Tag Archives: overweight

Does Pollution Cause Type 2 Diabetes?

Posted on January 2, 2016 | Comments Off on Does Pollution Cause Type 2 Diabetes?
See text for mention of pancreatic alpha and beta cells

See text for mention of pancreatic alpha and beta cells

A panel of university-based scientists convened by The Endocrine Society recently reviewed the available literature on health effects of endocrine-disrupting chemicals (aka EDCs). The executive summary is available free online. Some excerpts:

The full Scientific Statement represents a comprehensive review of the literature on seven topics for which there is strong mechanistic, experimental, animal, and epidemiological evidence for endocrine disruption, namely: obesity and diabetes, female reproduction, male reproduction, hormone-sensitive cancers in females, prostate cancer, thyroid, and neurodevelopment and neuroendocrine systems. EDCs such as bisphenol A, phthalates, pesticides, persistent organic pollutants such as polychlorinated biphenyls, polybrominated diethyl ethers, and dioxins were emphasized because these chemicals had the greatest depth and breadth of available information.

*  *  *

Both cellular and animal models demonstrate a role for EDCs in the etiology of obesity and T2D [type 2 diabetes]. For obesity, animal studies show that EDC-induced weight gain depends on the timing of exposure and the age of the animals. Exposures during the perinatal period [the weeks before and after birth] trigger obesity later in life. New results covering a whole range of EDC doses have underscored the importance of nonmonotonic dose-response relationships; some doses induced weight increase, whereas others did not. Furthermore, EDCs elicit obesity by acting directly on white adipose tissue, al- though brain, liver, and even the endocrine pancreas may be direct targets as well.

Regarding T2D, animal studies indicate that some EDCs directly target 􏰁beta and alpha cells in the pancreas, adipocytes, and liver cells and provoke insulin resistance together with hyperinsulinemia. These changes can also be associated with altered levels of adiponectin and leptin— often in the absence of weight gain. This diabetogenic action is also a risk factor for cardiovascular diseases, and hyperinsulinemia can drive diet-induced obesity. Epide- miological studies in humans also point to an association between EDC exposures and obesity and/or T2D; however, because many epidemiological studies are cross-sectional, with diet as an important confounding factor in humans, it is not yet possible to infer causality.

RTWT.

Bix at Fanatic Cook blog says foods of animal origin are the major source of harmful persistent organic pollutants, some of which act as ECDs.

Keep your eyes and ears open for new research reports on this critically important topic.

Steve Parker, M.D.

Book front cover

Book front cover

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Theoretical Support for the Healthfulness of the Paleo Diet

Posted on May 15, 2015 | 4 comments
See modern man walking off that cliff?

See modern man walking off that cliff?

Aren’t people healthier now, thanks to the Agricultural and Industrial Revolutions?

As a marker for health, we can look at life span and longevity. Humans started to see dramatic increases in longevity probably around 30,000 years ago, before the revolutions. Nevertheless, Kuipers, Joordens, and Muskiet note that average life expectancy after the start of the Agricultural Revolution 10,000 years ago fell from about 40 to around 20 years.

Other researchers report that average height in the Nile River Valley at the time of the transition fell by 4 inches (10 cm). The Agricultural Revolution allowed for rapid expansion of human populations through more births, but those folks still didn’t live very long. As before the revolution, infections and high infant/child mortality rates were devastating killers, dragging down average life spans. If you survived childhood, you had a shot at hitting 50 or 60.

At the dawn of the Industrial Revolution, life expectancy at birth was only 35–40 years, even in then-sophisticated cultures like Switzerland. Consider Thomas Jefferson, the principal author of the U.S. Declaration of Independence and the third U.S. president, who lived between 1743 and 1826 (he died on July 4, Independence Day). He and his wife Martha had six children; only two survived to adulthood, and only one past the age of 25. Martha died at age 33. This mortality picture was typical for the times.

Since 1800, life expectancy has doubled in industrialized countries, but it’s mostly due to public health measures and economic prosperity. Other than smallpox vaccination, it wasn’t until the mid-20th century that medical care advances contributed in a major way to longevity.

Overview: Conflict Between Our Paleolithic Genes and Modern Life

A number of diseases or conditions may result from the mismatch of our Paleolithic genes and modern lifestyle. If not caused by the mismatch, they’re aggravated by it. These are the so-called “diseases of civilization”:

  • type 2 diabetes
  • high blood pressure
  • overweigh and obesity
  • dental caries (tooth decay or cavities)
  • osteoporosis
  • fertility problems (polycystic ovary syndrome)
  • pregnancy complications (pre-eclampsia, gestational diabetes)
  • some cancers (colon, breast, prostate)
  • heart disease (such as coronary artery disease)
  • major and postpartum depression
  • autism
  • schizophrenia
  • some neurodegenerative diseases (Parkinsons disease, Alzheimer’s disease)
  • constipation
  • hemorrhoids
  • diverticulosis
"I ate well over 70 grams of fiber daily!"

“I ate well over 70 grams of fiber daily!”

