Sick in the Saddle

Well, back in the saddle might mean riding the horse, but writing the blog requires me to be illness free. And that I am not. Not that is until recently. My recent move must have presdisposed me to infection because shortly after arriving, I came down with what seems now to be an infulenza style illness. And after the baby started in daycare, the organisms have been free flowing at our house. Ever had diarrhea so bad you had to throw up in the trash can while embracing the toilet with the other end? I'll spare you the details.

Nevertheless, illness is a guaranteed weight loss vehicle. More soon.

WG

Back in the Saddle

The move is complete. I'm almost to the stage of calling us moved into the new house. Boxes and paper still dominate the landscape and I can't find a thing. Nothing shakes up life like moving to a new climate, a new house with new surroundings and a new position of gainful employment. Unfortunately nutrition has been on a back burner with most meals consisting of easily prepared semi-palatable industrial dishes of the fast food variety. I will say this: I'm almost certain I've lost weight during the entire process. Maybe a new diet?

Breastfeeding and Obesity: Is there a protective role for breast milk?

Obesity in infancy and childhood is a measure of adiposity that's a little more difficult to determine than the usual weight for height. In adults, the Body Mass Index or BMI is used to estimate the percent body fat. By most rigid definitions, in boys, a body fat mass of greater than 25% defines obesity, while in girls it moves up to greater than 32% body fat. It goes without saying that not all infants defined by the above criteria as obese will go on to become obese children. Likewise not all obese children will go on to become obese adolescents. And finally, not all obese adolescents will become obese adults . . . on the other hand many will.

The relationship between formula feeding and obesity implies breast fed infants have been given a step up in the fight to maintain fat mass within a non-obese range. The biologic plausibility relating the relationship between breast feeding and a protective effect from excessive body fat relies upon a few very nebulous factors. How might the intimate contact between mother and baby protect said child in later years from overeating? Is there some as yet undefined anti-obesity effect provided by the intimate contact of mother and baby? And what are the content factor or factors (often referred to) within breast milk that might modulate later eating practices? Infant formula might be deficient in some as yet not clearly defined hormone or protein factor which establishes weight control in the breast fed infant. Also, is there again some yet undiscovered factor that modulates adipose tissue proliferation and growth in infants and children while those bottle fed infants have no such modulation? And without those modulating factors, fat storage becomes uncontrolled in later life. Finally, might taste function become changed by the suckling of infant to breast such that breast fed infants spend a lifetime eating less due to the chemical environment of the breast milk on the developing taste organ? So many theories, so little evidence.

In all, the epidemiology of obesity as it relates to breast versus bottle feeding has numerous seemingly plausible biologic explanations for the observation that more obese children and adolescents were bottle fed, but offers nothing concrete. The ultimate answer to this question would involve a study taking all newborns, randomize them to either a breast feeding or bottle feeding regimen and measure their change in fat mass over the next thirty years. Short of that, observational studies with all the confounders and interfering factors will cloud the relationship between formula feeding and obesity.

Without citing studies, the hypothesis that formula feeding determines or sets the stage for later obesity presents a dilemma for treating the problem. Are the issues related to obesity not related to environmental factors, such as the number of hours watching television, and the family focus on good nutrition and physical activity? If the deterministic model of obesity is adopted, then treatment with lifestyle changes would be assumed to have no impact as the determining factor (breast versus formula feeding) has already occurred and damaged the system. The cornerstone of treating childhood and adolescent obesity are modifications in physical activity, diet and lifestyle such that more calories are burned and less time is spent in sedentary activities such as television watching and video games or computer games.

Finally, a study was published in the American Journal of Clinical Nutrition (2007;85:1578-1585) titled:

Infant Feeding Method and Obesity: Body Mass Index and Dual–energy X-ray Absorptiometry Measurments at 9-10 y of Age From the Avon Longitudinal Study of Parents and Children.

The long-winded title of the study addressed one of the critical factors in determining obesity, the measurement of fat mass. Since BMI only estimates percent body fat, a more accurate measure using Dual-energy X-ray Absorptiometry (DEXA) was used in children age 9 to 10 years from a large birth cohort. The goal of this study was to determine the relationship between percent total body and trunk adiposity and prior breast versus formula feeding. Of interest was the association between breast feeding and a number of factors. Included in that list and associated with breast feeding was less television watching, higher education, higher socioeconomic class, lower % who smoked and lower maternal BMI. Using multivariate linear regression the association between breast feeding and total body and trunk fat persisted (but was attenuated) after adjustment for all the above factors. Which points to the possibility that factors characteristic of those inclined to breast feed their children are determining fat mass and not the breast milk per se.

In conclusion there isn’t a definitive answer to this question and probably never will be. Wild speculation has led breast feeding advocates to run amok with notions of near perfect populations of babies if exclusively breast fed. Those same advocates recite lower rates of nearly every disease known to man including obesity, again, if all babies were breast fed. There is no doubt in my mind that breast feeding benefits the baby (and mother) in many subtle ways, but preventing obesity? I’m as always . . . a skeptic.

Formula Fed versus Breast Fed: Does one lead to Obesity?

Overweight and obesity have been proposed to have their origins in not just childhood but from dietary intake during the very early months and years of life. The proposal presumes that what a baby consumes during the perinatal and infant stages of development set the tone for weight gain later in life. In particular, the question posed by many a researcher is the following: Do formula fed babies tend to be overweight or obese later in life as children or even later as adults?

While a seemingly absurd proposal, the number of studies looking at this very issue is surprisingly large. The biologic plausibility of this proposal is based upon a fundamental set of observations regarding the comparison of breast fed versus bottle fed babies. Breast fed babies tend to gain less weight in the first 18 months of life when compared side by side to their bottle (formula) fed brethren. Which is surprising given the following comparison of an ounce of each:



Human Breast Milk versus Infant Formula

Kilocalories 22 /20
Protein (grams) 0.32 /0.41
Fat (grams) 1.35 /1.05
Carb (grams) 2.12 /1.93

Calcium (milligrams) 10 /16

Vit C (milligrams) 10 /2.4

Fats (grams)
Saturated 0.619 /0.436
10:0 0.019 /0.011
16:0 0.283 /0.224
18:1 0.454 /0.377
n-3 0.0 /0.003


Comparing the two, much of which I left out for the sake of saving time and coma producing numbers, one can see that infant formula manufacturers have mimicked breast milk in terms of most content. One small difference is in the caloric load. Breast milk is actually more calorically dense than infant formula (and I examined many different formulations). The variable of breast milk is in what the mother consumes. A mother consuming a diet rich in carotenoids or other phytochemicals would likely have breast milk rich in that component. Coastal and seafood eating communities show greater quantities of n-3 fatty acids in breast milk than inland communities. On the other hand, infant formula comes in a host of variations from cow’s milk to soy to fractionated protein and more. Most popular varieties contain arachadonic acid (ARA) and docosahexanoic acid (DHA) to “promote brain development” in babies.

How then might this comparison lead to breast fed infants consistently weighing less than bottle fed cohorts? There are really only two possibilities:

1. Breast milk contains some component or interaction that promotes normal weight gain. Conversely, infant formula lacks said component and promotes excess weight gain.

or

2. Bottle fed infants actually consume larger amounts because of the difference in delivery systems.

My feeling is bottle fed babies actually consume more liquid than breast fed babies. A study needing to answer this question might look at breast milk expressed into a bottle compared to infant formula from a bottle. Which would gain the most weight?

More later.

Infant Formula or Breast Milk: Is there a difference?

A tremendous has been written regarding the benefits of both breast-feeding and breast milk. From neurodevelopmental benefits in speech development to improved mucosal immunity and the subsequent incidence of infectious diseases such as otitis media, respiratory illness and diarrhea, to the subtle behavioristic changes brought about by bonding skin-on-skin and suckling from the mother’s breast, the advantages of breast-feeding have been promoted and elevated from a matter of opinion to in many cases an institutional policy. One of the more obvious reasons for opting to breast feed would include the following brush with common sense: What better food for a baby but the milk produced by his or her mother? In the age of synthetic and artificially produced food, hair, nails, skin, organs, happiness, longevity and more, why not an artificial breast milk?

