I Wish I Were Far From the Madding Crowd

August 6, 2010

A chemical pot pourri

This is a real hodge-podge of items.

Bisphenol A

The Environmental Working Group (EWG) recently announced the findings of a study that found BPA in a large percentage of paper receipts it had collected.  http://ewg.org/BPA_Found_In_Receipts

Chemicals in cosmetics

Another resource EWG maintains is the Skin Deep cosmetic safety database.

http://www.cosmeticsdatabase.com/

Speaking of cosmetics, Annie Leonard (“The Story of Stuff”) has come out with “The Story of Cosmetics”, a look at chemicals in cosmetics and personal care products.  The Story of Stuff blog looks at the cosmetics industry’s reaction.

Learning and developmental disabilities and other diseases and conditions

The Collaborative on Health and the Environment (CHE) covers a wide range of topics, from learning and developmental disabilities to the CHE Toxicant and Disease Database, a searchable database that summarizes links between chemical contaminants and approximately 180 human diseases or conditions, to the Metabolic Syndrome Discussion Group.

BP (not just oil spills)

The CHE site also includes news items like:

6 Aug Thousands sign on for $10 billion BP suit. The revelation that BP’s Texas City refinery emitted toxic benzene for more than a month has ignited a furor in the port community that has suffered its share of deadly industrial accidents and toxic spills. Houston Chronicle.

Yes, before the BP oil spill there was the BP Texas City refinery explosion.  The U.S. Chemical Safety Board conducted an investigation.  I believe that they are looking into whether these incidents show that BP fostered a culture of cutting corners.

Chemicals and depression?

Was reading Peter Kramer’s Against Depression, where he argued that depression is a true illness.  (At least that’s what I’m getting out of it.)  He makes a couple of points that struck me.  One, on p. 156 he states that there is a connection between diabetes and depression.  Unfortunately, he doesn’t cite a source for that.  And if true, it’s not clear which caused which.  That is, does having diabetes make it more likely that you would be depressed?  Or does depression in some way connected to the development of diabetes.  Or could diabetes and depression be caused by the same agent?  (Or some combination of the above.)

He also talks about how long-term stress can result in increased levels of corticotropin and that such stress can lead to depression and illness.  Of course, corticotropin is but one element of the neuroendocrine system.  And with many of these things, there are feedback loops that get out of whack if enough recovery time is not available.  That’s actually why some scientists have proposed that a chronic lack of sleep can cause obesity over the long haul.  The International Agency for Research on Cancer and NIOSH are looking at whether “shift work” (along with a number of chemicals) can be considered carcinogenic.

Leptin: An example of what we didn’t know

Leptin, the appetite hormone, was not discovered until 1994 (though its effects had been observed much earlier).  (Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (December 1994). “Positional cloning of the mouse obese gene and its human homologue”. Nature 372 (6505): 425–32. doi:10.1038/372425a0. PMID 7984236.) I mention that because chemical industry apologists seem to ignore the fact that we’ve learned a lot about the human body in the last 15-20 years.  And the more we learn, the more we discover how chemicals can mess up our systems.

Regarding leptin, I found the following using the National Library of Medicine’s MedlinePlus service.

A National Cancer Institute fact sheet on physical activity and cancer states that “increasing physical activity may influence insulin and leptin levels and influence breast cancer prognosis.”

An EPA report, “A Decade of Children’s Environmental Health Research:  Highlights from EPA’s Science to Achieve Results Program,” cites an EPA-funded study that found that “autistic children showed higher levels of leptin (a hormone that affects the regulation of body weight, metabolism, and reproductive function, and influences the immune system) in their blood when compared to typically developing children (Ashwood et al. 2007; R829388C002).”

Citation: Ashwood P., Kwong C., Hansen R., Hertz-Picciotto I., Croen L., Krakowiak P., Walker W., Pessah I.N., and Van de Water J. 2007. “Brief report: Plasma leptin levels are elevated in autism: association with early onset phenotype?” J. Autism Dev. Disord. Advanced online publication (DOI 10.1007/s10803-006-0353-1).  Abstract

So our bodies are these incredibly complex systems.  Some chemical companies would have you believe that the stuff they make, even the synthetic chemicals that human beings have never been exposed to before, have absolutely NO effect on our health.