Overweight and Obesity

The Paleolithic diet is lower in total carbohydrate calories compared to the standard American diet: 30-35% versus 50-55% of calories. The higher consumption today, especially of highly processed refined carbohydrates, contributes to overweight and obesity, diabetes, gallbladder disease, heart disease, and possibly dementia. Ian Spreadbury hypothesizes that carbohydrate density of modern foods may be the cause of obesity. Refined sugars and grains—types of acellular carbohydrates—are particularly bad offenders. These acellular carbs may alter our gut microorganisms, leading to systemic inflammation and leptin resistance, etc. Our Paleolithic ancestors had little access to acellular carbohydrates. Here’s how Spreadbury explains acellular: “Tubers, fruits, or functional plant parts such as leaves and stems store their carbohydrates in organelles as part of fiber-walled living cells. These are thought to remain largely intact during cooking, which instead mostly breaks cell-to-cell adhesion. This cellular storage appears to mandate a maximum density of around 23% non-fibrous carbohydrate by mass, the bulk of the cellular weight being made up of water. The acellular carbohydrates of flour, sugar, and processed plant-starch products are considerably more dense. Grains themselves are also highly dense, dry stores of starch designed for rapid macroscopic enzymic mobilization during germination. Whereas foods with living cells will have their low carbohydrate density “locked in” until their cell walls are breached by digestive processes, the chyme produced after consumption of acellular flour and sugar-based foods is thus suggested to have a higher carbohydrate concentration than almost anything the microbiota of the upper GI tract from mouth to small bowel would have encountered during our coevolution.” (Reference: “Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity,” in Diabetes, Metabolic Syndrome, and Obesity: Targets and Therapy. 2012; vol 5: 175–189. doi: 10.2147/DMSO.S33473 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/)

Added sugar provides 17 % of total energy in modern societies, contributing to overweight, obesity, tooth decay, and diabetes. Modern diets provide 15–20% of calories from protein, compared to 25–30% in the Paleolithic diet. To the extent that high protein consumption is satiating, lower consumption may cause over-eating of carbohydrates and fats, then overweight and obesity and all their associated medical conditions.

Heart Disease

I written elsewhere on the blog that the much lower omega-6 to omega-3 fatty acid ratio in the Paleolithic diet. There’s some evidence that today’s high ratio may contribute to systemic inflammation and chronic disease, heart disease in particular. Today’s ratio is quite high due to our consumption of industrial seed oils, such as those derived from soybeans, peanuts, corn, and safflower. And we don’t eat enough cold-water fatty fish, which are major sources of omega-3 fatty acids. Two long-chain polyunsaturated fatty acids, EPA and DHA, are essential fatty acids. That means our bodies cannot make them. We have to get them from diet. DHA and EPA are also cardioprotective omega-3 fatty acids.

High Blood Pressure

Most modern diets have much more sodium and much less potassium than the Paleolithic diet, perhaps contributing to high blood pressure, which in turn contributes to heart attacks, strokes, and possibly premature death. The higher magnesium content of the paleo diet may also help prevent high blood pressure.

Gastrointestinal Problems

We eat much less fiber these days, contributing to constipation, hemorrhoids, and diverticulosis. Some experts believe low fiber consumption adversely effects development of palate bones, jaws, and tooth placement.

Osteoporosis

Our lower vitamin D levels these days may cause osteoporosis (thin fragile bones) and raise the risk of diabetes and cancer. Our prehistoric ancestors spent more time in the sun, allowing their bodies to make vitamin D.

Type 2 Diabetes

Robert Lustig and associates looked at sugar consumption and diabetes rates in 175 countries and found a strong link between sugar and type 2 diabetes. It’s not proof of causation, just suggestive. From the scientific article abstract: “Duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner, while declines in sugar exposure correlated with significant subsequent declines in diabetes rates independently of other socioeconomic, dietary and obesity prevalence changes. Differences in sugar availability statistically explain variations in diabetes prevalence rates at a population level that are not explained by physical activity, overweight or obesity.” (Reference: Basu S, Yoffe P, Hills N, Lustig RH (2013) The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data. PLoS ONE 8(2): e57873. doi:10.1371/journal.pone.0057873)

A major diet change from Stone Age to modern diets is a reduction in magnesium consumption. This could be one reason type 2 diabetes is a problem today. A 2013 article at Diabetes Care suggests that higher magnesium consumption in modern populations may protect against type 2 diabetes (Reference: http://care.diabetesjournals.org/content/early/2013/09/23/dc13-1397.abstract.html?papetoc).

Dental Problems

Dentist John Sorrentino wrote at his blog in 2012: “The truth is that tooth decay is a relatively new phenomenon. Until the rise of agriculture roughly 10,000 years ago, THERE WAS NO TOOTH DECAY IN HUMANS. Let that sink in for a moment. Humanity is 2,500,000 years old. For the first 2,490,000 years no one ever had a cavity. If we understand that tooth decay started when people started farming instead of hunting and gathering for a living clearly you realize that tooth decay is a disease or mismatch between what you are eating and what your body expects you to eat. If we examine the past as prologue it becomes clear that the path to proper health starts in the mouth and the answers are so simple that not only did a Cave Man do it. They perfected it.” (Reference: http://www.sorrentinodental.com/blog.html?entry=why-teeth-decay-i)

To be fair and balanced, a research report from 2014 found a very high incidence of caries (cavities) in a Stone Age population living in what is now Morocco. The authors attributed the cavities to heavy consumption of acorns, which are rich in carbohydrates and sticky, to boot.

Orthodontist Mike Mew, BDS, MSc, made a presentation at the 2012 Ancestral Health Symposium titled “Craniofacial Dystrophy—Modern Melting Faces.” Dr. Mew says 30% of folks in Western populations have crooked teeth and/or malocclusion, and the mainstream orthodontic community doesn’t know why. But they’ve got expensive treatment for it! Dr. Mew thinks he knows the cause and he shared it at the symposium. The simple cure is “Teeth together. Lips together. Tongue on the roof of your mouth.” And eat hard food that requires lots of chewing, like our ancestors did, ideally in childhood before age 9. Older people also benefit, he says.