Enter powdered or liquid infant and newborn formula. Infant formula is a mixture of protein, fat, carbohydrate vitamins and minerals developed as a substitute for breast milk. Infant formula is produced by the likes of Nestlé, Mead Johnson, Ross, Gerber, Wyeth and others under the scrutiny of the United States Food and Drug Administration, designed for babies from premature to 1 year of age. From the age of 1 year on the ability to handle a larger protein load allows for the introduction of cows milk.

The evolution of artificial breast milk or infant formula began in the early 19th century with the establishment of first wet nurses giving way to “dry nursing” with a variety of available milk based products. Dry nursing took a giant leap forward with the development of the artificial nipple by Elijah Pratt in 1845. From there, the science, analysis and monitoring of artificial formulations to feed newborns accelerated to where we are today. We have cow’s milk based protein formulations, soy based formulations, formula with iron, without iron, formula with docosahexanoic acid (DHA) and arachidonic acid (ARA) or without it, and many more.

The question posed by this article is as follows: Does breast-feeding offer an advantage to growing babies developing into children then into adolescents and into adulthood all other factors being equal? By that, is it a stretch to offer some relationship between adult disease and breast feeding versus formula feeding some thirty to fifty years earlier?

Because of the extent of the literature related to this subject, I’ll break it up into three or four articles covering as much literature and as many relevant topics as possible. From the outset, relating an exposure such as breast feeding or infant formula to disease some years later is without a doubt going to be fraught with mixed results. Confounding between the exposure and outcome of interest is at best a tricky business and at worst impossible. For example, the association between breast feeding versus infant formula feeding and the subsequent development of otitis media or ear infections necessarily needs to account for other (usually older) children in the house, daycare exposure, parental smoking, family history of allergies, cleft palate, and other possible exposures predisposing to otitis media or ear infection. At that, a paper showing an association between infant formula feeding and subsequent predisposition to otitis media without taking into account the aforementioned known predisposing factors listed above, may gain popular support because it lends credence to the opinions of some; however, it needs to be viewed for what it is: a flawed analysis. Also, the results may now be obsolete as infant formula has evolved over the years.

The debate over the benefits of breast feeding over the use of infant formulas has also ignored one subset of feeding practices: The breast expressed (using a breast pump) but bottle fed baby. Is it strictly the breast milk or the practice of putting baby to breast?

Flaxseed Oil

I’m currently watching a lot of television as a new addition to the family is feeding every two hours. Babies are amazing little things. Their tiny feet and hands and innocent little pursed lips and occasional open eyes distract from the time warp one enters. They have the uncanny ability to blur the distinction between waking and sleeping or even days of the week. We’ve literally been living in cycles of two hours with no distinction between day and night. Needless to say, I turn to the television on some of my watches.

I became interested in a Bravo Network show the other night called “Top Chef” as one of the panel of “judges” or “experts” in cooking and food claimed that flaxseed was effective at reducing cholesterol in humans and foods with flaxseed were good for those wishing to lower their cholesterol. I paused and scratched my head. Maybe I had missed something?

Flaxseed is rich in fiber if taken whole and if crushed into an oil, is very high in Alpha Linolenic Acid, an 18 carbon Omega-3 fatty acid. Flaxseed oil is also called “linseed” oil and has been used in industrial and commercial processes for ages. As an aside, flaxseed oil is also rich in monounsaturated fatty acid as well as the saturated fatty acid palmitic acid.

The question comes down to an examination of the scientific evidence that an 18 carbon Omega-3 fatty acid (alpha linolenic acid or ALA) will lower cholesterol on its own (that is no dietary changes other than adding the fat supplement have been made). Flaxseeds are high in fiber and impart a fiber load with the consequent cardioprotective properties of any dietary fiber if eaten whole and chewed; however, for most foods, whole flaxseed is not consumed in significant amounts and flaxseed oil or flaxseed supplements with ALA are what the Top Chef is referring to.

A recent study published in the Journal of Nutrition (2006 Nov;136(11):2844-8) did a very slick experiment with double blinding and lots of daily ALA in the test supplements.
What they found was as follows: Lipoprotein levels were no different between groups, LDL, HDL and total cholesterol was unchanged after 26 weeks. In their words,

“In conclusion, ALA does not decrease CVD risk by altering lipoprotein particle size or plasma lipoprotein concentrations.”

So be careful what your Top Chef tells you!

Changes

I apologize for the break in entries but I’ve been preparing for one or two of those life-changing events. I resigned my current position, we’re moving to another state, my wife is having a baby (any day) and we have been selling our house. Now some might see that as more than a confluence of stressful events. I see it as a confluence of stressful events.

A new baby is a fantastic event. I love babies. They represent a fresh look at life, a new perspective on humanity, and a passing along of hundred million year old genetic adaptation. A new career position is usually an opportunity to see problems from a different perspective. Meeting new people, doing daily tasks with a different cadence and being confronted with new and different problems always adds to a cumulative career of needed experiences. Moving out of a house you have lived in for many years has no redeeming qualities.

The stress of the events listed above is without question a risk factor for any of a number of bad outcomes. One of the more common expressions of stress is to overeat. Eating supplies a sudden sense of physiologic comfort and gives a brief period of rest in a tumultuous time. With the initial shock of life changes, adaptation to change is a fulcrum of tolerable reactions versus maladaptive reflexes. Overeating is just one small maladaptive change. Alcohol is another self-medicating approach to stress. Depression, evolution of cardiovascular disease and other medical expressions of stress might surface at any time.

When all is settled: new house, new state, new career path, new baby; the phenomenon of stress is very real and needs constant addressing.

Public Health Response to Obesity

The case of Connor McCreaddie, an 8yo obese boy living with his mother in Wallsend, North Tyneside, a distance north of London, raises some interesting questions. I happened to rediscover this story as I was looking up some references on genetics and obesity. If you haven’t heard about the story here’s the short version: Connor is 8 years old, currently in the third grade and weighs somewhere in the range of 200 lbs. The story was plastered over the newswires last February/March as local social services, who had been working with the family for some undetermined amount of time, considered Connor at risk of health sequelae from his obesity. Not really a story worth consideration at that, until the authorities considered taking little Connor into custody because his mother was unable to keep him from eating junk food.

To quote Dr. Colin Waine, the Director of the National Obesity Forum in Nottingham, England, Connor’s lifestyle was “extremely dangerous” and might lead to diabetes, heart disease and nervous system disease in his early 20’s. He added, “He’s really at risk of dying by the age of 30.”

That’s still not the real story here.

The issue has less to do with obesity and more to do with state-run management of a public health service. In more modern-day examples of epidemics, or the worst possible case, a pandemic, the forces that manage health on a grand scale need to have a plan of action. A model of the worst possible scenario in recent history was the influenza epidemic of 1918. The pandemic flu was responsible for the deaths of between 20 and 40 million people worldwide. The epidemic called the “Spanish Flu,” probably originated in China but struck early in Spain for unknown reasons. The virulence of the influenza virus was thought to be due to spontaneous genetic recombination—a technique viruses utilize to overcome herd immunity—creating a strain particularly lethal to humans. Chance recombination did it then and might do it again in the future. What then could the forces of today do in the face of a public health crisis such as an influenza pandemic? And might we model our public health fight against obesity in the same way?

The short answer is no. Pandemics with rapid respiratory transmission and short incubation times requires an entire population to isolate themselves from others. A friend of mine is currently working on a pandemic response model.
I asked him, “What do we do in a pandemic?”
He put it simply, “Stay home. Don’t go to the grocery store, don’t go to work, don’t go to a shopping mall or a movie. Isolate yourself. And if you must go out, wear a mask.”

So how does any of this relate to childhood obesity and Connor McCreaddie? Returning from the model of a pandemic, the obesity issues of childhood worldwide are quite often being referred to as an epidemic. And with that designation comes a public health response. Enter the authorities with the capacity to create sanitariums for tuberculosis patients and quarantines for infected households. Could the easy access to cheap, high calorie foods lead to government run sanitariums where those among us who become obese are housed and fed government sanctioned low calorie foods? I wont say it isn’t possible, but short of that, what can the hamstrung public health services do to stem the tide of obesity?

