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.

Omega-3 Zeitgeist

I’m going to try an experiment. Throughout the post, I’m placing a couple of the top ten search terms from 2006 as defined by Google Zeitgeist. I’m doing this not to attract surfers by casting a wider net, but to actually capture them and force them to read about Omega-3 fats. After they read about Omega-3 fats, and like any catch-and-release program, I will let the unwary surfers go.

Paris Hilton, the low calorie gadabout tabloid princess, consumes Omega-3 fat like a skinny kid popping gummy bears.

Most Omega-3 fatty acid comes as either the variety found in flaxseed oil or the longer carbon chain variety found in fish and fish oil supplements. The question for years has been: How much of the smaller carbon chain fat found in flaxseed oil is converted to the far superior longer carbon variety found in fish oil? The answer seems to be, it depends on your gender. If you’re a woman, you convert quite a bit of the small chain Omega-3 fat to the longer chain fat. If you’re unfortunate enough to be male, you convert some of the small chain fat found in flaxseed oil (alpha-linolenic acid) to the longer chain fish oil fat, but only to a limited extent. Therefore, men are forced to either eat fish or cut bait . . . I mean, take a supplement.

My 17yo daughter, Orlando Bloom, read through my blog the other day and proclaimed chemistry to be dead.

“Surfers checking out blogs will immediately click out if they see a chemical formula,” she declared. “Just give ‘em the facts, like how Omega-3 fats or whatever will affect my complexion? Or, what do I need to eat fish for? Stuff like that. Anyway, people who eat a lot of fish usually stink.”

Therein lies my challenge. Is it possible to explain the conversion of eicosapentanoic acid and docosahexanoic acid to 3 series prostaglandins and leucotrienes with lower inflammatory potential without diving into the biochemistry of it all? Is it possible to understand the finer points of any dietary element’s impact on health without explaining it in biochemical terms? Give it a go and render an opinion.

Omega-3's: Do they prevent heart disease?

Our current fascination with Omega-3 oils including flax oil, fish oil supplements and fish intake, assumed to promote good health, is really a reflection of our observations over the years of how Inuits, Eskimos and other northern clime cultures live. Living in a land frozen most of the year, traveling over icy tundra and ice floes on dog sleds, hunting in mukluks and skins, rubbing noses, and existing only on fish, whale blubber and seal meat for months on end, has us spinning in our imagination chairs. How do they survive healthy long lives not eating salads, veggies and fruits regularly?

Living more in the southern climes, driving SUV’s and hunting for foods at Safeway, Whole Foods and Albertsons in our Birkenstocks, we’ve opted instead to live the way we do and pop either flax seed oil or fish oil capsules daily. What we’re silently hoping daily Omega-3 supplements will deliver is a little piece of the Inuit experience—that Omega-3 fats will impart a healthy high-fish glow and keep our hearts healthy like Inuit and Eskimo hearts.

In a typical review of fatty fish consumption, fish oil supplements and other sources of Omega-3 fatty acids, the benefits always seem to outweigh the controversies. In most cases, the scientific evidence is shrouded by health and science writers reciting the popular beliefs and feeding into the supplement spin machine.

One of the most blatant abuses of that review process is an ignorance of the endpoints of investigations leading many to believe fatty fish, fish oil supplements and other Omega-3 supplements are, in general terms, “Good for your heart,” or another favorite, “Heart Healthy.” While there is speculation about the connection between specific Omega-3’s and the health of ones heart, there is by no means an overwhelming consensus of data leading to that velvet conclusion.

As I’ll show with an objective review of the scientific literature, fatty fish and fish oil supplements are certainly acting as anti-arrhythmics; that is, if you have a heart attack, the omega 3 fatty acids found in fish and fish oil supplements appear to impart a benefit in preventing dangerous rhythm disturbances of the heart. All of which may save lives and allow those having a heart attack to live long enough to receive treatment. Everyone would agree the benefit of saving lives after a heart attack is pretty darn significant, and probably worth the investment in fish oil supplements.

But do they prevent a heart attack from occurring? By that I mean, if I currently have no history of heart disease at the ripe young age of fifty years, and I start taking fish oil supplements, will they keep me from having a heart attack? The quick answer is probably not. Supplementing fish oils and other Omega-3’s for saturated fats is without question a measure that will prevent the development of cardiovascular disease in most individuals. However, does one conclude that fatty fish and fish oil supplements are good for the heart? Heart Healthy? Or are they only good for those having a heart attack? I’ll explore the differences between those concepts in a future blog. In short here is what fish oil will and wont do:

1. Fish intake and Fish Oil Supplements (EPA and DHA) appear to prevent sudden cardiac death following a heart attack.


2. Fish intake and Fish Oil Supplements will not prevent a heart attack.

Omega Chemistry?