NPR (National Public Radio) in February, 2013, ran an article called “Ancient Choppers Were Healthier Than Ours,” by Audrey Carlsen. An excerpt: “Hunter-gatherers had really good teeth,” says Alan Cooper, director of the Australian Centre for Ancient DNA. “[But] as soon as you get to farming populations, you see this massive change. Huge amounts of gum disease. And cavities start cropping up.” And thousands of years later, we’re still waging, and often losing, our war against oral disease. Our changing diets are largely to blame. In a study published in the Nature Genetics, Cooper and his research team looked at calcified plaque on ancient teeth from 34 prehistoric human skeletons. What they found was that as our diets changed over time — shifting from meat, vegetables and nuts to carbohydrates and sugar — so too did the composition of bacteria in our mouths. Not all oral bacteria are bad. In fact, many of these microbes help us by protecting against more dangerous pathogens. (Reference: http://www.npr.org/blogs/health/2013/02/24/172688806/ancient-chompers-were-healthier-than-ours)

Dentist Mark Burhenne wrote the following at Huffington Post – Canada: “It is generally well accepted that tooth decay, in the modern sense, is a relatively new phenomena. Until the rise of agriculture roughly 10,000 years ago, there was nearly no tooth decay in the human race. Cavities became endemic in the 17th century but became an epidemic in the middle of the 20th century (1950). If we understand that tooth decay started when people started farming, rather than hunting and gathering, it’s clear that tooth decay is the result of a mismatch between what we’re eating and what our bodies are expecting us to eat based on how they evolved….The recent changes in our lifestyle create a “mismatch” for the mouth, which evolved under vastly different environments than what our mouths are exposed to these days. Our mouths evolved to be chewing tough meats and fibrous vegetables. Sugar laden fruit was a rare and special treat for our paleolithic ancestors. Now, our diets are filled with heavily processed foods that take hardly any energy to chew — smoothies, coffees, and sodas high in sugar, white bread, and crackers to name just a few.” (Reference: http://www.huffingtonpost.ca/mark-burhenne/paleo-diet-oral-health_b_4041350.html)

Shrinking Brains

Since the end of the Stone Age, human brain size has been shrinking. That’s not good, is it? Anthropologist John Hawks has noted that over the past 20,000 years, the average volume of the human male brain has decreased from 1,500 cubic centimeters to 1,350 cc, losing a chunk the size of a lemon. The female brain has shrunk proportionately. Anthropologists don’t know why. Is it modern nutrition? The experts aren’t sure what it means for our future. As for me, I think the answer is in Mike Judge’s movie, “Idiocracy.”

His brain was bigger than yours

His brain was bigger than yours

Death By Sugar

Sugar-sweetened beverages kill almost 200,000 worldwide annually, according to a Gitanjali Singh, Ph.D., a postdoctoral research fellow at the Harvard School of Public Health. How could that be? Sugar-sweetened beverages contribute to obesity, which in turn leads to diabetes, cardiovascular disease, and some cancers. (Reference: Singh, GM, et al “Mortality due to sugar-sweetened beverage consumption: A global, regional, and national comparative risk assessment,” American Heart Association Epidemiology and Prevention/Nutrition, Physical Activity and Metabolism 2013 Scientific Sessions, Abstract EPI-13-A-879-AHA.) Reducing consumption of sugar-sweetened beverages was one of the major points in the American Heart Association’s 2010 guidelines for reducing heart disease.

Elderly Cognitive Impairment

Diets high in sugar and other carbohydrates raise the risk of elderly cognitive impairment, according to recent research by the Mayo Clinic. Mild cognitive impairment is often a precursor to incurable dementia. (Most authorities think dementia develops more often in people with diabetes, although some studies refute the linkage.) Researchers followed 940 patients with normal baseline cognitive functioning over the course of four years. Diet was assessed via questionnaire. Study participants were ages 70 to 89. As the years passed, 200 of them developed mild cognitive impairment. Compared with those eating the lowest amount of sugar, those eating the most sugar were 1.5 times more likely to develop cognitive impairment. Looking at total carbohydrate consumption, those eating at the highest levels of carbohydrate consumption were almost twice as likely to develop mild cognitive impairment. The scientists note that those eating lower on the carbohydrate continuum were eating more fats and proteins. (Reference: Mayo Clinic website, published October 16, 2012 http://www.mayoclinic.org/news2012-rst/7128.html)

Is a Paleolithic-Style Diet the Healthiest Way to Eat?

Certified paleo-compliant, plus high omega-3 fatty acids

Certified paleo-compliant, plus high omega-3 fatty acids

The jury’s still out on that one! My strong sense is that it’s definitely more healthful than the Standard American Diet. Maybe the traditional Mediterranean diet or DASH diet is even healthier. Don’t hold your breath waiting for the randomized controlled trials that would answer the question definitively.

If the paleo diet is the healthiest, which version is best? That’s a question for another day (or year).

The most healthful diet for you depends on your genetic make-up and any medical conditions you have.

Steve Parker, M.D.

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Do Sugar Substitutes Cause Overweight and T2 Diabetes?

Posted on January 30, 2015 | 2 comments

We don’t know with certainty yet. But a recent study suggests that non-caloric artificial sweeteners do indeed cause overweight and type 2 diabetes in at least some folks. The study at hand is very small, so I wouldn’t bet the farm on it. I’m not changing any of my recommendations at this point.

exercise for weight loss and management, dumbbells

Too many diet sodas?

 

The proposed mechanism for adverse metabolic effects of sugar substitutes is that they alter the mix of germs that live in our intestines. That alteration in turn causes  the overweight and obesity. See MedPageToday for the complicated details. The first part of the article is about mice; humans are at the end.

Some quotes:

“Our results from short- and long-term human non-caloric sweetener consumer cohorts suggest that human individuals feature a personalized response to non-caloric sweeteners, possibly stemming from differences in their microbiota composition and function,” the researchers wrote.

The researchers further suggested that these individualized nutritional responses may be driven by personalized functional differences in the micro biome [intestinal germs or bacteria].