We’re back once again to a response model of an epidemic. Each response needs to systematically deliver prevention and sequestration of the elements that create the epidemic. And how that might work with obesity is an fascinating consideration with few easy answers. Food is everywhere and present at every event. Here’s a few observations:

1. Government Consensus Panel Nutrition Advice: Toothless. The advice being delivered mutely over already chaotic media and internet portals is sadly inadequate and haphazardly delivered. The answer here needs to begin with primary education and adult re-education. Short of that, the panels will convene and deliver diatribes on the wisdom of drinking milk or eating beef and the evil that resides in Big Food as they deliver soda pop, chips and corndogs.

2. Isolation: Extremist. Taking Connor McCreaddie into custody and isolating him from the outside (junk food) world solves the problem on a small scale but at what price to human freedom?

3. Legislative Action: Not out of the realm of possibilities. Taxation of foods considered “unhealthy” might sound easy, but determining which foods are unhealthy has been a struggle against an army of special interest lobbyists and food freedom fighters. Any healthy food, such as a carrot, might be rendered unhealthy with the right cooking technique and sauce.

4. Government Run Food Sources: Stand up George Orwell. A very futuristic solution, which offers a state-run grocery store where your scanned card tells how many calories you are purchasing for a designated number of family members. “Sorry sir, you cant purchase cheese. You’re over your cheese budget for the month.”

I say so what if Connor McCreaddie has a shortened life expectancy. That's right, so what. Might not all the homeless citizens in poorer areas and near homeless shelters have a shortened life expectancy as well? What then do we do to offset the epidemic of homelessness? The solution seems rather easy. Build them homes. And what about mountain climbers and skydivers? Don’t they have a mortality rate that mirrors obesity? Should we collectively save them from themselves? A certain amount of freedom is necessary, and the freedom to overeat is unfortunately one of those inalienable rights.

San Diego

A conference in San Diego brought some street level observations into focus. First, the number of homeless in this city is large and from what I can see, there isn’t much in the way of a safety net for them to fall back on. But then, I’m conferencing and staying on the affluent waterfront, what would I expect? A walking tour took me to the upper part of the city and the location of the homeless shelter. As I passed a man was yelling obscenities at no one in particular and appeared in desperate need of mental health counseling. I scurried past.

On the waterfront, the USS Midway is a spectacular museum piece with a variety of naval aircraft on display to chronicle the history of carrier-based aviation. In the tiny park in front of the USS Midway a sometimes-large collection of the homeless have found a place to congregate and sleep. I sat and spoke with a woman.

“Where are you from?” I asked her.
“Here there and everywhere. Mostly Cincinnati is where I grew up.”
“What brought you here?”
“It’s just where I ended up.”
“Do you like living here?”
She looked long and hard. “Expletive. Do I look like I like living here?”

The San Diego homeless population is divided up into homeless urbanites and homeless agricultural workers. The urban homeless make up the bulk of the two groups currently estimated to be 6,300 persons in San Diego proper. The woman I was talking to started to become agitated so I dropped the probing questions.

“Have you eaten today?”
“Just the ‘expletive’ people leave in the trash. You know you people leave food around like it doesn’t matter. Yur kids eat a corndog halfway and toss it. I never lived that way.”
“We do have a lot.”
“Damn right you have a lot. You have no idea how much you have.”

From Foreign Protein to Dead Pets

The protein content of food has recently been thrust into the media spotlight by a spate of pet food contaminations and deaths. The culprit it seems was finally determined to be melamine, or as they call it in China, “melamine scrap” added to animal feed. Why then we have to be asking, would anyone add melamine scrap to animal feed or grain? To understand the ruse we need to travel to the heavily contaminated region of Northeast China, where the practice is common.

The first order of business is defining melamine and in particular, “melamine scrap.” Retrogressing from there, and more fundamental, why add it to foods? Melamine is a nitrogen containing compound (shown above) with a chemical structure similar to urea, the nitrogen waste vehicle of mammals. Melamine can be produced in industrial style processes using urea and very high pressure. Melamine is used in those same industrial processes to produce a number of plastics and a variety of fire retardant clothing. In yet other large industrial processes in China, producing fertilizers and again plastics, a residue left over in chunks falling to the bottoms of vats is called “melamine scrap” which instead of being discarded, is sold to local agricultural middlemen. The white chunks of melamine are crumbled and broken up into a protein containing food, like a single grain product or flour, or a combination of milled grains. By adding the chemical the middleman in the process artifically boosts the protein content, without having to buy expensive protein powder. In reality to all comes down to testing. The process of testing the food or flour, as I'll outline, is fooled by the presence of melamine and the protein content using current testing methods shows an elevated level of protein in the product.

Boosting the "apparent" protein content of grains
Melamine is a nitrogen containing molecule with amine group side chains. That’s not amino acid side chains, but rather amine side chains. Thus in the two methods used to test a bulk lot of feed or grain for protein, both the Kjeldahl Method and the Dumas Method assay for nitrogen. From there, the relationship between the nitrogen content of the sample and the protein content is extrapolated. However, if there is a nitrogen containing molecule in the feed or grain, like “Melamine Scrap” the nitrogen content is artificially boosted and the extrapolation to protein content is also incorrectly boosted. Since the food purchasers are primarily interested in the protien content, and the middle man can boost "apparent" protein content with melamine scrap, crude measures of nitrogen content allow for both to claim their product is protein rich. Thus the cheap "melamine scrap" from industrial processes is worth it’s weight in gold to a Chinese middleman peddling bulk grains or feeds.

Toxicity to Humans
In a nutshell: no one knows. However, having stated that, the FDA out of an “abundance of caution” declared 6,000 hogs to be contaminated due to consuming melamine tainted chow. The porkers were excluded from the human food chain. The Pesticide Action Network (PAN) of North America lists melamine but regards it as a virtual unknown. The WHO and EPA both essentially have no information on it, or in the case of the EPA, limited information. The FDA and USDA are currently investigating the pet food scare and establishing methods of screening for melamine in foods. Many of the animals apprear to have simply died of ammonia exposure from the metabolism of melamine. The final tally is melamine one, understanding of human toxicity from chronic exposure to melamine, zero.

Trust
Now we get into the issue of trust. Having learned about this very sinister way the analysis of a food for protein content can be manipulated with melamine, a tasteless, odorless nitrogenous compound, the question remains, should the marketplace respond in kind? As consumers of grain and protein containing foods, how would you view a product containing protein if it were produced in China? And how many Western food producers purchase protein products or grain products from China and add them to commonly consumed foods?

In short, I trust the food supply a little less and will scrutinize packed products a little closer now that I’ve learned how commonplace it is in Northeast China to spike foods with melamine. In the end, the words of William Shakespeare say it all: “Love all, trust a few. Do wrong to none.”

Depression and Obesity: Which disorder begets which?

The relationship between obesity (BMI >30) and depression has been characterized as the chicken/egg dilemma. Which came first? It seems self evident that depression might lead one to seek out the solace and sensory rewards of foods. And viewing that seemingly self-evident proposal in the mirror; obesity might lead to social isolation, discrimination and other real or perceived losses all associated with social stigmata, which might lead inevitably to a depressive state. The question that might be posed is: Do those with obesity have mood disorders (specifically depression) more often than those without obesity?

Research in the past has shown that obesity is significantly associated with depression and other mood disorders. What the research hasn’t been able to show is a cause and effect relationship between obesity and depression. There are a small number of studies examining the possibility of depression leading to obesity[1]. And an equally small number of studies showing that obesity might lead to depression[2]. The research in general doesn’t really lend a direction to this dilemma.

A recent study published in the Archives of General Psychiatry sought to better define the population of obese individuals at risk for depression. Or if you look at it from the other perspective, depressed individuals that happen to be obese. The study looked at a cross section of America[3] and simply examined the association between obesity and mood disorders.