Truth is, despite the Environmental Defense Fund saying that we’re not guinea pigs, we all are.  (See previous post: “Tired of being a guinea pig?“)

“Would you like BPA with those fries?”

April 18, 2010

Sugar is sugar … or not?

If you’ve followed any of the discussion about high fructose corn syrup (HFCS) vs. sucrose, you’ve probably heard representatives of the soft drink industry and HFCS refiners repeatedly say that fructose is no different than sucrose and that they’re metabolized the same (which, according to more and more research, is debatable).  I’ll get to that a little further on.

How much sugar we’re consuming

Amber Waves article “Behind the Data: Estimating Consumption of Caloric Sweeteners.” (April 2003)

Amount of HFCS and refined sugar delivered to food and beverage manufacturers in 2001

Intake levels represent the difference between total deliveries of calorie sweeteners for food and beverage use and estimated losses
Graphics from http://www.ers.usda.gov/AmberWaves/April03/Indicators/behinddata.htm

Make note of that 31.1 teaspoons per day figure for 2001.  (Daily intake in teaspoons = average annual intake in pounds / 365 days per year x 16 ounces per pound x 28.3495 grams per ounce / 4.2 grams per teaspoon.)

Think about the last item in that formula.  If the label on a box of cereal says 9 g of sugars, that means that a single serving contains 2 tsps of sugar.  A 12 oz. soda containing 39 g of sugars contains more than NINE teaspoons of sugar.  You get the idea.

According to Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005 (see references), for 2005 it was down to 30 teaspoons per day.

What does this tell us?

Several points, one, representatives of the Corn Refiners Association and beverage manufacturers are right when they say that whether it’s fructose or sucrose doesn’t really matter.  If you’re consuming almost 4 times the amount of added sugars you should be, you are going to have problems!

Two, sucrose contained in beverages begins to undergo hydrolysis once it’s bottled and separates into its component parts (that is, fructose and glucose).  So in many cases when you’re drinking a sugar-sweetened soda you’re not drinking sucrose in solution, but sucrose, fructose, and glucose.  If enough time goes by most of the sucrose turns into free fructose and glucose.

A number of studies have shown that fructose is metabolized differently than glucose, but other studies seem to indicate that’s not as much of a concern, except possibly in two cases: one, when the ratio of fructose to glucose consumption is high, or in cases of high consumption of calories.  I would say that we have a combination of those, a relatively high ratio of fructose to glucose consumption (look at the relative amounts of HFCS to refined sugars used by beverage manufacturers!) together with consuming too many calories from sugar.  (And remember, that’s just the average amount.  Some people are consuming even larger amounts of sugar.)

Background on high fructose syrups

I recently came across a very interesting article, coauthored by John S. White, who is, or at least has been, a consultant to the Corn Refiners Association.

“Manufacturing, composition, and applications of fructose.”  L. Mark Hanover and John S. White.  American Journal of Clinical Nutrition, 1993, v.58(suppl.), 724S-732S.
http://www.ajcn.org/cgi/content/abstract/58/5/724S

The article describes the manufacturing and refining process of HFCS (or, as the authors call it, HFS), the composition of various grades of HFCS (as well as crystalline fructose and crystalline fructose syrup), functional properties and uses, and regulatory status.

What I found so fascinating about this particular article though, were these bits of information scattered throughout it.  According to the authors , HFS-42 (that is, HFCS that is 42% fructose) was the “first generation syrup of commerce.”  (p.726S)

They go on to note that :

Japanese and US manufacturers were producing HFS containing 55% fructose by the late 1970s.  HFS-55 was adopted by the carbonated-beverage industry and became the predominant sweetener in colas by late 1984. (p.726S)

On p. 727S, a table showing the typical composition of the various grades of fructose (ranging from 42% all the way up to 80% and 95%).

  • HFS-42 is 42% fructose, 53% dextrose (i.e. glucose), and 5% oligosaccharides
  • HFS-55 is 55% fructose, 42% glucose, and 3% oligosaccharides
  • HFS-80 is 80% fructose, 18% glucose, and 2% oligosaccharides
  • HFS-95 is 95% fructose, 4% glucose, and 1% oligosaccharides

One of the minor differences between HFS-80 and HFS-95 is that they, unlike the other two, contain less sulfated ash and no sulfur dioxide.  (Okay, the HFS-42 and -55 contain only 2 parts per million.)