***

Diabetes researcher Robert Rizza, MD, of the Mayo Clinic in Rochester, Minn., who was not involved with the research, called the findings “fascinating.”

He noted that earlier research suggests people who eat large amounts of artificial sweeteners have higher incidences of obesity and diabetes. The new research, he said, suggests there may be a causal link.

“This was a very thorough and carefully done study, and I think the message to people who use artificial sweeteners is they need to use them in moderation,” he said. “Drinking 17 diet sodas a day is probably a bad idea, but one or two may be OK.”

I won’t argue with that last sentence! (Unless you have phenylketonuria and want to use aspartame.)

Finally, be aware that several clinical studies show no linkage between human consumption of non-caloric artificial sweeteners and overweight, obesity, and T2 diabetes.

Steve Parker, M.D.

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How Did the Agricultural and Industrial Revolutions Change Human Diets?

Posted on January 1, 2015 | 1 comment

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With the advent of the Agricultural Revolution 10,000 years ago, mankind took a giant leap away from two million years of evolutionary adaptation. The Industrial Revolution that started in the late 18th century—about 240 years ago—was yet another watershed event. The Agricultural Revolution marks the end of the Old Stone Age and the start of the Neolithic period. The Neolithic ended four to six thousand years ago, replaced by the Bronze Age (or Iron Age in some areas).

EFFECTS OF THE AGRICULTURAL REVOLUTION

The Agricultural Revolution refers to farming the land on a large scale, and all that entails: gathering and planting seeds, nurturing the soil, breeding plants for desirable traits, storing crops, processing plants to maximize digestibility, domesticating wild animals and enhancing them by selective breeding, setting down roots in one geographic location, etc. The revolution allowed for the expansion of reliable food supplies and an explosion of human populations. Less time was needed for hunting and foraging, allowing for the development of advanced cultures.

It wasn’t all sunshine and roses, however. We have evidence that human health deteriorated as a result of the revolution. For instance, some populations declined in height and dental health.

EFFECTS OF THE INDUSTRIAL REVOLUTION

The Industrial Revolution starting in the late 18th century brought its own changes to our diet. Progressive industrialization and affluence changed the composition of our “energy foods.” For instance, peasants in poor developing countries derive about 75% of their calories from high-fiber starchy foods. With modernization, fiber-free fats and sugars become the source of 60% of calories. U.S. consumption of cereal fiber decreased by 90% between 1880 and 1976. In addition to lower fiber content, refined wheat products also had fewer vitamins and other micronutrients. Machinery allowed the production of margarine and vegetable oils. Sugar imports and snacking increased in the Western world.

Obesity suddenly became very common in the upper classes of Europe and England toward the end of the 17th century and even more so in the 18th. Weights also increased throughout populations of developed countries. For instance, if we look at U.S. men of average height between the ages of 30 to 34, average weights were 148 lb (66 kg) in 1863, but were up to 170 lb (77 kg) in 1963. Our current obesity epidemic didn’t even start until around 1970.

Let’s look at a few major U.S. diet changes from 1860 to 1975. Energy derived from protein rose from 12% to 14–15%. Energy from fat rose from 25 to 42% of calories. Energy from starches fell from 53 to 22%. Calories from sugar rose from 10 to 24%. Total carbohydrate calories fell from 63 to 46%.

It only takes a few decades to see major changes in a population’s food consumption. For instance, U.S. per capita consumption of salad and cooking oils increased from 21.2 pounds per person in 1980 to 54.3 pounds per person in 2008 (USDA data). I refer to these oils as industrial seed oils, and they include soybean, corn, and sunflower oil. We’re not entirely sure what effect these have on health. Some suspect they are related to obesity, heart disease, and other “diseases of civilization.” Per capita soybean oil consumption in the U.S. increased over a thousand-fold between 1909 and 1999, to 7.4% of total calories. It’s in many of our processed foods. Linoleic acid is a predominant omega-6 fatty acid in seed oils. Linoleic acid consumption increased by 200% in the last century. Thanks to increasing omega-6 fatty acid consumption, the omega-6/omega-3 ratio increased from 5.4:1 to 9.6:1 between 1909 and 2009. (Reference: Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. “Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century.” Am J Clin Nutr. 2011 May;93(5):950-62. doi: 10.3945/ajcn.110.006643. Epub 2011 Mar 2.)

The Industrial Revolution also introduced into our diets large amounts of man-made trans-fats, which are highly detrimental to cardiovascular health. Public outcry has lead to diminishing amounts of dietary trans-fats over the last decade.

An occasional teaspoon of sugar probably won't hurt you

Added sugars: table sugar in coffee, high-fructose corn syrup in ketchup

At his Whole Health Source blog, Dr. Stephan Guyenet and Jeremy Landen produced a graph of U.S. sugar consumption from 1822 to 2005. Dr. Guyenet wrote, “It’s a remarkably straight line, increasing steadily from 6.3 pounds (2.9 kg) per person per year in 1822 to a maximum of 107.7 pounds (49 kg) per person per year in 1999. Wrap your brain around this: in 1822, we ate the amount of added sugar in one 12 ounce can of soda (360 ml) every five days, while today we eat that much sugar every seven hours.” Note that added sugars overwhelmingly supply only one nutrient: pure carbohydrate without vitamins, minerals, antioxidants, protein, fat, etc.

