I Wish I Were Far From the Madding Crowd

April 3, 2010

Obesity, HFCS, and fatty liver disease in children (as well as increased heart disease risk)

I personally am very interested in this topic because just over three years ago I had gone in to see my doctor because of abdominal pain.  My triglycerides and LDL were high.  He thought it might be my gallbladder so I went in for an ultrasound, which revealed that I had a fatty liver.

Fatty liver disease has not been considered a children’s disease, so it’s disturbing to read that children and adolescents are developing it, especially since there are usually few symptoms until the disease has progressed to a more advanced stage of steatohepatitis (aka hepatosteatosis) and scarring has already occurred.

According to the American Heart Association, more than 6 million children in the United States are affected.

High Fructose Corn Syrup Linked to Liver Scarring (HealthDay, March 19, 2010)

Reports on a study, “Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease,” which found that increased consumption of HFCS led to increased fibrosis (scarring) in patients suffering from NAFLD.

Fatty Liver Disease May Raise Heart Disease Risk in Overweight, Obese Kids (American Heart Association, April 3, 2010)

A fatty liver disease that is not well-known in overweight and obese children may be a precursor of cardiovascular disease, researchers reported in Circulation: Journal of the American Heart Association.

The overweight children with NAFLD had significant cardiovascular risk including higher levels of fasting glucose, insulin, total cholesterol, low-density lipoprotein (LDL, “bad” cholesterol), triglycerides and higher systolic and diastolic blood pressure than the control group.

NAFLD is the most common cause of liver disease in children and is associated with metabolic syndrome, a clustering of risk factors for the development of cardiovascular disease and type 2 diabetes. NAFLD is characterized by the presence of oily droplets of triglycerides in liver cells. More than 6 million children in the United States are affected.

NAFLD in overweight children is strongly associated with metabolic syndrome. The association is independent of both body mass index and insulin sensitivity.

Fatty liver disease often has no outward symptoms, which contributes to it going undetected. Although some children will have symptoms such as abdominal pain or fatigue, the majority remain symptom-free until the disease is in very advanced stages.

American Heart Association Scientific Statement on Metabolic Syndrome in Children and Adolescents (2009)

Since 2003, substantial new information has emerged in children on the clustering of obesity, insulin resistance, inflammation, and other risk factors and their collective role in conveying heightened risk for cardiovascular disease and type 2 diabetes. A constellation of these interrelated cardiovascular risk factors in adults has come to be known as the metabolic syndrome.

The scientific statement covers the following topics:

Selected References

Steinberger J, Daniels SR. Obesity, insulin resistance, diabetes and cardiovascular risk in children: an American Heart Association scientific statement from the Atherosclerosis, Hypertension, and Obesity in the Young Committee (Council on Cardiovascular Disease in the Young) and the Diabetes Committee (Council on Nutrition, Physical Activity, and Metabolism). Circulation. 2003; 107: 1448–1453.[Free Full Text]

Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Spertus JA, Costa F. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement [published corrections appear in Circulation. 2005;112:e297 and 2005;112:e298]. Circulation. 2005; 112: 2735–2752.[Free Full Text]

Non-alcoholic fatty liver disease (NAFLD)

Once considered an illness of adults over 40, more and more children are being diagnosed with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH).  NAFLD can be a precursor to NASH, which can progress to cirrhosis.

According to Children’s Memorial Hospital in 2005 an estimated 1.6 million children were affected with fatty liver disease

But the American Heart Association now says that 6 million children have NAFLD (see above).

Note: The Children’s Memorial Hospital’s NASH program is a member of the NASH clinical research network.  In 2005, the NASH clinical research network launched a trial for treatment of liver disease in children. The NASH CRN website contains links to related information for patients.  Most of the website, however, is technical and requires an account to access.)

When complications such as cirrhosis cannot be controlled with treatment or when the liver becomes so damaged from scarring that it completely stops functioning, a liver transplant is necessary.