They found in their cross-section of America that from 2001 to 2003 in a random sampling of the 48 contiguous states, that 25.5% of us have a BMI greater than or equal to 30. That is, 25.5 % of us are obese or larger. Further, 18.6% of those with a BMI > 30 had a major depressive disorder at one time in their lifetime. I’ll sum up the other findings:

1. White (non-hispanics) were more often depressed if obese than non-whites
2. Depression was more common in those obese individuals with higher levels of educational attainment
3. As age increased, obesity was more often associated with depression

Cross-sectional analysis such as the study above might be more a snapshot of America than an analysis of trends, but the snapshot shows some interesting associations. In higher socioeconomic circles there might be more pressure to be normal weight and those with obesity are shunned to a greater extent than those in lower socioeconomic circles. Cultural and ethnic analyses show that in some racial groupings, depression is low and may be low due to greater acceptance of obesity by peers. And those attaining higher levels of education may feel guilt and loss of self-control (with subsequent depressive episodes) due to a contrast between the self-control and will power it takes to attain higher levels of education and the state of obesity.

Which begets which? I think after examining a sampling of the studies it appears to work both ways. In some cases, possibly those in higher social strata with higher levels of education, obesity might lead to social isolation and depression. However in some (not so clearly identified by the above research study), depression and isolation may lead to overeating and sensory rewards which can lead to obesity. I think the forces leading one disorder to the other are situation specific and not amenable to generalized identifying markers or settings.
WG

[1] Goodman, et al. A Prospective Study of the Role of Depression in the Development and Persistence of Adolescent Obesity. Pediatrics 2002; 110, 497-504
[2] Roberts EE, et al. Prospective Association between Obesity and Depression. Int J Obesity Rel Met Disorders 2003;27: 514-26
[3] Simon et al. Association Between Obesity and Psychiatric Disorders in the US Adult Population. Archives of General Psychiatry. 2006;63:824-30

Happy Feel-good Reward

In the course of an interview today I had the opportunity to observe an interesting exchange between a mother and her 2 year old daughter. Interesting, in the sense that it gave me a reason to pause and think about the roots of obesity briefly and the factors we as parents promote by encouraging overeating, and eating what we would all consider the wrong kinds of foods. It’s a surprisingly common approach to children’s behavior and in this case the child was acting fine; she was making faces at me and acting goofy, but nothing out of the ordinary for a 2 year old. The mother made the remark to her daughter, as we were discussing her 2 year old daughter’s health, that if she’s good during the interview, she would be rewarded with a trip to McDonald’s.

The mother in this case was herself obese (roughly 5’4”, 250lbs) and it struck me that the reward to the child might possibly be rewarding the parent as well. So what did I learn from that short exchange? Food is being given to children as a reward. There’s nothing fancy or scientific about it. There is nothing profound to say, other than the carrot being dangled in front of this small child is a trip to McDonalds. More than that, it’s teaching the child about a reward system which offers up fast food at the end of that sequence of promises.

Turning the universe upside down, what would happen in The Land of Nutritionally Correct Foods, if the mother offered up something simple like an apple or an orange as a reward if the child’s behavior was exemplary? More to the point, why in any circumstance are we offering food rewards to children based upon good behavior?

Garlic: Good for the Heart or Bad for the Breath?

The answer to the title appears to be: Bad for the breath. In a study published recently in the Archives of Internal Medicine, the impact of oral garlic either through supplementation or raw cloves, had no impact on Low Density Lipoprotein concentration (that cholesterol moiety we all call “Bad Cholesterol”).

In a randomized trial of raw garlic versus two varieties of garlic supplement versus placebo, four groups were followed over the span of 6 months whereby intake of said smelly phyto-therapeutic bulb was taken six of seven days and lipid levels were monitored. On the seventh day breath mints were handed out.

In a nutshell, by the end of the 6 month study, the groups showed no statistically significant differences in lipid levels and in particular in LDL-C levels. The study follows up other studies which have found no lipid lowering effect of garlic. It may do other things, like flavor stews or pasta dishes, but it wont prevent heart disease.

Food Policy

Nutrition policy might appear to be a concrete concept describing something meaningful and weighty, but it has no greater impact and no greater importance than the individual’s perception of the need to change—and more fundamental than that, the actual changes it induces. In a nutshell, the government and private health organizations can promote change all they like, but if the citizenry makes no change based upon the policy, the policy has done nothing.

Applying Benford’s Law of Controversy to nutrition policy: Passion in the generation of public nutrition policy is inversely proportional to the amount of information available. That is, we may be passionate in creating a policy, setting daily limits on certain macronutrients and food groups, but we risk the effect of scientific research updating current understanding and potentially showing our “policy” to be at best outdated and at worst flat wrong.

The public was universally confused in just this manner with the butter versus margarine debates over the past thirty years (actually the last 100 years). Many who flipped back to butter after the trans fat scare of the late 1990’s, are now filtering back to margarines with low trans fat content. However, ask the average shopper about the health risks of either and you get a rambling confused diatribe of concepts and fears brought on by the conflicts between science and public health policy.

Nutrition policy is ideally designed to inform and change behavior based upon a consensus of information derived from current and past science. The implication is that changing eating behavior rewards the individual with a more favorable health outcome. An example might be directed at children: Eat fewer calories, more fruits and vegetables and less saturated fats from animal sources, and enjoy lower rates of heart disease, obesity, type 2 diabetes and a host of other issues and problems. The policy, however, is actually directed at their parents and the public institutions where they learn. The policy is directed toward the prevention of obesity, heart disease and the other conditions mentioned, without directly targeting the susceptible audience (a roundabout bid once again for essential nutrition education in classrooms). What that implies, is the significance of nutrition policy is disease specific, asks a caretaker (parent or government) to administer the policy and offers no real roadmap to accomplishing the terms of the policy. It tells the parents and schools, in essence:

“We’ll tell you what to feed your children for the next twenty to thirty years, even though it’s less satisfying and offers a somewhat reduced taste experience. And we have no idea how to discourage them from eating all the good tasting, bad-for-you foods. After that, we’ll see if it prevents disease.”

And there are few real world examples of a policy that takes 30 years to bear fruit. In fact, no policy can be 100% sure of all outcomes and a policy that prevents a disease 30 years in the future is vulnerable to say the least.

The seatbelt law represents a wonderful example of a public policy that had legislative backing and thus moved quickly from policy to law. The change is immediate if one encounters another car head on at just forty miles-per-hour. However, food policy takes decades to see potential benefit. And what if the policy makers overlooked an intervening exposure? Intake of certain fruits and vegetables over time with low levels of pesticides may be found to promote certain cancers. What would we tell the populous in twenty years if the last assertion were found to be true? In truth, no policy can capture all possible conditions and situations. And no policy is perfect. But nutrition policy to prevent lifestyle accumulating disease is without question on a very buttery slope.

All-you-can-eat

The all-you-can-eat buffet is based upon a couple of very basic marketing principles and engages two very fundamental human characteristics. In an effort to scratch out another blog on this very topic, my wife and I visited a local buffet restaurant chain in an effort to see first hand the aforementioned principles in action. We both agreed that we would not enjoy the experience, although I swore to keep an open mind and evaluate the concept and the restaurant based strictly upon my senses and what I was about to observe.

The marketing principles at work in this particular establishment are:
1. Make the atmosphere as appealing as possible.
2. Deliver highly palatable foods in large quantities.

The human characteristics augmenting those principles are:
1. The need to be satisfied by the foods consumed with a variety of taste experiences.
2. The perception of a “good deal” or “bargain” based upon the price paid for the quantity and quality of food received.

The combination of marketing principles with human characteristics has allowed all-you-can-eat buffets to flourish. This particular restaurant is located near a shopping mall in an area with fairly high traffic. It’s a national chain and well-known locally.

We drove into the parking lot in stealth mode. I checked each license plate against a database of friends and coworkers to ensure anonymity. We both donned sunglasses and hats. Upon entry, the crowd gets funneled into a series of cash registers where you identify how many in your party (as well as the ages) and order drinks. The all-you-can-eat breakfast was $7.49 with coffee and tea as add-ons. The bill came to $18.00 and change. We were given a tray with six large plastic plates with two wraps of silverware.

After sitting down we each took one of the six plates and walked over to the food. It was divided up into a High Fat section and a High Refined Carbohydrates section. I started with some cantaloupe and grapefruit from the scant offerings of fresh fruit. My empty plate with fruit immediately drew numerous stares.

“Look, someone’s eating the fruit?”

In keeping with the theme I walked over to what was quite literally a mound of freshly cooked bacon. There was easily seven to ten pounds of bacon dripping with fat in a large pan. I was stupefied. I can’t remember the last time I saw that much bacon in one tray. My wife silently gave me a stern look and a nod such that I should back away from the bacon. To my amazement, a series of patrons recognizing the freshness of the bacon, lurched in front of me with elbows flared and piled the bacon on their plastic plates.