 

Think about the typical Western or Standard American Diet (SAD) eaten by an adult these days. It provides an average of 2673 calories a day (not accounting for wastage of calories in restaurants; 2250 cals/day is probably a more accurate figure for actual consumption). Added sugars provide 459 of those calories, or 17% of the total. Grains provide 625 calories, or 23% of the total. Most of those sugars and grains are in processed, commercial foods. So added sugars and grains provide 40% of the total calories in the SAD. That’s a huge change from the diet of our prehistoric ancestors. Remember, we need good insulin action to process these carbohydrates, which is a problem for diabetics. Anyone going from the SAD to pure paleo eating will be drastically reducing intake of added sugars and grains, our current major sources of carbohydrate. They’ll be replacing them with foods that generally require less insulin for processing. (Figures are from an April 5, 2011, infographic at Civil Eats: http://www.civileats.com.)

FUN FACTS! (from the U.S. Dept. of Agriculture)

  • A typical carbonated soda contains the equivalent of 10 tsp (50 ml) of table sugar.
  • The typical U.S. adult eats 30 tsp (150 ml) daily of added sweeteners and sugars.
  • U.S total grain product consumption was at record lows in the 1970s, at 138 pounds per person. By 2008, grain consumption was up by 45%, to 200 pounds per person.
  • Total caloric sweetener consumption (by dry weight) was 110 pounds per person in the 1950s. By 2000, it was up 39% to 150 pounds.
  • Between 1970 and 2003, consumption of added fats and oils rose by 63%, from 53 to 85 pounds. (How tasty would that be without starches and sugars? Not very.)
  • In 2008, “added fat” calories in the U.S. adult diet were 641 (24% of total calories).

Steve Parker, M.D.

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Americans Eat Too Much

Posted on September 23, 2014 | 3 comments

The U.S. adult population in the 1970s ate an average of 2400 calories a day. By the 2000s, our calories were up to 2900.

Putting a face on the statistics

Putting a face on the statistics

What did average adult weight do as we increased daily calories by 500? It increased by 8.6 kg, from 72.2 to 80.6 kg. In U.S. units, that’s a 19 lb gain, from 159 to 178 lb.

Children increased their average intake by 350 cals/day over the same time frame.

If I recall correctly, I’ve seen other research suggesting the daily calorie consumption increase has been more like 150 to 350 per day (lower end for women, higher for men). I suspect these latter figures are more accurate.

Details are in the American Journal of Clinical Nutrition.

The study authors don’t say for sure why we’re eating more, but offhand mention an “obesogenic food environment.”  They don’t think decreased physical activity is the cause of our weight gain; we’re fatter because we eat too much.

Steve Parker, M.D.

h/t Ivor Goodbody

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Pollution May Be Causing T2 Diabetes and Obesity

Posted on August 5, 2014 | 2 comments

It sounds like Jerome Ruzzin is convinced that’s the case. I put some thought into it last August and was skeptical—still am, but I’m keeping an open mind. Mr. Ruzzin has a review article published in 2012 at BMC Public Health (“Public health concern behind the exposure to persistent organic pollutants and the risk of metabolic diseases”). Here’s his summary:

The global prevalence of metabolic diseases like obesity and type 2 diabetes, and its colossal economic and social costs represent a major public health issue for our societies. There is now solid evidence demonstrating the contribution of POPs [persistent organic pollutants], at environmental levels, to metabolic disorders. Thus, human exposure to POPs might have, for decades, been sufficient and enough to participate to the epidemics of obesity and type 2 diabetes. Based on recent studies, the fundaments of current risk assessment of POPs, like “concept of additive effects” or “dioxins and dl-PCBs induced similar biological effects through AhR”, appear unlikely to predict the risk of metabolic diseases. Furthermore, POP regulation in food products should be harmonized and re-evaluated to better protect consumers. Neglecting the novel and emerging knowledge about the link between POPs and metabolic diseases will have significant health impacts for the general population and the next generations.

Read the whole enchilada.

The cold-water fatty fish I so often recommend to my patients could be hurting them. They are major reservoirs of food-based POPs.

Steve Parker, M.D.

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Is Dining Out Making Us Fat?

Posted on April 7, 2014 | Comments Off on Is Dining Out Making Us Fat?
So easy to over-eat!

So easy to over-eat!

The U.S. trend of increasing overweight and obesity started about 1970. I wonder if eating away from home is related to the trend. I found a USDA report with pertinent data from 1977 to 1995. It also has interesting info on snacking and total calories consumed. Some quotes:

“We define home and away-from-home foods based on where the foods are obtained, not where they are eaten. Food at home consists of foods purchased at a retail store, such as a grocery store, a convenience store, or a supermarket. Food away from home consists of foods obtained at various places other than retail stores (mainly food-service establishments).”

***

“Over the past two decades, the number of meals consumed has remained fairly stable at 2.6 to 2.7 per day. However, snacking has increased, from less than once a day in 1987-88 to 1.6 times per day in 1995. The increased popularity in dining out is evident as the proportion of meals away from home increased from 16 percent in 1977-78 to 29 percent in 1995, and the proportion of snacks away from home rose from 17 percent in 1977-78 to 22 percent in 1995. Overall, eating occasions (meals and snacks) away from home increased by more than two-thirds over the past two decades, from 16 percent of all eating occasions in 1977-78 to 27 percent in 1995.”

***

“Average caloric intake declined from 1,876 calories per person per day in 1977-78 to 1,807 calories per person per day in 1987-88, then rose steadily to 2,043 calories per person per day in 1995.”

***

“These numbers suggest that, when eating out, people either eat more or eat higher-calorie foods or both.”

Parker here. I’m well aware that these data points don’t prove that increased eating-out, increased snacking,  and increased total calorie consumption have caused our overweight and obesity problem. But they sure make you wonder, don’t they? None of these factors was on a recent list of potential causes of obesity.

If accurate, the increased calories alone could be the cause. Fast-food and other restaurants do all they possibly can to satisfy your cravings and earn your repeat business.

If you struggle with overweight, why not cut down on snacking and eating meals away from home?

Steve Parker, M.D.