As a child I was tortured on many fronts by all the usual combatants: girls, pimples, bullies, bad hair, the wrong clothes, no respect, and a houseful of high-octane sibling rivalry. Nothing in that assault, matched my grandmother’s reliance on concoctions and over-the-counter goos to treat my colds and flu. I didn’t live with my grandmother, but we seemed to visit her on the occasions I was ill. To make matters worse, she was a big, forceful woman—so all I could do was lodge a protest. Despite my spindly arms waving in disapproval, she was always successful at placing a large tablespoon (sometimes two) of cod liver oil down my throat during the most minor of upper respiratory infections.

Plugging my nose didn’t help—it was like a fish oil explosion in my mouth. I usually gagged. “This fish oil,” she would stand erect and proclaim, “is how you’re gonna get better.” I can still remember the aftertaste; it was something between licking a week old fish lollipop and gargling with stale seawater. At night she would slather my chest down with Vicks directly after the cod liver oil inquisition, making me feel like a fish basted in mentholated paste. Was there some health benefit associated with cod liver oil? Or was my grandmother secretly attempting to turn me into a sea creature?

In that vein, the next consideration along the road to Omega understanding is the various forms the Omega fatty acids come in. To reiterate information from the last blog, Omega fats are simply a way of numbering the double bonds. Since we are talking about fats with double bonds, all Omega fatty acids are unsaturated fats. If the double bond is at the third carbon-carbon link counting from the left, we call it an Omega-3. If it’s at the sixth carbon we call it an Omega-6 fatty acid; however, for all practical purposes, the Omega-3 fatty acids are the only fats made relevant to this discussion. As I will show, actually one of the most important fatty acids is an Omega-6 fatty acid, linoleic acid.

Most unsaturated fatty acids contain more than one double bond. More than one double bond implies it is a polyunsaturated fatty acid. If it contains just one double bond it’s a monounsaturated fatty acid. Therefore, the Omega-3 designation is rather generic and implies just one of the many double bonds begins in the “3” position. More on the relative importance of the “3” position later. As you might have seen in the last blog, another way to designate the Omega fats is through the “N” system. Thus an N-3 fatty acid is the same as an Omega-3 fat. An N-6 fatty acid is the same as an Omega-6 fatty acid. And indeed one of the most important fatty acids is Linoleic Acid, which happens to be a polyunsaturated N-6 fatty acid. It’s also an essential fatty acid.

Linoleic Acid (18:2 N-6)

C ― C ― C ― C ― C― C = C ― C ― C = C ― C ― C ― C ― C ― C ― C ― C ― C OOH


Why is Linoleic acid essential? Because the human body doesn’t have the enzymes to produce the double bond in the Δ9 position (9 carbons from the Dela end, or 9 carbons from the Omega end). We have to consume foods that contain Linoleic Acid or develop essential fatty acid deficiency. More later.

Omega Madness

The names of fatty acids, and in particular Omega-3 fats, describes a nomenclature unique to and based upon the location of double bonds along the fatty acid carbon skeleton. Let me simplify that: a fat is nothing more than a string of carbon atoms bonded together. In addition to that, fats are really fatty acids as the fat portion has an added carboxylic acid attached to one end. The acid portion physiochemically makes the molecule both fat soluble and water soluble. For naming purposes, we count from the bare carbon end (Omega) or the acid end (Delta) to the first double bond and name the fat. Incidentally, and to confuse matters more; another name for Omega-3 fats is N-3 fats, with the N naming system cluttering an already confusing nomenclature. So if you hear about N-3 fats, that represents yet another way of indicating Omega-3 fats and at that I wont mention it again. What follows is a typical 16 carbon fatty acid.

(Omega end) C-C-C-C-C-C-C-C-C-C-C-C-C-C-C-COOH (Delta end)

To describe an Omega-3, means count in from the Omega end three carbons and place a double bond. Count in 6 carbons and place a lone double bond and you get an Omega-6. You get the picture.