Not surprisingly, the atmosphere and tables were nicely adorned with ranch-style hominess. The tables were clean and the floor spotless. Contrary to my perceptions of trough rugged seats worn through by obese patrons eating in a miasma of bacon smoke, the restaurant was well ventilated and kept immaculate.

My wife took the first bite and declared, “Industrial food. I hope they don't get their wheat gluten from China."

Metabolic Syn-drone

Metabolic syndrome is a play with a cast of millions. It's full of characters we all see daily. We see them in shopping malls, restaurants, bars, city streets, on the job, and nearly everywhere (in Western society). B.R., one of my recent encounters, so typifies this syndrome I had to present his case en-blog, to show the somewhat typical and blissfully ignorant face of this illness/modern distillation.

B.R. is a 46 year old male (not his initials and not exactly his age, but close) with non-insulin dependent diabetes (a blood sugar today of 176), obesity, hypertension, hyperlipidemia, sleep apnea (untreated), gastric reflux and a heaping of denial and ignorance that might now be considered epidemic. In a human play involving this constellation of signs and symptoms (he also doesn’t sleep well and feels exhausted all the time) the drama from my perspective involves a backdrop which shows a sheer lack of insight and offers a rich look into what appears to be going wrong with a large segment of society. He is retired/disabled due to a back injury. We open with the interview:

I ask B.R. an open ended question, “You have high blood pressure?”
He chuckles and replies, “Yeah, that’s what they tell me.” His wife, who is also obese, chuckles in response to his reply.
I continue, “Your blood pressure is 155/95 today. It’s not well controlled”
“Yep . . . I don’t always take my medication,” he admits.
I move on, “You have diabetes as well?”
He chuckles again, “I control it with diet.”
His wife corrects him, “No doctor X gave you medication, don’t you remember?” She looks at me, “He takes it once in the morning and once at night.”
He turns to her, “Do I?”
“Don’t you remember?”
His weight is 284 lbs and he’s 5’10” tall. (BMI of 40.2)
He has shortness of breath with minimal exercise, has what may be developing angina, all of which leads to a fairly sedentary life.

The frustration is: Where do you start with someone like B.R.? Is he a lost cause and do we move on to the next generation or do we all simply plod along with him and wait for the wake-up call; the heart attack the stroke the severe angina the coronary artery stent, the peripheral neuropathy the diabetic foot ulcers and the amputations? Usually by then it’s too late and the connection between the gallon of ice-cream and the below the knee amputation isn’t ever made. As B.R.’s metabolic syndrome worsens due to his increasing central obesity, insulin resistance, hyperlipidemia, and more, the treatment is simply to eat less and exercise more. The treatment isn't a medication or a high-tech procedure, but a simple dietary and lifestyle change. But in B.R.'s case the disease processes are setting in solidly and the diet and lifestyle changes, while desperately needed, will without question require medications and expensive procedures to maintian his life over the next 10 years. And what about the cost?

A to Z weight Loss Study

One of the more startling results of the A to Z Weight Loss Study is the interpretation of the results. Again, the study found that after 12 months, those participants on the Atkins diet lost more weight and ended with a metabolic (cardiovascular disease) profile no worse than those on the comparison diets thought to be “healthy” diets. Those participants in the Atkins diet arm of the study on average consumed significantly more saturated fat, more protein and less dietary fiber than the other diets (Table 2 of the study in question[1]). They in essence ate large amounts of foods that might be considered unhealthy by most current nutritional standards. And after a year (granted that’s a fraction of the time needed to prove it a safe and healthy diet) the participants lost the most weight and didn’t suffer with metabolic indices indicative of unhealthy eating.

One critical aspect of this study to keep in mind is the brief glimpse it gives. Dietary lifestyles take many times ten to twenty years of exposure to impact for example the cardiovascular system. While indices of cardiovascular risk are within the range of other “healthy” diets, the indices measured may not tell the entire story. As a case in point, the genesis of atherosclerosis is thought to be due to trapped Low Density Lipoproteins (LDL) stuck in the arterial walls, consumed by tissue macrophages which expire in the arterial wall leaving thick goo. The goo expands into the arterial lumen and the nidus of a plaque is created. With that genesis in mind, might the Atkin's diets impact the oxidizability of LDL, leaving the absolute amount of LDL unchanged?

Another important consideration: The study was conducted in women. Is the result generalizable to both women and men? Or is another study with the same methodology needed for men? And what if the results were different, what could we conclude? The answer from my perspective is: it depends on the winds of nutritional change. Trans fats were never found to be unhealthy (lead to adverse cardiovascular indices) in men yet the unsavory results of the Nurses Health Study were generalized to men (never mind the results of the Physicians Health Study, which found no adverse metabolic effects of trans fats in men). But that’s another soap box.

What do the authors of the study conclude? I’ll quote one the study authors ending remarks:

“Physicians whose patients initiate a low-carbohydrate diet can be reassured that weight loss is likely to be at least as large as for any other dietary pattern and that the lipid effects are unlikely to be of immediate concern.”

So there you have it. The whole nutrition cycle begins to churn again. Fat is good for you, carbohydrates are evil and the Atkins diet we all shunned for so many years because of the perceived adverse effects of eating bacon, pork and fatty foods, is shown to be as healthy as all the other dietary approaches. As Daniel Boornstein was quoted as saying,

“The greatest obstacle to discovery is not ignorance—it is the illusion of knowledge.”


[1] Christopher D. Gardner et al. Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women: The A TO Z Weight Loss Study: A Randomized Trial JAMA. 2007;297:969-977.

Contribution or Consternation: The A to Z Weight Loss Study

The diet and weight loss chronicles received a retro boost recently with the publication of a study in the Journal of the American Medical Association. The A to Z weight loss Study randomized willing participants to one of four diets: Atkins, Zone, Ornish or LEARN.

Studies such as this, examining the most effective method of losing weight, have been plagued with methodological and patient related issues. High dropout rates, poor compliance with diet protocols and short duration of study have left the conclusions drawn from these studies nebulous at best. Layer that with popular diet authors espousing the virtues of low carbs, zone eating, eliminating refined sugar, or in the case of the American Heart Association, eating by the dictates of the No Fad Diet, and the public becomes confused.

So to further the confusion and nebulousness, we have the A to Z weight loss Study. The A to Z Weight loss Study published in JAMA compared the Atkins, Zone, Ornish and LEARN diets in premenopausal women. Naturally media-reported ultra-short sound-bite analysis declared the Atkins diet the winner. The Atkins Diet, you ask in dismay? Didn’t they go away after bankruptcy and weren’t the virtues of this diet debunked? Apparently not.

Let’s look at the study. The endpoints of the study examined weight loss, changes in lipid profiles (total, LDL, HDL cholesterol and triglycerides) as well as changes in waist to hip ratio, % body fat and a few other variables. The participants were generally obese women in the age range 25 to 50 years with a BMI range of 27 to 40 (average in the 31 to 32 range) followed for 12 months with frequent follow-up visits. The interesting point of this study is that it addressed some of the prior problems plaguing similar weight loss studies. Lets look at them individually:

Drop out rate: The study randomized 311 participants to one of four diet groups listed above. Atkins had 77, Zone 79, LEARN 79 and Ornish 76. Of the four diet groups the number of dropouts respectively were 9, 18, 18, 17 which isn’t a terribly bad drop out rate.

Regression to a regular diet: This is where the low carbohydrate dieters start eating higher percentages of carbs and likewise the low fat dieters eat more fat. In short, the dieters regress to a normal diet and give up the basic principles of the diet. Again, in this study, regression to a normal diet resulted, but wasn't terribly bad.

The result: Much to the chagrin of the scientific world, (and the authors of the losing diet plans)the Atkins protocol won the horse race. Those on the Atkins diet lost a significantly greater percent of BMI, had lower % body fat, and had significantly lower triglycerides with no change in LDL cholesterol. The authors of the study concluded there were no adverse metabolic effects for those women following the Atkins diet regimen.