Update:

Here’s a pie chart I found with more current and detailed information from the U.S. government (h/t Yoni Freedhoff):

feb13_feature_guthrie_fig03

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Does Dining Out Cause Obesity?

Posted on March 14, 2014 | 2 comments
Home-cooked meal

Home-cooked meal

The U.S. trend of increasing overweight and obesity started about 1970. I wonder if eating away from home is related to the trend. I found a USDA report with pertinent data from 1977 to 1995. It also has interesting info on snacking and total calories consumed. Some quotes:

“We define home and away-from-home foods based on where the foods are obtained, not where they are eaten. Food at home consists of foods purchased at a retail store, such as a grocery store, a convenience store, or a supermarket. Food away from home consists of foods obtained at various places other than retail stores (mainly food-service establishments).”

***

“Over the past two decades, the number of meals consumed has remained fairly stable at 2.6 to 2.7 per day. However, snacking has increased, from less than once a day in 1987-88 to 1.6 times per day in 1995. The increased popularity in dining out is evident as the proportion of meals away from home increased from 16 percent in 1977-78 to 29 percent in 1995, and the proportion of snacks away from home rose from 17 percent in 1977-78 to 22 percent in 1995. Overall, eating occasions (meals and snacks) away from home increased by more than two-thirds over the past two decades, from 16 percent of all eating occasions in 1977-78 to 27 percent in 1995.”

***

“Average caloric intake declined from 1,876 calories per person per day in 1977-78 to 1,807 calories per person per day in 1987-88, then rose steadily to 2,043 calories per person per day in 1995.”

***

“These numbers suggest that, when eating out, people either eat more or eat higher-calorie foods or both.”

Parker here. I’m well aware that these data points don’t prove that increased eating-out, increased snacking,  and increased total calorie consumption have caused our overweight and obesity problem. But they sure make you wonder, don’t they? None of these factors was on a recent list of potential causes of obesity.

If accurate, the increased calories alone could be the cause. Fast-food and other restaurants do all they possibly can to satisfy your cravings and earn your repeat business.

If you struggle with overweight, why not cut down on snacking and eating meals away from home?

Steve Parker, M.D.

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Heresy! Sleep Deprivation NOT Linked to Adult Obesity

Posted on September 22, 2013 | Comments Off on Heresy! Sleep Deprivation NOT Linked to Adult Obesity
Paleobetic diet

I bet she’s faking

It’s currently popular to blame inadequate sleep time for overweight and obesity. I found a study supporting that idea in children, but not adults. Here’s the authors’ conclusion:

While shorter sleep duration consistently predicts subsequent weight gain in children, the relationship is not clear in adults. We discuss possible limitations of the current studies: 1.) the diminishing association between short sleep duration on weight gain over time after transition to short sleep, 2.) lack of inclusion of appropriate confounding, mediating, and moderating variables (i.e. sleep complaints and sedentary behavior), and 3.) measurement issues.

I found another analysis from a different team that is skeptical about the association of sleep deprivation and obesity in adults.

Everybody knows adults are getting less sleep now than we did decades ago, right? Well, not really. From Sleep Duration Across the Lifespan: Implications for Health:

Twelve studies, representing data from 15 countries and a time period of approximately 40 years, attempted to document changes in sleep duration over that time period. They found that, overall, there is no consistent evidence that sleep durations worldwide are declining among adults. Sleep duration decreased in six countries, sleep duration increased in seven countries, and mixed results were detected in two (one of which was the USA). In particular, the data from the USA suggest that although mean sleep duration may have actually increased slightly over the past 40 years, the proportion of short sleepers (six hours per night or less) also seems to have increased over the past several decades.

See, it’s complicated. Don’t believe everything you read. Not even this.

Steve Parker, M.D.

PS: It’s fun being an iconoclast now and then!

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Do Environmental Contaminants Cause Type 2 Diabetes or Obesity?

Posted on August 22, 2013 | Comments Off on Do Environmental Contaminants Cause Type 2 Diabetes or Obesity?
"Today we're going to learn about odds ratios and relative risk."

“Today we’re going to learn about odds ratios and relative risk.”

A month ago I watched part of a documentary called “Plastic Planet” on Current TV (Now Al Jazeera TV). It was alarming. Apparently chemicals are leaking out of plastics into the environment (or into foods contained by plastic), making us diabetic, fat, impairing our fertility, and God knows what else. The narrator talked like it was a sure thing. I had to go to work before it was over. A couple chemicals I remember being mentioned are bisphenol A (BPA) and phthalates. I sorta freaked my wife out when I mentioned it to her. I always take my lunch to work in plastic containers and often cover microwaved food with Glad Press’n Seal plastic wrap.

A few days later I saw a report of sperm counts being half of what they were just half a century ago. (It’s debatable.) Environmental contaminants were mentioned as a potential cause.

So I spent a couple hours trying to figure out if chemical contamination really is causing obesity and type 2 diabetes. In the U.S., childhood obesity has tripled since 1980, to a current rate of 17%. Even preschool obesity (age 2-5) doubled from 5 to 10% over that span. In industrial societies, even our pets, lab animals (rodents and primates), and feral rats are getting fatter! The ongoing epidemics of obesity and type 2 diabetes, and our lack of progress in preventing and reversing them, testify that we may not have them figured out and should keep looking at root causes to see if we’re missing anything.

Straightaway, I’ll tell you it’s not easy looking into this issue. The experts are divided. The studies are often contradictory or inconsistent. One way to determine the cause of a condition or illness is to apply Bradford Hill criteria (see bottom of page for those). We could reach a conclusion faster if we did controlled exposure experiments on humans, but we don’t. We look at epidemiological studies and animal studies that don’t necessarily apply to humans.

Regarding type 1 diabetes and chemical contamination, we have very little data. I’ll not mention type 1 again.