(Omega end) C(1)-C(2)-C(3)=C-C-C-C-C-C-C-C-C-C-C-C-COOH (Delta end)

Silly, you thought that’s all there was to it. The Delta designation is there for a reason. In the
IUPAC system (International Union of Pure and Applied Chemistry) the fatty acid is numbered from the opposite end (acid end) of the molecule where the first carbon is numbered from right to left as follows:

(Omega end) C-C-C-C-C-C-C-C-C-C=C-C-C-C-C-COOH (Delta end)

This would be called a Delta-6 fatty acid or in the lingo of pure and applied chemists, it would be denoted as a 16:1 Δ6. Is this shades of college chemistry or what?

Not to bore you with all the nomenclature, the Omega numbering system usually applies only to fatty acids with double bonds close to the Omega end; thus, Omega-3 fatty acids are all you really hear about.

A key to understanding fatty acids is an understanding of some very basic terminology that’s thrown around daily. An unsaturated fatty acid has at least one double bond like this fragment: (Actually a monounsaturated fat)

― C ― C = C ― C ―

And a saturated fatty acid has no double bonds like this fragment:

― C ― C ― C ― C ―

The key when all this is said and done, is how much chemistry do you really need to know to be able to understand Omega-3 fats? The simple answer is: really, not that much. As Albert Einstein was quoted as saying, “Imagination is more important than knowledge.” And at that I’ll finish this later.

Obesity and Legal Matters

Quite recently a commentary was published in the Journal of the American Medical Association (JAMA) giving a legal perspective on the obesity epidemic. The title of the commentary was: Law as a Tool to Facilitate Healthier Lifestyles and Prevent Obesity[1] written by a member of the O’Neill Institute for National and Global Health Law, Georgetown University Law Center.

According to the author the obesity epidemic has resulted in obesity-attributable medical expenditures in 2003 to the tune of $75 billion just in the United States.[2] He goes on to discuss how the cost is at least 50% paid by general taxpayers through increased payments to Medicare and Medicaid with employers picking up the rest. That burden on taxpayers, as outlined in the commentary, should potentially shift from society to those individuals with obesity and obesity-related health issues. In short, for those individuals living a lifestyle of reckless food consumption, the state and federal government should not be made to pick up the tab for obesity related disease.

The pithy proposal of this commentary asks the question: What can the law do to prevent the obesity epidemic? The author then went on to present 8 potential areas where he felt the law might have an impact. I’ll present all eight with some commentary of my own.

1. Disclosure: As with cigarettes, a warning on a pack of donuts would inform and assist in allowing the consumer to understand that food can be dangerous to your health (not exactly as the author presented it). My opinion: put a warning on everything; the air in Los Angeles, the water in the Chesapeake, the dirt in Hanford, the sun in Hawaii and the conversation at Georgetown University. Please, please . . . no more warning labels.

2. Tort Liability: Again, as with big tobacco, sue the food industry. The food industry has inadequately prepared us for the culinary delights of the new millennium. Informed consent should accompany every order of French fries at Burger Central. As the author noted, many states prevent this kind of litigation with commonsense laws. Commonsense . . . how you do that?

3. Surveillance: This is where the ghost of George Orwell takes note. I have no idea what the author was alluding to with the inclusion of surveillance, but maybe a new government agency is needed: The Central Obesity Agency. Instead of the CIA we call it the COA. Let’s keep track of who’s getting fat and intervene with agents from the COA. "Sir, you've reached critical mass, and you'll have to come with me." What does surveillance have to do with the law anyway? Ask the Watergate conspirators.

4. Targeting Children and Adolescents: Targeted advertising by the food industry directed toward children and adolescents has at a minimum become part of the equation relating the environment to childhood obesity. Important in that exposure is the relationship between intake of specific foods and advertising. Regulation of advertising content directed at children is the upshot of this approach. I’m trying to imagine how that would play out in modern-day America? Replace the Trix rabbit with the attorney general? Replace Ronald McDonald with the Surgeon General? How about this: Parents, don’t let your kids buy all that junk we all see advertised. And that didn’t even require a law.

5. Taxation: This is by far my favorite. Impose a tax on unhealthy and calorie dense foods. As the theory goes, tax the heck out of certain foods and everyone will quit eating them. Call it the “Twinkie tax” for lack of a better term. First of all, who would determine which foods are healthy and which are unhealthy? I can only imagine the lobbying effort for that one. And governments given tax dollars have a tendency to blend all those dollars together (as opposed to setting the money aside for obesity related disease). Broccoli is healthy; but broccoli with béarnaise sauce might be considered unhealthy. I’m so confused!

6. School and Workplace Policies: On this issue I side with the author. Admittedly, most public schools have not been able to offer what anyone would consider a healthy lunch. And with vending machines making up for the lack of choice at most schools, many kids are munching on chips and cola and calling it lunch. I have no advice to give other than schools need to take this issue seriously.