As Sir William Bragg (1862-1942) was quoted as saying, “The important thing in science is not so much to obtain new facts as to discover new ways of thinking about them.” What if, after digesting Sir Williams quote, the important thing about diet, health and weight loss wasn’t so much what you ate, but how much of it you ate (in terms of calories)? More commentary later.

Othorexia Nervosa

As Oscar Wilde said, “I am not young enough to know everything.” And likewise the concept of a person being too concerned about eating healthy food, might have traction. It might just make sense in the context of my own life: I might be too concerned about my health, my bank account, my children’s activities, my carbon footprint, my automobile emissions, my lack of knowledge of the arts, my lack of knowledge of auto mechanics and on ad infinitum. Volley along now, I too might be the creator of a new DSM IV category: Dysplernecess.

Dysplernecess: Eating until it hurts.
Anyone with Dysplernecess has the unavoidable compulsion to eat whatever comes to mind without pre-conception or planning. When in a bakery they point to each and every pastery and state, “I’ll have one of those, one of those, oh, and one of those,” until the glass case is quite empty. They make up diagnoses, accuse others of focusing too much on healthy eating, and publish a book to prove their point(s).

Take the 10 point test to see if you qualify:

Two points for each yes:
1. Did you publish a book recently titled “Health Food Junkies”?
2. Is your last name Bratman?
3. Is the point of eating to achieve a pleasurable state?
4. If eating a twinkie is fun, would you eat ten?
5. Do you frequent all-you-can-eat buffets without remorse?
6. Does your waistline keep expanding?
7. Do you eat anything you like and not think twice?
8. Do you spend more than three hours a day thinking about new DSM IV diagnostic criteria to describe healthy eaters?
9. Do you feel a sense of achievement when you eat the most pie at a pie eating contest?
10. Has the rate of heart disease and obesity gone up in those around you?

A score of 6 to 8 you may have Dysplernecess. If you scored more than 10, you probably need to be put on a statin, have a treadmill test and get frequent blood pressure checks. Also; purchase a bathroom scale.

All tongue-in-cheek of course, but moral absolutists that consider watching what you eat to be a sin, need desperately to consider the trends. Where did the obesity trend come from? Answer: Not paying attention to what foods are composed of and allowing too much of said undescribed and tasty foods to enter the oral orifice. Where did the trend in hypercholesterolemia come from? Answer: See last answer. I could go on.

Road Food

Traveling and dining out for each meal brings home some interesting observations on Western society. It doesn’t take a brilliant critic of our current food culture to very quickly notice patterns in food intake while on the road. First off, the food choices available to travelers in essence involves marketing a taste driven machine; and it’s not a process we want to intellectualize about very much. Nutrition information is not just lacking, it’s suppressed. By that I mean it might be a bit depressing for the causal nutrition clerk to tally the day-in day-out calories, saturated fat and lack of fiber when jumping from one national chain restaurant to the next. Avoid the national chains you offer as an armchair quarterback? Try as I might, and knowing what I know, the local grocery stores didn’t offer up what the weary traveler needs. Like the battered fighter on the ropes, at some point you give in to the chain restaurants and order up. Like a “tractor beam” from the old Star Trek series, we were drawn in by the smell, the anticipation and the ease of entry. But honestly, we tried to avoid them.

Theoretical arguments against eating at chain restaurants are workable from the safety of home. However, on the road, after numerous hours on dreary pock marked pavement with the nearly constant hum of the engine wearing senses thin, a city or town rises in the neon light like an all-you-can-eat Phoenix. Neon signs proclaim Burger King and Pizza Hut with enticing visions of reprieve from the constancy of the road. And taste experience is king in neon food chain land as each establishment announces savory meals offered up at the likes of Tony Roma’s and Applebee’s. Tony Roma’s advertises in bold letters a “Slab-Fest” going on. I paused at that trying to imagine what the patrons of the restaurant engaging in the slab gluttony might look like. Hardee’s advertises a gigantic monster burger with many too many pounds of ground beef on thick slices of cheese all covered in the usual suspect fixins and a secret sauce to boot.

Seeking out the less common establishments like the backstreet Thai restaurants or corner bistros might offer up more international flavors with gourmet dishes (and higher price tags per meal), but the nutrition clerk in me was tallying up the saturated fat and calories next to the check, trying to figure out which is the larger. I usually based the tip on some fractional multiple of the total grams of saturated fat. Needless to say the wait staff made a fortune off of me.

In the final analysis, each time I travel it makes me wonder about all those road weary truckers, travelers and communters who frequent the aforementioned neon establisments regularly. Health implications and cost aside, the taste experience alone is akin to mainlined heroin, making it nearly impossible to return to fruit and granola as a snack and the simplicity of vegetable rich meals as a norm. And the number of obese patrons I saw reinforced my conviction: We are truly a society and culture addicted to food. Not food for sustenance and nourishment, but food strictly for the taste experience.

Vitamin B12 (Part Deux)

This complex and confusing mass of chemical scribble to the right is B12. Most publications regarding vitamin B12 will neglect to reflect on a few fascinating facts regarding the molecule. Complex as it looks, the molecule itself is speculated to have been around for 3 to 4 billion years. That’s billion years.

The next fascinating factoid regarding B12 is it’s made by some our bacterial arch enemies, including Klebsiella pneumoniae, Salmonella typhimurium and E-coli (if offered a precursor, cobinamide). Not arch enemies in a strict sense, as many of the colonic bacteria indeed reside happily in our colons coexisting in harmony with us and making loads of vitamin B12 (only to have us excrete it), but arch enemies in the sense that if given the opportunity, in a weakened host, will kill us.

Is this beginning to seem like a good bacteria/bad bacteria story? If they coexist in our colons, performing innocent fermentation functions, living happy healthy lives, but have the capacity to cause disease and death in their human hosts, all the while producing a molecule critical to our survival, what would you call that? That’s more than symbiosis, that’s co-dependence.

Absorption and Disposition of B12
When again considering the sources of B12 many would point to those sources as evidence of animal consumption for many millions of years. Although geophagy and coprophagy are possible sources of the vitamin, there’s minimal evidence of either from anthropological data. And while strict vegans might argue the point, that leaves meat eating as the only consistent source of B12 over the history of man.

The absorption of vitamin B12 from dietary sources requires a chorus of activities and proteins to effect the separation and transport through the intestinal wall and into vital tissues, organs and cells. After chewing a B12 containing food a molecule called Haptocorrin binds B12 to shuttle it through the upper stomach and small intestine to keep it safe from either acid damage or bacterial consumption. In the small intestine a protein call Intrinsic Factor (IF)—which is secreted by the stomach—binds B12 and shuttles it to a receptor in the ileum. From the receptor, the IF-B12 complex is absorbed by endocytosis and the B12 is transferred to another shuttle protein called transcobalamin-II. The transcobolomin-II B12 complex is taken to tissues and taken up by an as yet unknown mechanism into cells.

B12 body stores are adequate enough to last for 3-5 years without any intake before a deficiency state sets in. Those as greatest risk of a B12 deficiency are individuals with minimal animal food sources, such as vegans and strict vegetarians, and the elderly consuming a series of “tea and toast” style meals as well as those with missing IF or short guts due to surgery.

A deficiency of B12 leads to a host of problems the least of which is a severe anemia. The anemia can take two forms:

1. Pernicious Anemia: Lack of IF

2. Megaloblastic Anemia: Lack of dietary B12

Deficiency of B12 can lead to devastating and permanent central nervous system degeneration with ataxia, numbness and spinal cord degeneration.

Note: I'll be traveling for a week or so.

Vitamin B12

Vitamin B12 or cyanocobalamin (not the active form of B12) is one of the most complex molecules required for the human body. B12 comes in different active varieties depending upon the reaction it catalyzes. Methylcobalamin catalyzes the conversion of homocysteine to methionine (by adding a methyl group) and adenosylcobalamin catalyzes the conversion of certain amino acids and three carbon fatty acid fragments into molecules funneled into energy production.

The term “cyano” comes from the method of purifying the vitamin (using cyanide) and cobalamin comes from the cobalt complexed in the center of the molecule. That cobalt ring is generically called a corrin ring. There is no cyanide in naturally occurring B12.