What Does the Science Tell Us?

For this post I read a couple pertinent scientific reviews published in 2012, not restricting myself to plastics as a source of chemical contaminants.

The first was REVIEW OF THE SCIENCE LINKING CHEMICAL EXPOSURES TO THE HUMAN RISK OF OBESITY AND DIABETES from non-profit CHEM Trust, written by a couple M.D., Ph.D.s. I’ll share some quotes and my comments. My clarifying comments within a quote are in [brackets].

“It should be noted that diabetes itself has not been caused in animals exposed to these chemicals [a long list] in laboratory studies, but metabolic disruption closely related to the pathogenesis of Type 2 diabetes has been reported for many chemicals.”

“In 2002, Paula Baillie-Hamilton proposed a hypothesis linking exposure to chemicals with obesity, and this is now gaining credence. Exposure to low concentrations of some chemicals leads to weight gain in adult animals, while exposure to high concentrations causes weight loss.”

“The obesogen hypothesis essentially proposes that exposure to chemicals foreign to the body disrupts adipogenesis [fat tissue growth] and the homeostasis and metabolism of lipids (i.e., their normal regulation), ultimately resulting in obesity. Obesogens can be functionally defined as chemicals that alter homeostatic metabolic set-points, disrupt appetite controls, perturb lipid homeostasis to promote adipocyte hypertrophy [fat cells swelling with fat], stimulate adipogenic pathways that enhance adipocyte hyperplasia [increased numbers of fat cells] or otherwise alter adipocyte differentiation during development. These proposed pathways include inappropriate modulation of nuclear receptor function; therefore, the chemicals can be termed EDCs [endocrine disrupting chemicals].”

Don't assume mouse physiology is the same as human's

Don’t assume mouse physiology is the same as human’s

Literature like this talks about POPs: persistent organic pollutants, sometimes called organohalides. The POPs and other chemical contaminants that are currently suspicious for causing obesity and type 2 diabetes include arsenic, pesticides, phthalates, metals (e.g., cadmium, mercury, organotins), brominated flame retardants, DDE (dichloro-diphenyldichloroethylene), PCBs (polychlorinated biphenyls), trans-nonachlor, dioxins.

Another term you’ll see in this literature is EDCs: endocrine disrupting chemicals. These chemicals mess with hormonal pathways. EDCs that mimic estrogen are linked to obesity and related metabolic dysfunction. Some of the chemicals in the list above are EDCs.

The fear—and some evidence—is that contaminants, whether or not EDCs, are particularly harmful to embryos, fetuses, and infants. For instance, it’s pretty well established that mothers who smoked while pregnant predispose their offspring to obesity in adulthood. (Epigenetics, anyone?) Furthermore, at the right time in the life cycle, it may only take small amounts of contaminants to alter gene expression for the remainder of life. For instance, the number of fat cells we have is mostly determined some time in childhood (or earlier?). As we get fat, those cells simply swell with fat. When we lose weight, those cells shrink, but the total cell number is unchanged. What if contaminant exposure in childhood increases fat cell number irrevocably? Does that predispose to obesity later in life?

The authors note that chemical contaminants are more strongly linked to diabetes than obesity. They do a lot of hemming and hawing, using “maybe,” “might,” “could,” etc. They don’t have a lot of firm conclusions other than “Hey, people, we better wake up and look into this further, and based on the precautionary principle, we better cut back on environmental chemical contamination stat!” [Not a direct quote.] It’s clear they are very concerned about chemical contaminants as a public health issue.

Here’s the second article I read: Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review. About 50 experts were empaneled. Some quotes and my comments:

“Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes. There was also support for the “developmental obesogen” hypothesis, which suggests that chemical exposures may increase the risk of obesity by altering the differentiation of adipocytes [maturation and development of fat cells] or the development of neural circuits that regulate feeding behavior. The effects may be most apparent when the developmental [early life] exposure is combined with consumption of a high-calorie, high-carbohydrate, or high-fat diet later in life.”

“The strongest conclusion from the workshop was that nicotine likely acts as a developmental obesogen in humans. This conclusion was based on the very consistent pattern of overweight/obesity observed in epidemiology studies of children of mothers who smoked during pregnancy (Figure 1) and was supported by findings from laboratory animals exposed to nicotine during prenatal [before birth] development.”

I found some data that don’t support that conclusion, however. Here’s a graph of U.S. smoking rates over the years since 1944. Note that the smoking rate has fallen by almost half since 1983, while obesity rates, including those of children, are going the opposite direction. If in utero cigarette smoke exposure were a major cause of U.S. childhood obesity, we’d be seeing less, not more, childhood obesity. I suppose we could still see a fall-off in adult obesity rates over the next 20 years, reflecting lower smoking rates.  But I doubt that will happen.

The CDC suggests a slight drop in childhood obesity in recent years (2010 data).

“The group concluded that there is evidence for a positive association of diabetes with certain organochlorine POPs [persistent organic pollutants]. Initial data mining indicated the strongest associations of diabetes with trans-nonachlor, DDT (dichloro-diphenyltrichloroethane)/DDE (dichloro-diphenyldichloroethylene)/DDD (dichloro-chlorophenylethane), and dioxins/dioxin-like chemicals, including polychlorinated biphenyl (PCBs). In no case was the body of data considered sufficient to establish causality [emphasis added].”

“Overall, this breakout group concluded that the existing data, primarily based on animal and in vitro studies [no live animals involved], are suggestive of an effect of BPA on glucose homeostasis, insulin release, cellular signaling in pancreatic β cells, and adipogenesis. The existing human data on BPA and diabetes (Lang et al. 2008; Melzer et al. 2010) available at the time of the workshop were considered too limited to draw meaningful conclusions. Similarly, data were insufficient to evaluate BPA as a potential risk factor for childhood obesity.”