7. Zoning: The government needs to step in and zone, cities and living regions appropriately such that parks, walking paths and bike paths are given a priority. As with issue #6, I couldn’t agree more.

8. Food Prohibitions: The prohibition against trans fat has occurred because of suspected associations between significant intake (5% of total calories or more) and cardiovascular disease. What that has to do with obesity is beyond me. Prohibiting foods that are known to lead to obesity might have been another argument in this vein. Placing restrictions on cakes, candies, chips, fried foods, frostings, ice cream . . . the list is endless.

In the final analysis, the commentator brought up two good points, those being #6 and #7 above. The rest appears to be health policy gone awry.

[1] Lawrence O. Gostin, JD, JAMA Jan. 3, 2007 297;1: 87-90
[2] Finkelstein EA, Fiebelkorn IC, Wang G. State-Level estimates of annual medical expenditures attributable to obesity. Obesity Research 2004;12:18-24

The Wisdom of a Serving Size

I normally don’t like to rant, but on Rudd Sound Bites a question arose regarding the use of the word “lean” by Nestle foods to describe their “grab and go” foods like lean pockets or pizza squares. Recently the FDA approved Nestle’s request to allow the word “lean” on the aforementioned foods. What then does any of that have to do with serving size? Well, the arguments used to sway the FDA depended upon a measure very much like the serving size called the Reference Amount Customarily Consumed. What it all conjured up in my mind was the proliferation of “nutri-babel” from government agencies mired in finding paper solutions to the obesity epidemic.

As outlined in the Federal Register Vol. 70 #63 Docket 2004N-0456, a serving of a food is defined as:
“An amount of food customarily consumed per eating occasion by
persons 4 years of age or older, which is expressed in a common
household measure that is appropriate to the food.”

There are two fundamental reasons to establish a serving size:

1. To standardize foods for labeling purposes: Not a bad notion as I might want to compare a serving of whole wheat bread to a serving of rye bread. But what if a standard slice of rye is larger than a slice of wheat?

2. To induce healthy portion consumption: Also not a bad notion. In the era of portion distortion might it be instructive to understand what amount constitutes a serving of broccoli? Or hold on there; does serving size really relate to healthy foods? Is it as important to understand a serving size for broccoli as it is for French fries? In the world of macro and micro nutrition, are we really concerned about people eating too much broccoli?

Starting with #1
1. To standardize foods for labeling purposes has been a monumental failure. I hate to always seem to throw cold water on the government’s attempts to standardize and regulate our lives, but in this case it simply isn’t working. Food manufacturers have so manipulated the serving size it has been relegated to the terminology junk pile. Here’s why:

Purchase a common food, a breakfast muffin, and the label reads: 240 cal in 2.5 servings. My muffin it seems is not a complete unit of food. Not only is it not a complete unit, it’s not a single serving, it’s 2.5 servings. But the muffin is without question a discrete unit of food, isn’t it? Taking out my calculator I divide the muffin into servings. If there are 2.5 servings per muffin, then what fraction of the whole represents a serving? The answer isn’t at all easy. First we need either the weight or the volume of the muffin. Using weight, I assume it weighs 6 ounces. The implication then is that 2.4 ounces of the 6 ounce muffin is a serving. In other words, 40% of the muffin is a serving. Without a scale, how might one excise 40% of the muffin to satisfy eating a single serving from the 2.5 serving muffin? Needless to say, the scaling by the manufacturer sought to hide the fact that if you ate the whole muffin, you took in 600 calories. In the end, most people eat the whole muffin.

2. To induce healthy portion consumption and relate nutrition information to an established quantity of food is certainly important. Here again, the public has been the one left out. The government docket cited above is rife with cogitation regarding how much an idealized serving size ought to be. Experts in the field bat at the concept of servings size as a quick means of controlling the obesity epidemic. Please (experts in the field) get a clue. The free market and independent free living people make daily decisions regarding how much they are going to eat—at each sitting. The average person eating the average meal does not consult USDA tables of servings per food item. The only thing served by the serving size cogitations is the self-serving (ego) size of the cogitator. If the government decides that a serving of pizza is one slice weighing 4.5 ounces, what difference does it really make to the average consumer?