Vitamin B12 is made exclusively by bacteria and archaea, and can be found in organisms that have a symbiotic relationship with bacteria. Mollusks and organ meats such as liver are an excellent source of B12 as are muscle meats and varieties of other foods such as milk eggs and a host of seafoods including fish and shellfish. The requirements for B12 are fairly well known and the sources encompass primarily the organisms that harbor the vitamin producing bacteria. The Dietary Reference Intake for most adults is 2.4 µg per day. Most multivitamins contain 6µg.

What does B12 do? Again, B12 functions in methyl group transfers and has been found important in two human biochemical reactions:

1. Conversion of the amino acid Homocysteine to Methionine

2. Energy conversion in specific amino acids and odd chain fatty acid fragments


How humans evolved to require the water-soluble vitamin is still somewhat of a mystery and certainly beyond the scope of this blog. Needless to say, there are no artificial means of acquiring B12 outside of bacterial production. Why bacteria produce B12 in the first place is unknown as well. And human bacteria living lives in our colons do indeed produce B12 but it isn’t absorbed in appreciable quantities. Instead, it’s lost in the feces.

There are basically three ways to acquire B12 from the environment. One method is to consume soil containing bacteria which produce B12, a practice call “geophagia” and not good on the teeth. Another less savory method involves a practice called “coprophagia” where feces are consumed, presumably to acquire those lost vitamins and nutrients. Chimpanzee’s and numerous other animal species practice coprophagia, presumably to acquire the vitamin B12 content, but that’s speculation as well.

The final and most common approach to acquiring B12 is through the consumption of other animals, mollusks or algal species which themselves live in symbiosis with the bacteria that produce the B12.

Body Mass Index and Mortality

The ultimate measure of body shape and size, lifestyle and eating pattern is the answer to the following question: Will it (the eating pattern, lifestyle or body makeup) impact my overall risk of mortality? Health problems like the numbered stack I’ve listed below might arise, and there are well-know relationships between diet, fat distribution patterns and specific disease entities, but is there a healthy overweight category? Can someone have a BMI of 28, exercise regularly and still be considered healthy with a low risk of mortality? Maybe. Or maybe not.

By implication, the categories of BMI don’t lend any apparent wiggle room. That is to say, the overweight category, BMI 25 to 29.9, might seem innocent (since many if not the majority of the population now falls into this category) but is there a basis for stating that being overweight is unhealthy to the point of increasing the chance of mortality? More concrete than that, if my BMI is 26 am I at any more risk of death than some0ne with a BMI of 24?

Taking the liberal skeptics approach, if not, then all this wrangling to call more than half of all Westerners overweight and by implication, unhealthy, is an exercise in futility. A persons diet, body habitus, fat distribution and lifestyle may increase the risk of certain disease processes, but if it doesn’t impact mortality is it worth pursuing? Risking an argument that invokes quality of life questions and the economics of health care, if I'm overweight and I have a mortality rate the same as someone not overweight, don't preach weight loss to me.

According to widely held beliefs, when comparing those at ideal BMI (18.5 to 24.9), to obese individuals (BMI greater than 30) the risk of chronic medical problems attributed to that increase in weight is rather large. What follows is a number of health problems associated with a BMI greater than 30:
1. Diabetes
2. Hypertension
3. Heart disease
4. Stroke
5. Cancer
6. Decreased life expectancy
7. Sleep apnea

However, lets examine the most recent mortality data.

In a study[i] published in the Journal of the American Medical Association on April 20th 2005, Katherine Flegal and others examined data from the National Health and Nutrition Survey (NHANES) to report on excess mortality due to overweight and obesity. NHANES is a cross-section of Americans who are periodically interviewed and examined by representatives from the National Center for Health Statistics. The authors took data from NHANES I (1971-1975), NHANES II (1976-1980) and NHANES III (1988-1994) examining mortality data from each of the three groups sampled.

The first noteworthy trend found by comparing all three NHANES data sets, is a growing percent of individuals in America (and probably most of Western society) with a BMI greater than 35. In NHANES I the percent of individuals with a BMI greater than 35 was just 4.4%, but by NHANES III that number had risen to 8.3%.

The shocker in this study wasn’t that the excess mortality due to obesity wasn’t statistically significant (except for a BMI greater than or equal to 35); the jolt was that in the overweight category (BMI from 25 to 29.9) the actual excess mortality was less than zero. An excess mortality less than zero is interpreted to mean that relative to a normal BMI (18.5 to 24.9), those individuals categorized as overweight had a lower relative risk of mortality than those individuals in the normal BMI category.

In other words, the proposed health impact of overweight might not be considered unhealthy. And extending that thought, it might offer a benefit. According to this study, the excess weight appears to offer a very low risk of mortality to those overweight individuals, and might, in the current environment, offer an advantage. While the findings of a lower rate of death in the overweight category is tantamount to blasphemy, the study’s lead author hails from the National Center for Health Statistics, Centers for Disease Control and Prevention. More Later.

[i] Flegal et al., Excess Deaths Associated With Underweight, Overweight, and Obesity JAMA, April 20th 2005, Volume 293, pages 1861-67.

Body Mass Index Dissected

What follows is a little closer inspection of what BMI actually reflects. The formula once again is as follows:

Body Mass Index
Metric: = weight in Kilograms / (height in Meters)2
American: = weight in Pounds x 703/ (height in Inches)2

The following has been proposed to describe body mass classes:

Underweight: Less than 18.5
Normal Weight: 18.5 – 24.9
Overweight: 25 – 29.9
Obese: 30 or more

The mathematical model renders a number with the units of Kg/meter2 or mass per square meter. A natural question might be, wouldn’t it make more sense to measure mass per cubic meter? By that, cube the height and arrive at a mass per unit volume? It might seem to make sense but in correlation studies using a gold standard to measure percent body fat, the height squared actually correlates much better with percent body fat than the height cubed.

Again, the BMI is a mathematical model used to estimate CHANGES in % body fat. And population-wide that model does indeed hold true in nearly all cases. Most adults with an increase in BMI have a corresponding increase in % body fat. The running backs, competitive weight lifters and short distance sprinters with very low % body fat (but a high BMI, which gets higher with increases in muscle mass) make up only a very small fraction of the population and would be classified as outliers as they don't fit the mathematical model. The reason for that obviously relates to the greater density of muscle and lean tissue compared to adipose or fat tissue. With muscle weighing more than fat, a body builder adding muscle (building up for a competition) would have an increasing BMI with a decreasing % body fat!

Information BMI does not give:

1. Distribution of Body Fat
A high BMI as a number doesn’t necessarily describe percent body fat and absolutely doesn't define where on the body the fat might be distributed. Centrally, hips, thighs or evenly distributed over the entire body, the value give no information. And distribution as it turns out is probably more important than the absolute value of BMI.
2. Absolute Percent Lean Body Mass
Using the weightlifter with heavy muscle mass, as #1 above, the value of his/her BMI is meaningless as a reflection of percent body fat. And by corollary, gives no information about lean body mass.
3. Absolute Percent Body Fat
Although it’s an assumption that as an individuals BMI increases, the percent body fat increases, the value has no real relationship to percent body fat.

Body Mass Index Unraveled

Formulas to reflect body habitus or body makeup have in recent years defaulted to the calculation for body mass index (BMI). BMI has without question become the universal yardstick used by both clinical and research science to approximate percent body fat. The ultimate goal of any measure or calculation utilizing body weight or weight for height is to arrive at an estimate of the percent body fat. Inherent in the BMI classification system is a categorical assignment into one of the following based upon height and weight:

1. Underweight
2. Normal weight
3. Overweight
4. Obese.


The formula for BMI is simple and reflects mass per square meter:

Metric: BMI = weight in Kilograms / (height in meters)2
American: = weight in pounds x 703/ (height in inches)2

Lambert Adolphe Quetelet, a Belgian mathematician (1796-1874) developed concepts and definitions for determining the “average” man. In his quest to define the average man, he developed the Quetelet index which is the same formula for what we now call the BMI. The BMI has become one of the most utilized indices of “normal” weight for height. Other formulas, measures and scales of ideal body weight have been used by various organizations, but the BMI has yet to be replaced by a simpler measure reflecting the variation in weight for height.