Both NASH and NAFLD are becoming more common, possibly because of the greater number of Americans with obesity. In the past 10 years, the rate of obesity has doubled in adults and tripled in children. Obesity also contributes to diabetes and high blood cholesterol, which can further complicate the health of someone with NASH.  (From the NASH page on the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) website.)

From “Fatty Liver Disease is Common in the US

Source: Spare the exercise, spoil the liver

More information about fatty liver can be found on the American Liver Foundation’s Fatty Liver page and in their Fatty Liver Brochure.

In case you’re wondering what I did after my diagnosis…

At the ultrasound the technician had said, “Your gallbladder is fine, but you have a fatty liver.”  The way she said it made it sound like it was more than just a casual observation, so when I got home I did a quick search on the National Library of Medicine’s website, where I found a lot of information about NAFLD.  (I’m not a teetotaler, but I don’t drink much.)

The progression from NAFLD to NASH to cirrhosis to needing a liver transplant or you die got my attention. Even before I got the formal diagnosis from my doctor I changed my diet (I started eating fish, raisins, and nuts, as well as more fruit, nuts, raisins, whole grains, leafy green vegetables, and fiber (even tried quinoa); and fewer sugar-sweetened drinks) and lots more exercise.  I dropped about twenty pounds in four months and, more importantly, my triglyceride level dropped a lot.

I had relapsed a bit since then, but after viewing Dr. Lustig’s presentation on the effects of fructose (and having done some follow up reading on the topic) I have once again cut back on sugar consumption and have started working out more regularly once more.

If you’re been sort of blasé about fructose you might find yourself changing your mind if you look at the slides on the “Detrimental Effects of Fructose” from a presentation he gave at the National Institute of Environmental Health Sciences (NIEHS) (pp. 15-27, with final slides on p. 27 showing the end result) and look at how fructose metabolized by the liver ultimately results in the creation of lipid droplets (these are what create a “fatty liver”), FFA (free fatty acids) (which help trigger insulin resistance), and triglycerides (TG), resulting in higher blood pressure and inflammation (among other things).

April 2, 2010

Metabolic syndrome and exposure to persistent organic pollutants

Take a spoonful of sugar, add a pinch of chemicals that accumulate in fatty tissue, and voila, metabolic syndrome! So while Dr. Lustig may be on to something, it looks like fructose might not be the only thing to blame for the obesity epidemic.

The reason why persistent organic pollutants (POPs) are a problem is that they can bioaccumulate in fatty tissue.  (If fructose causes metabolic syndrome as Dr. Lustig says, and metabolic syndrome results in increased obesity, which in turn means more fatty tissue, and more fatty tissue can absorb more POPs, we would seem to have started a rather vicious cycle.)

The Editor’s Summary explains why the findings of this study are especially important (emphasis added).

The authors conclude that exposure to POPs through a diet high in fatty fish is capable of inducing insulin resistance and impairing both lipid and glucose metabolism. Furthermore, they found that n-3 polyunsaturated fatty acids failed to counteract the harmful metabolic effects of dietary POP exposure. This finding is important because the presence of n-3-polyunsaturated fatty acids in fish oil has been reported to have a wide range of beneficial effects, including protection against high-fat diet–induced insulin resistance. The authors conclude that there is a need to continue efforts to limit human exposure to dietary POPs even in foods containing protective factors such as polyunsaturated fatty acids.

Persistent Organic Pollutant Exposure Leads to Insulin Resistance Syndrome, Jérôme Ruzzin et al. Environmental Health Perspectives, 118(4) Apr 2010.

Related EHP news item:

Chew on This: Persistent Organic Pollutants May Promote Insulin Resistance Syndrome

March 14, 2010

The toxic effects of … sugar

UCSF Lecture on Sugar & Obesity Goes Viral as Experts Confront Health Crisis

March 10, 2010 UCSF news release (University of California San Francisco)

Background

Metabolic syndrome (from National Library of Medicine) – a group of conditions that put you at risk for heart disease and diabetes. These conditions are

See also Metabolic Syndrome from the Nemours Foundation.