Let’s not approach obesity paternalistically. Is it realistic for a government entity to develop a policy regarding food intake and expect the written policy to control individual food intake? Historically, the only way to control individual food intake is to severely limit supply or severely punish the wrongdoers. Or wait, is there a third method? Education? No that wouldn’t work, it’s more important for our children to know the capital of Peru than why essential fatty acids are essential. There’s my rant. I feel better.

Micro and Macroscopic Fat

Under the microscope, fat cells are massed together in packets of cells like a Kowloon high-rise. The cells specialized to store excess energy are colloquially called fat cells, but to the histologists and pathologists of the world, they’re called adipocytes. If examining the block of fat under a microscope, the fat cells collectively bunch together shoulder to shoulder and take the name adipose tissue. Even in fairly thin individuals with very low overall % body fat, pinching deeply around the lower belly reveals a fold or two of thick, loose tissue, the bulk of which is adipose tissue.

The focus of fat distribution has characterized individuals as either “Pear” or “Apple” with the descriptive pear assuming a more hips, thighs and legs distribution of fat, and apple as central fat distribution. The evolutionary justification for each is simple. Both in the final analysis are “centrally” distributed with apple fat being carried higher than pear fat. Both allow for free use of limbs and unobstructed senses.

Consider the physiological options with energy accumulation in obesity. If fat accumulated in the chest cavity, breathing would be impaired at very low adipose expansion. If fat were only accumulated on the arms, the arms would become useless and survivability of the organism would be rapidly diminished. Fat around the head and neck in any location to the same capacity of apple or pear distribution, would render the head enlarged with large cumbersome folds of fat around the eyes or engrossing the neck. The natural result of fat accumulation is to render preservation of an unencumbered organism with far too much stored adipose. Still, the organism can move, sense, survive and become limited by the accumulation of fat, but retains survivability skills.

From skin to adipose the layers are epidermis, dermis, hypodermis and adipose. And beneath the adipose tissue is the abdominal musculature—the “abs” or rectus abdominus. Going a level deeper, through the peritoneum and into the abdominal cavity, fat again proliferates on and in the omentum. The omentum is difficult to describe to the novice. Think of the omentum as a large gangly growth of adipose and loose connective tissue covering and surrounding the bowel. Central obesity is a massive collection of fat within the hypodermis (sometimes many centimeters thick) and a large collection of internal fat within the omentum. In some circles, omental fat is really what describes central obesity and the risk factors for the metabolic syndrome.

The tenants of this project I call adipose tissue are not even loosely thought of as an organ like the cells making up the liver or the spleen; but make no mistake, they collectively form a specialized kind of cell that lives for the sole purpose of storing excess energy in the form of triglyceride or fat.

Again, concentrating in certain locations, like around the mouth, nose or eyes, adipose tissue could obviously become a problem. Therefore the tissue is diffusely located in specific distributed locations such that the accumulation of storage fat would not impede day-to-day activities. As more and more excess energy is accumulated, the back of the arms, riding over the triceps muscles and in many cases encircling the entire upper arms, collects large deposits of adipose tissue. The thighs widen, or the abdomen becomes pendulous as more triglyceride accumulates in adipocytes.

Again, by design, the fat encircling the upper arm is less intrusive upon daily tasks than say a collection of fat surrounding the lower arms or fingers. An inspired quote by Eliel Saarinen, a Finnish-American architect and city planner, has applications to biological systems as well as the distribution of fat tissue around the human body:

“Always design a thing by considering it in its next larger context—a chair in a room, a room in a house, a house in an environment, an environment in a city plan.”

At that Eliel Saarinen described the evolution of human development. As an aside, the popular term, “cellulite” coined in the early 1970’s by non-medical beauty solon types, was thought to be a collection of “fat gone bad” by incorporating fat with water and a collection of “toxic wastes” leading to dimpling of the skin over the fat. The dimpling is actually a result of the connective tissue networks making up globular collections of adipocytes near the surface of the skin. The connective tissue holds the adipocytes firmly in groups and pulls on the surface as it expands. The term cellulite lead to a raft of possible snake oil cures including plastic pants, massage techniques, oil treatments and rollers and skin brushes to allow the cellulite to disappear. An excellent history and chronicle of the alleged treatments of cellulite are outlined nicely by Stephen Barrett M.D. on a wonderful website called Quackwatch.[i]

All adipocytes are cells with the primary purpose of holding a central core of energy dense fat or triglyceride within the cells matrix. The image above shows a cell with a large droplet of fat or triglyceride inside the cell. The nature and origin of triglyceride will be discussed shortly as the term “fat” is further dissected and defined. Again, those particular sites of collection described above have evolved as a distribution pattern allowing excess energy to be stored but not collecting in such a way to disrupt daily activities. Running with a moderate collection of adipose around the upper legs or thighs may slow the pace slightly, but it shouldn’t offer a significant obstruction to the mechanical motion of the legs. Moving up the body, lifting a heavy object with adipose around the upper arms or with adipose in the central portion of the abdomen ringing the belly like a donut, will not keep the object from being lifted or manipulated.