The crystalline fructose and crystalline fructose syrup are both 99.5% or greater fructose.

What is interesting is that the authors note, p. 731S, that HFS-55 was being used in colas by late 1984, but that in 1988 the FDA had “proposed to recognize the long history of safety for fructose and reaffirm the GRAS status of HFS as a direct human food ingredient.” (FDA, 1992, 21 CFR 182.1866)  GRAS = “Generally Recognized As Safe” (for particular uses of a substance), CFR = Code of Federal Regulations

They go on to note: “The petition is specific for HFS-42, but may include HFS-55 on review of its additional processing steps.”

I’m not a lawyer, but to me that sounds like HFS-55 had not actually been approved for use as a direct human food ingredient at the time that cola manufacturers were starting to use it.  (I guess they must have just done that after the fact.)

HFS-55 vs. HFS-42

“The carbonated beverage industry is the largest user of HFS-42 and -55.” (p. 729S)  HFS-42 is primarily used in non-colas and HFS-55 in many colas, though colas can also be made using more HFS-42.  (See the graphic above about the use of sugar vs. HFCS by food vs. beverage manufacturers.)

In 1993 more than than 90% of energy-containing carbonated beverages produced in the U.S. were sweetened with HFS.

If I understand Hannover and White correctly, before 1984 most colas apparently were sweetened with HFS-42 and after 1984 with HFS-55.  In other words, the HFCS had approximately a 13% increase in the amount of fructose in it after the switch.

More importantly, the ratio of fructose to glucose changed from 42:53 to 55:42.  Why is that important?

Fructose malabsorption

Too much fructose in the diet can cause irritable bowel syndrome and other gastrointestinal problems.  However, studies have found that the problems are reduced when fructose is consumed with glucose.  (A certain percentage of the population is more prone to this, but it doesn’t seem to be an issue for most people.)

This is where you run into the problems of fructose metabolic products related to metabolic syndrome.   (The results of some studies also suggested that fructose malabsorption and metabolism problems were more likely to be associated with copper deficiency.)

Is HFCS the biggest problem?

I was going to say that HFCS is not the innocent player some portray it to be, then I realized that’s not really accurate.  The use of HFCS is not in and of itself the problem; the problem is food and beverage manufacturers putting it in almost every food and beverage they can.  It’s cheaper than refined sugar.  And most fast food places and restaurants reportedly make a higher profit margin off of soft drinks.  Once HFCS was introduced soft drink ingredients became so inexpensive that a lot of places started offering free refills.  I’m sure someone has brought that up before, but perhaps free refills are one of the main contributing factors to the increase in obesity (!?).   When people had to pay for a second glass of soda, they drank less.  Sorry, I don’t have a citation for that, but that seems obvious.  (Okay, I had to check.  I did a search on Google Scholar on +”obesity epidemic” +”free refills” and got 21 hits.   Google Scholar searches the scientific literature and books, as opposed to the entire Web.)

One example (with excerpt containing search terms):

Fructose, insulin resistance, and metabolic dyslipidemia

H Basciano, L Federico, K Adeli – Nutrition & Metabolism, 2005 – biomedcentral.com
in humans and animals, but the emphasis on fat reductions has had no significant benefits relative to the obesity epidemic. bombarded by huge million-dollar advertising campaigns for soft drinks, offered extra-extra-large serving sizes with free refills.

Apparently this is known as “portion distortion.”

Put that together with chronic overconsumption of sugar (regardless of whether they’re fructose or sucrose), unbalanced diets (deficiencies in vitamin D?), and not as much exercise as we should be getting.

Then throw in genetics, add a good dose of epigenetics in the form of gene-environment interactions, and you have all the conditions for development of metabolic syndrome and an obesity epidemic.

More on this in another post.

References

Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005, by Hodan Farah Wells and Jean C. Buzby, Economic Information Bulletin No. (EIB-33) 27 pp, March 2008, http://www.ers.usda.gov/Publications/EIB33/

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 19, 2010

Update on fructose – Dr. Lustig on Nightline

From post by Michelle Burton – “Dr. Robert Lustig on ABC’s Nightline”

Check out Dr. Robert Lustig on ABC’s Nightline discussing sugar and the damage it is taking on American’s Health.  (See post for link to video.)

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