Connection between sugar and the metabolic syndrome

The news release includes a presentation by Dr. Robert H. Lustig, UCSF, on “Sugar: The Bitter Truth” (approx. 1h, 30min.)

Dr. Lustig explores the damage caused by sugary foods. He argues that fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic through their effects on insulin. Series: UCSF Mini Medical School for the Public [7/2009].  (In case you don’t have an hour and a half to spare, I found a basic version of Lustig’s presentation on the NIEHS website.  Also includes a QuickTime version of the presentation Lustig gave at that workshop.)

I’m still convinced that environmental chemicals could be contributing to occurrence of metabolic syndrome, but Dr. Lustig’s presentation was eye-opening.  I don’t understand all the biochemistry, but he makes what I think is a convincing argument that fructose, whether from high fructose corn syrup (HFCS) or from refined sugar (sugar = fructose + glucose), is responsible for the development of metabolic syndrome.

The basic reason is not because we’re taking in too many calories, but that fructose is metabolized differently than glucose is.

Lustig goes through the history of sugar in drinks and food and the production of HFCS before diving into biochemistry.  He compares the metabolism of glucose, ethanol, and fructose, covering all the metabolic pathways for each.

All of the cells in the body can metabolize glucose, some ethanol is absorbed bv the gastrointestinal tract, then metabolized by the brain and liver.

Fructose is primarily metabolized by the liver.  I won’t go into the details here, but fructose increases the level of triglycerides, messes with the insulin and leptin processes, makes the pancreas work harder, and has other negative effects on your body.

Dr. Lustig makes a very convincing argument that overconsumption of fructose has causes metabolic syndrome and had led to the obesity epidemic.

Some people argue that it’s Americans’ eating habits and lack of exercise that have caused the obesity epidemic.  Lustig asks, if that’s true, how do you explain the epidemic of obese six-month-olds? (Lustig looks at the amount of sugar contained in many formulas.)

Lustig also notes that the role of exercise isn’t really to burn calories, but to keep our bodies’ metabolic processes running smoothly and discusses the important role of fiber in fructose metabolism.

From the NIEHS website (a basic version of Lustig’s presentation)

(presented at a workshop on “Children’s Environmental Health Research: Past, Present & Future,” Jan. 2007) – this workshop had sessions focusing on lead and neurotoxicity, asthma, metabolic disorders, and ADHD)

Summary

Fructose (sucrose or HFCS) consumption has increased in the past 30 years, coinciding with the obesity epidemic

  • Fructose is everywhere
  • Fructose is not glucose

• Hepatic fructose metabolism leads to all the manifestations of the Metabolic Syndrome:

      • hypertension
      • de novo lipogenesis, dyslipidemia, and hepatic steatosis
      • inflammation
      • hepatic insulin resistance
      • obesity
      • CNS leptin resistance, promoting continuous consumption

• Fructose ingestion interferes with obesity intervention
• Fructose is a chronic toxin (it’s metabolized like ethanol)

Links (from UCSF)

UCSF Center for Obesity Assessment, Study & Treatment (COAST)

WATCH Clinic
UCSF Children’s Hospital

Adult Weight Management Program
UCSF Medical Center

New Center to Focus on Effects of Stress, Socioeconomic Status on Obesity
UCSF Today, August 11, 2009

Sugar is a Poison, Says UCSF Obesity Expert
Science Café, June 25, 2009

The Biology of Fat (or Why Literally Running Away from Stress Is a Good Idea)
Science Café, July 6, 2007

Note: A much briefer (and less rigorous) discussion of the harmful effects of HFCS can be found at High-Fructose Corn Syrup Truth, Still Not Sexy, HFCS.

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