Finally and contrary to popular belief, the collections of adipose tissue are not for the most part responsive to the muscle groups they surround. That means doing more sit-ups will not decrease belly fat if the energy balance falls in excess of the energy needs. And upper arm fat will not respond specifically to biceps and triceps exercises. Instead, the muscles of the abdomen and upper arm will most likely become strengthened and may actually enlarge or hypertrophy beneath the pad of adipose. However, adipose tissue reacts to global energy needs not spot exercising.

The individual tenants of this complex referred to above live for one reason only: the storage of excess energy. The single adipose cell is rather large and dominated by a considerable amount of fat or triglyceride in the cell cytoplasm, appearing somewhat like a tanker truck. The truck and the driver (the nucleus of the cell, in purple) are dwarfed by the huge tank full of yellow fat. In the case of the adipocyte, a thin layering of cell cytoplasm surrounds the huge fat droplet, which as the figure shows, pushes the other cell components out to a thin layer around the fat droplet. The typical ingress and egress of triglyceride from the adipocyte, as above, occurs as a result of global energy needs. Hormone sensitive lipase is the key to moving fat in and out.

[i] Barrett S. “Cellulite” Removers. Quackwatch. http://www.quackwatch.org/

Surgical Fat: The Tummy Tuck

In my world, plastic surgeons make people beautiful again with sometimes intense and lengthy surgical procedures. I’ve had the occasion to sit in on a number of these procedures with plastic surgery colleagues and wanted to lend a little insight (and a break from the tedium of trans fat) into the process.

One of my least favorite procedures to observe is the abdominoplasty. The abdominoplasty or “tummy tuck” as it’s commonly called is a procedure which removes a significant portion of abdominal subcutaneous fat. Tummy seems innocent enought and tuck doesn't nearly describe the size of the incision. In fact, the fat is usually excised (cut out) in large blocks, by making rather large incisions across the lower abdomen. Being the curious one, I poked and prodded at the newly excised big block of yellow fat.

The yellow color of human fat actually depends on the dietary intake of carotenoids from carrots, yellow peppers and other colorful vegetables; a diet low in those vegetables gives the fat a paler, pastier color. The technical term for yellow fat is actually “White Fat” or simply "adipose tissue" which is held in distinction to “Brown Fat” a form of fat much more metabolically active. Brown fat actually gets its brown color from a clustering of mitochondria within each cell, allowing for intense metabolic activity. Bears and hibernating mammals use brown fat to slowly metabolize fat stores and survive the winters. Adult humans use very little if any brown fat.

With gloved hands I lifted the block of fat to test the weight of said extra tissue. It was weighty, but more than that, it was awkward not attached to the middle of the patient’s body—it slipped and flopped around like a shifty slab of fish. I set the block down and ran the corner of pure fat between my fingers. To foreigners outside the daily environment of the operating room, this process might sound a bit nauseating; but to those working in an operating room on a daily basis, the site of a tissue mass such as this is nothing short of benign. The fat seemed to come off in globules connected by a cellophane thin membrane breaking the fat up into discrete packets of thumb-sized tissue. Pressing the tissue between my finger and thumb instantly gave my gloves a greasy covering as the actual fat (triglyceride) held tight within the cells was partially ruptured, spilling out over my gloves.

Upon closer inspection, a spider web of tiny blood vessels laced itself through the tissue to offer a connection between the adipose (fat) cells containing the triglyceride (storage form of fat) and the systemic circulation—it was a liquid conduit of connectivity not in any way different than the plumbing system of a typical house or apartment. A mesh of fine nerve fibers was networked between the cells and complemented the wiring system of the house. Like any living tissue with function and purpose, fat cells need connectivity with blood and nerve fibers to integrate that specialized tissue to the greater functioning of the organism. With the naked eye, that’s about the extent of what an inspection of a block of human fat might reveal. Beyond that, a high-powered microscope is needed to reveal the minute world the fat cell resides within.
More on their microscopic world later.

