1000%.  During those two decades, the incidence of overweight and obesity nearly doubled.  Many wonder if this is more than just coincidental. Most of this fructose is in soft drinks.  Soft drink consumption per person in 1942 was two servings per week.  In 2000, consumption was two servings per day.  Of course, these drinks typically have few nutrients other than sugars.
I wrote about fructose possibly being “the new trans fat” almost two years ago.

Dr. Lustig is convinced that high fructose corn syrup (HFCS) is a chronic toxin, at least in the amounts many of us eat, and the cause of our current epidemic of childhood and adult obesity and overweight.  Even if this idea is not new to you, you may be interested to hear the biochemistry and physiology behind his position.  If you didn’t enjoy college lectures or are not a food science geek, you probably won’t be able to sit through this 1.5-hour video. 

I enjoyed the heck out of it!  Made me feel like I was back in college again.  Few of my professors were as good as Dr. Lustig at lecturing. 

Here are a few of his other major points:

  • HFCS was invented in Japan in the 1960s, then introduced to U.S. markets in 1975
  • sucrose and fructose are both poisons
  • in the U.S. we eat 63 pounds (28.6 kg) of HFCS and 141 pounds (64.1 kg) of sugar per year [he didn’t define “sugar” in this context]
  • he praises Yudkins book, Pure, White, and Deadly [I’ve written about the Cleave-Yudkin carbohydrate theory of chronic disease]
  • the triglyceride/HDL ratio predicts heart disease much better than does LDL cholesterol
  • chronic high fructose intake causes the metabolic syndrome [does he think it’s the only cause?]
  • only the liver can metabolize fructose, in contrast to every other tissue and organ that can use glucose as an energy supply
  • high fructose consumption increases the risk of gout and high blood pressure
  • fructose interferes with production of our body’s production of nitrous oxide—a natural circulatory dilator—leading to higher blood pressures
  • fructose increases de novo lipogenesis—in other words, it creates body fat
  • fructose interferes with natural chemical messengers that tell your brain you’ve had enough food and it’s time to stop eating
  • high fructose intake reduces LDL particle size, potentially increasing the future risk of cardiovascular disease such as heart attacks [small, dense LDL cholesterol is more damaging to your arteries that large, fluffy LDL]

So What? 

You don’t need polititians to reduce your consumption of sugary soft drinks and high fructose corn syrup—do it yourself starting today.  Read food labels—HFCS is everywhere.  I’ve found it in sausage! 

The food industry greatly reduced use of trans fats in response to consumer concerns, before the polititians ever dabbled in it.  HFCS can go the same route.  Consumption of soft drinks, sports drinks, and other sugary beverages—the major sources of HFCS—is up to you.

Steve Parker, M.D.

PS: The Advanced Mediterranean Diet and Ketogenic Mediterranean Diet are naturally low in fructose.

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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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