“It was not possible to reach clear conclusions about BPA and obesity from the existing animal data. Although several studies report body weight gain after developmental exposure, the overall pattern across studies is inconsistent.”

“The pesticide breakout group concluded the epidemiological, animal, and mechanistic data support the biological plausibility that exposure to multiple classes of pesticides may affect risk factors for diabetes and obesity, although many significant data gaps remain.”

“Recently, the focus of investigations has shifted toward studies designed to understand the consequences of developmental exposure to lower doses of organophosphates [insecticides], and the long-term effects of these exposures on metabolic dysfunction, diabetes, and obesity later in life. [All or nearly all the studies cited here were rodent studies, not human.] The general findings are that early-life exposure to otherwise subtoxic levels of organophosphates results in pre-diabetes, abnormalities of lipid metabolism, and promotion of obesity in response to increased dietary fat.”

In case it’s not obvious, remember that “association is not the same as causation.” For example, in the Northern hemisphere, higher swimsuit purchases are associated with summer. Swimsuit sales and summer are linked (associated), but one doesn’t cause the other. Swimsuit purchases are caused by the desire to go swimming, and that’s linked to warm weather.

In at least one of these two review articles, I looked carefully at the odds ratios of various chemicals linked to adverse outcomes. One way this is done is too measure the blood or tissue levels of a contaminant in a population, then compare the adverse outcome rates in animals with the highest and lowest levels of contamination. For instance, if those with the highest contamination have twice the incidence of diabetes as the least contaminated, the odds ratio is 2. You could also call it the relative risk. Many of the potentially harmful chemicals we’re considering have a relative risk ratio of 1.5 to 3. Contrast those numbers with the relative risk of death from lung cancer in smokers versus nonsmokers: the relative risk is 10. Smokers are 10 times more likely to die of lung cancer. That’s a much stronger association and a main reason we decided smoking causes lung cancer. Odds ratios under two are not very strong evidence when considering causality; we’d like to have more pieces of the puzzle.

These guys flat-out said arsenic is not a cause of diabetes in the U.S.

Overall, the authors of the second article I read were clearly less alarmed than those of the first. Could the less-alarmed panelists have been paid off by the chemical industry to produce a less scary report, so as not to jeopardize their profits? I don’t have the resources to investigate that possibility. The workshop was organized (and paid for, I assume) by the U.S. government, but that’s no guarantee of pure motivation by any means.

You need a break. Enjoy.

You need a break. Enjoy.

My Conclusions

For sure, if I were a momma rat contemplating pregnancy, I’d avoid all those chemicals like the plague!

It’s premature to say that these chemical contaminants are significant causes of obesity and type 2 diabetes in humans. That’s certainly possible, however. We’ll have to depend on unbiased scientists to do more definitive research for answers, which certainly seems a worthwhile endeavor. Something tells me the chemical producers won’t be paying for it. Universities or governments will have to do it.

You should keep your eyes and ears open for new evidence.

There’s more evidence for chemical contaminants as a potential cause of type 2 diabetes than for obesity. Fetal and childhood exposure may be more harmful than later in life.

If I were 89-years-old, I wouldn’t worry about these chemicals causing obesity or diabetes. For those quite a bit younger, taking action to avoid these environmental contaminants is optional. As for me, I’m drinking less water out of plastic bottles and more tap water out of glass or metal containers. Yet I’m not sure which water has fewer contaminants.

Humans, particularly those anticipating pregnancy and child-rearing, might be well advised to minimize exposure to the aforementioned chemicals. For now, I’ll leave you to your own devices to figure out how to do that. Good luck.

Why not read the two review articles I did and form your own opinion?

Unless the chemical industry is involved in fraud, bribery, obfuscation, or other malfeasance, the Plastic Planet documentary gets ahead of the science. I’m less afraid of my plastic containers now.

Steve Parker, M.D.

Additional Resources:

Sarah Howard at Diabetes and the Environment (focus on type 1 but much on type 2 also).

Jenny Ruhl, who thinks chemical contaminants are a significant cause of type 2 diabetes (search her site).

From Wikipedia:

The Bradford Hill criteria, otherwise known as Hill’s criteria for causation, are a group of minimal conditions necessary to provide adequate evidence of a causal relationship between an incidence and a consequence, established by the English epidemiologist Sir Austin Bradford Hill (1897–1991) in 1965.

The list of the criteria is as follows:

  1. Strength: A small association does not mean that there is not a causal effect, though the larger the association, the more likely that it is causal.
  2. Consistency: Consistent findings observed by different persons in different places with different samples strengthens the likelihood of an effect.
  3. Specificity: Causation is likely if a very specific population at a specific site and disease with no other likely explanation. The more specific an association between a factor and an effect is, the bigger the probability of a causal relationship.
  4. Temporality: The effect has to occur after the cause (and if there is an expected delay between the cause and expected effect, then the effect must occur after that delay).
  5. Biological gradient: Greater exposure should generally lead to greater incidence of the effect. However, in some cases, the mere presence of the factor can trigger the effect. In other cases, an inverse proportion is observed: greater exposure leads to lower incidence.
  6. Plausibility: A plausible mechanism between cause and effect is helpful (but Hill noted that knowledge of the mechanism is limited by current knowledge).
  7. Coherence: Coherence between epidemiological and laboratory findings increases the likelihood of an effect. However, Hill noted that “… lack of such [laboratory] evidence cannot nullify the epidemiological effect on associations”.
  8. Experiment: “Occasionally it is possible to appeal to experimental evidence”.
  9. Analogy: The effect of similar factors may be considered.

Science-Based Medicine blog has more on Hill’s criteria.

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