Trans Fatty Acid: Unhealthy or Undebated (4) Final Analysis

Finally, the epidemiologic evidence to either support or refute the claimed association between trans fat intake and heart disease will be presented below. There are just six studies with overt examination of trans fat intake and it’s association with heart disease. Below is a list of the important studies, followed by a discussion of the strengths and weaknesses of each.

Study Findings: No association between trans fat intake and heart disease
1. Euramic Study: (1995)
2. Health Professionals Study (1996)
3. Scottish Heart Study (1996)


Study Findings: Association found between trans fat intake and heart disease
4. Finnish Study (1997)
5. Nurses Health Study (1997)
6. Zutphen Elderly Study (2001)


The No Association Studies
Of the studies listed above not finding an association between trans fat intake and heart disease is one that has been basically swept under the rug. The Health Professionals Followup Study followed a group of 43,757 men from 1986 to 1992 looking at a number of risk factors for heart disease including trans fat intake. The key is fiber intake. In those with high trans fat intake, fiber intake was low. In those with low trans fat intake, fiber intake was high. When the authors of the study adjusted for fiber intake, the statistical significance between trans fat intake and heart disease disappeared. The message seems to be that a dietary regimen low in fiber is a marker for a diet high in trans fat. High fiber intake has without question shown to be associated with a lower risk of heart disease. Thus one might conclude that fiber intake and not trans fat was the factor in their diets most associated with (or offering protection from) heart disease.

The Scottish Heart Study simply found no association between trans fat intake and heart disease in a widely followed cohort of men in Scottland.

The Euramic Study is widely criticized by those promoting the ill effects of trans fat (primarily those investigators at the Harvard School of Public Health). The Study sampled from 10 separate centers in 9 countries. The bottom line is this: No association between trans fat intake and heart disease was found. Detractors like to post hoc the findings and state that if Spain’s results were pulled out, there would be a significant finding. Sorry, too late. Taking two large centers (making up one-sixth of all those studied) out of the study is too convenient.


Studies Finding An Association
Of the studies finding an association between trans fat intake and heart disease, the Zutphen Elderly Study is the most compelling, but with marginal statistical significance. The one criticism I might level from the start is the study looked at an older population, age 64 to 84. We all know the risk of heart disease rises with rising age, and the key to significance in this study was making sure the participants were really disease free at the start of the 10 year analysis. The study began in 1960 and followed 878 men from Zutphen, Netherlands born between the years 1900 and 1919. Of the 878 men, 667 were given a questionnaire in 1985 regarding dietary intake. Of those 667 men, 435 and 225 were again surveyed in 1990 and 1995. Those with overt disease, angina or post myocardial infarction were excluded from the start. Doing the math, at the final analysis in 1995, the youngest member of the study would be 76 years old. At that age, we might find an association between nearly any variable and heart disease. The authors found that in the highest intake of trans fat (4.8% of calories) after fully adjusting for other possible confounding variables, there was an association between trans fat and heart disease. However the data were so marginal, that asking the question what is the risk of heart disease from various sources of trans fat for each 0.5% increase in energy, found no statistically significant data.

The Nurses Health Study is widely cited as the nail in the coffin for trans fat. The study followed 80,082 women over many years. The study found a very significant relationship between trans fat intake and heart disease. However, the authors noted that those consuming the highest amount of trans fat consumed the lowest amount of fiber. And those in the lowest intake of trans fat had the highest intake of fiber. The authors did not adjust their findings for fiber intake. A fatal flaw.


Conclusion:
The evidence attributing trans fat intake to heart disease is equivocal at best. The authors of the cited studies finding an association have heralded the elimination of trans fat from foods without hard evidence (other than the Nurses Health Study) that it might be harmful. Studies necessarily need to control for fiber intake to be taken seriously. However, no study has attributed trans fat intake in American men (Health Professionals Follow-up Study) to heart disease. Indeed, if the authors, primarily a small group of investigators from the Harvard School of Public Health, advocated as rigorously to include more dietary fiber in the average diet, trans fat intake would not be an issue. To attribute so fervently that trans fat is without question associated with heart disease makes me suspicious. Possible sources of secondary gain (again, primarily from those at the Harvard School of Public Health) include all the following trappings of large university syndrome:
1. Grant monies from the NIH,
2. Being identified as a world leader in public health
3. Lending credibility to a science that is so fraught with variable findings

In the end, trans fat doesn't have a study which anyone could identify as a smoking gun. Although the Nurses Health Study is widely cited as the final answer to the association between trans fat intake and heart disease, again, the authors did not adjust the findings for dietary fiber intake. And even if this study was the definitive answer, it was conducted in women and thus generalizable only to women. Any serious analysis of the studies leaves one skeptical about the strength of the public health message compared to the results found. As an aside, the industry is changing and any further study of trans fat will be difficult at best.