Pierre Paul Broca, a French surgeon developed what was probably the first set of calculations to define ideal body weight in 1871. What his guidelines really amounted to was a rule of thumb:

Women: should weigh 100 lbs up to five feet in height, then five pounds for each additional inch.

Men: should weigh 110 lbs for five feet of stature and five additional pounds for each inch above five feet.”

Louis Dublin: The historical basis for ideal body weight in the United States began in 1942 when Louis Dublin, a statistician with the Metropolitan Life Insurance Company, categorized nearly 4 million subscribers according to frame size, height and weight. What he found was those who maintained an ideal body weight from the age of twenty-five into later years, had the best chance of survival. The Metropolitan Life Insurance Company revised those numbers in 1959 and again in 1983 allowing slightly higher average weights for respective heights to be categorized as normal. Planted in this line of thinking is what we call a “normal” weight individual or “weight appropriate” individual given their height.

Realize that this hypothetical normal weight range seems to be flexible as seen by the Metropolitan Life Insurance Company increasing the “normal” weight for height as the years progressed from the original 1942 study to the 1983 publication. Some argue the original ideal weight from the 1942 study should be considered the standard, while others are using the 1983 standards.

Absurd as it might seem, the concept of what constituted a healthy body was based upon what would earn Louis Dublin’s company the most money and keep people alive longer to pay more insurance premiums. Other factors that we now know affect life expectancy, like smoking and other lifestyle exposures, the quality of healthcare, the level of stress and other potential mitigating factors, weren’t factored in. As absurd as it might seem, in the initial studies by Dublin, smoking wasn’t considered a risk factor for early mortality—the association between smoking and lung cancer was not made until much later.

Many consider the Metropolitan Life Insurance Company’s appropriate weight for height given a frame size to be unusable, in part because the frame size was never really well defined by the company. However, the scale persists to this day and is still relied upon by a few organizations to risk-stratify individuals according to height, weight and frame size.

Omega-3 Fats: Concluding Remarks

There is much more to Omega-3 fats than this series of blogs lets on. I tend to focus on heart disease and the associations between foods and the risk of heart disease—basically because that’s my shtick. Omega-3 fats are proven effective in treating Hypertriglyceridemia and appear to be effective in preventing Sudden Cardiac Death. Its use in the primary prevention of heart disease is more controversial and hasn’t been shown to be definitively effective outside of other lifestyle factors and exposures.

I’ll briefly run through some of the suspected benefits of consuming Omega’s:

1. Alleviation of Psychiatric Illnesses: Bipolar disorder, Depression, ADHD, schizophrenia
2. Prevention of Macular Degeneration
3. Relapse rate of Chron’s Disease
4. Relapse rate of Relapsing Remitting Multiple Sclerosis
5. Lowered catecholamine levels
6. Treatment of Cancer anorexia
7. Alleviation of symptoms in Acute Pancreatitis

There are many more suspected benefits of Omega-3 fatty acids all of which seem to have a common thread. Omega-3 fatty acids produce inflammatory cytokines with a lower biologic/pharmacologic activity than cytokines produced from say Omega-6 fatty acids. Although this may not seem important, it represents one of the important reasons to consume Omega-3 fatty acids. Also, Omega-3 fatty acids become incorporated in phospholipids making up cell membranes and lipoproteins. That storage depot of fatty acids may be important in alleviating some of the disease entities listed above.

Sources of Omega-3 Fatty acids:
α-Linolenic Acid: Oils: Flaxseed oil, walnut oil, canola oil. Foods: Cauliflower, walnuts, spinach, pinto beans, tofu, and more.

EPA and DHA: Oils: Menhaden oil, cod liver oil, salmon oil. Foods: Salmon, oysters, mackerel, tuna, sea bass, shark, trout and many more sea food and fresh water fish species.

Amount to Take:
This is where things get a little sticky. Treatment of Hypertriglyceridemia is fairly straightforward and dose dependent; that is, consuming 4 grams a day is more effective at lowering the triglyceride count than consuming 2 grams a day.

If levels of DHA and EPA are your goal, to enable a reduction in inflammation from any of the above conditions in which Omega-3 fatty acids are suspected to help, the consumption of α-Linolenic Acid may or may not help. The problem is the conversion of α-Linolenic Acid to DHA and EPA is not reliable. In particular, it’s not reliable in men. In women, the conversion appears to depend upon global energy needs. In cases of severe caloric restriction, much of the α-Linolenic Acid may be metabolized for global energy needs. In a eucaloric state (a state where calories meet energy needs), the Linolenic Acid is effectively converted in DHA and EPA in women.

Dose to prevent Sudden Cardiac Death:
Sudden Cardiac Death is defined as death following a cardiac event, usually a myocardial infarction or heart attack. A number of observational studies have found that in those people either eating fatty fish or taking a supplement, the rate of death following a heart attack is much lower.

The optimal dose of daily fish or fish oil supplement to prevent sudden cardiac death after a heart attack, however, is a bit sketchy. There is some guidance based upon a dozen or so epidemiologic studies. But in reality, the precise information depends upon which study you bet the farm on. One salmon (or other fatty fish) dinner per week will supply about 1.5 grams of DHA and EPA which appears to be about the minimum intake to see a favorable outcome after a heart attack. The American Heart Association recommends healthy adults eat two fatty fish meals per week and include oils rich in α-linolenic acid like flaxseed oil, walnuts and canola oil.

Most supplements have a combined amount of DHA and EPA in the range of 500mg to 1 gram per gel capsule. Based upon the baseline benefit of one fatty fish meal per week, one capsule a day (1 gram combined of DHA and EPA) or even one capsule every other day would more than offset the minimum of one fish meal per week in preventing sudden death following a heart attack. The alternative is to eat the fatty fish once a week, which if cooked right, can be a far more rewarding experience than popping a fish oil capsule and burping up chicken-of-the-sea all morning.

Final Note on Omega-3 fats
I’ve noticed over the years when a food appears to offer some benefit, for example, eating fatty fish once a week, the elements of that beneficial food end up in supplements, soaps, skin creams, shampoo, and any of a number of other consumer products. Rubbing Omega-3’s on your skin might sound like a good thing, but there’s no evidence it impacts skin integrity, elasticity or longevity. Let there be no mystery regarding how I feel about food and product marketing. Marketing new products (especially new skin products) is tantamount to a criminal act until proven otherwise.

Omega-3's and Death

The ultimate test with any supplement or dietary protocol is as follows: Does the change make sense both from a scientific standpoint and more important, does it make sense at the dinner table. Therefore, based upon the consumption of Omega-3 fats, obviously the focus of these latest blogs, does consuming Omega-3 fats impart such a health benefit that we should all consider taking them?

Numerous alternative approaches to diet have espoused the magic of Omega-3’s. Mainstream medicine has found them efficacious in one setting: Preventing sudden cardiac death. Many, many other associations are being studied. If one simple supplement or diet management technique appears to be a panacea for all that ails us, Omega-3’s have apparently become a candidate.

There are really only three Omega-3’s to keep in mind:

1. Linolenic Acid: 18 carbons: 3 double bonds: found in flaxseed oil, walnut oil, canola oil and as a supplement.
2. Eicosapentanoic Acid: (EPA) 20 carbons: 5 double bonds: found in seafood, and as a supplement
3. Docosahexanoic Acid: (DHA) 22 carbons: 6 double bonds: found in seafood, and as a supplement

The question naturally arising from an examination of the above fatty acids is: Can the α-linolenic acid in the above foods, namely, flaxseed oil or walnut oil, be elongated and have two more double bonds added to make EPA and eventually DHA? Biochemically, the human body has the enzymes and machinery to do just that. A bigger question and one without a solid answer is: How much of consumed α-linolenic is converted to DHA and EPA? Is α-linolenic acid totally, partially or never converted to DHA and EPA? Can anyone take α-linolenic acid and not have to put up with fish oil and still achieve the same result in terms of a decrease in the risk of sudden cardiac death?

The short answer and reiterating yesterday’s blog is: It appears to depend on your gender. Women apparently convert a greater percentage of α-linolenic acid to the larger DHA and EPA than men do. Speculation has it that a woman’s hormonal environment favors that conversion and a man’s doesn’t. Why do we care so much about the conversion of α-linolenic acid to DHA and EPA? Stay tuned.