Trans Fatty Acids: Unhealthy or Undebated 3

It goes without saying we avoid trans fat to avoid heart disease. The natural question to come from that simple observation is how strong is the evidence that consuming foods with trans fat, in substantial quantities, will lead to heart disease? The answer isn’t at all easy as only a handful of epidemiologic studies have been conducted to answer that question. And based upon the world’s paranoia regarding trans fat, those few studies are probably all we’ll ever have to draw conclusions from.

A Brief Description of Atherosclerosis
First and most important is the fact that heart disease or coronary artery disease is a cumulative disease (developing over twenty to forty years in most cases). In that time frame, atherosclerotic (fatty) plaques form in the artery wall, leading to potential occlusion of the artery (usually when a plaque ruptures). Tissues downstream and served by that artery describe the damage from the disease; thus an acute coronary occlusion leads to a heart attack and a carotid artery occlusion leads to an ischemic stroke.

Damage to those two end-organs is the focus of cardiovascular disease, although renal artery occlusions can occur. The fat in the fatty plaque comes primarily from circulating LDL-C particles that migrate into the artery wall and become trapped in the intimal layer. After being trapped, the rapidly oxidizing LDL-C particle signals a response similar to an inflammatory signal, which incites circulating monocytes to enter the artery wall. As the monocytes enter the artery wall they become tissue macrophages which function to consume the trapped, oxidized, LDL-C particles. Consuming the LDL-C particles en mass, the tissue macrophages become themselves overwhelmed and eventually die in the artery wall. As more die, the fatty goo builds up and the bump of fat starts to occlude the artery. Thus goes a simplified and quick version of how atherosclerosis develops.

How does that Relate to Trans Fatty Acid?
From the last blog, remember that trans fats can elevate LDL-C and lower HDL-C if consumed in quantities greater than roughly 5% of total daily calories. That increase has been cited as the physiologic basis for the relationship between trans fat intake and the development of atherosclerosis and heart disease.

The ultimate study of trans fat would take a population of representative citizens and randomize them to either receive trans fat or not, usually in a double blind fashion. Follow that group for roughly twenty to forty years and assess the development of atherosclerosis at the end of the study in all participants. That assessment, of course, would be blinded to the intake of trans fat. If this seems a little far-fetched, it’s because it is. The closest thing we have to the above definitive study is the epidemiologic approach to approximate the above study (if conducted rigidly).

Epidemiologic Evidence that Trans Fat intake Leads to Heart Disease
The closest thing to a real randomized and blinded trial over the time frame of disease development is as stated above, the epidemiologic study. It’s sometimes called an observational study because instead of controlling the study, one observes the participants. The observational study seeks to replace what we simply can’t do in the real world.

In the case of trans fat, the typical epidemiologic study follows a large group of participants (called a cohort) over a long period of time—usually five to ten years—and reports the average dietary intakes (derived from periodic questionnaires), relating that intake to some endpoint like heart attack or death. One of the most famous of all cohorts is the Framingham Study, which spun off numerous epidemiologic analyses of environmental exposures as they relate to disease. Other well recognized cohort studies are for example the Health Professionals Follow Up Study and the Nurses Health Study, both utilizing a large group of health care professionals.

Typically, at the outset the groups are asked to report their usual food intake from a very detailed questionnaire, then followed-up after a variable period of time with more questionnaires and possibly physical and laboratory analyses. At the end of some pre-specified time frame, the entire cohort is examined to see how many have died, how many had heart attacks and what the repeated food intake questionnaires revealed about the relationship between what they ate and the rate of heart attacks or cancer or some other specified endpoint.

The studies and the analyses are expensive and complex, but model as closely as possible the effect of a particular food or environmental factor relating exposure to disease. In the case of trans fat intake, the number of studies have been somewhat limited and have generated variable results.

For the sake of brevity I will continue this blog with an analysis of the actual studies. Each has strengths and weaknesses, but as I will show, there is no real evidence to condemn the usual (2.6% of energy) intake of trans fat.

Trans Fatty acids: Unhealthy or Undebated 2

The American Heart Association (AHA) recommends limiting saturated fat intake to less than 10% of calories and trans fat to less than 1% of calories. One would assume the evidence from prior studies suggests that limiting trans fat intake to less than 1% of calories prevents changes that might increase the risk of cardiovascular disease.

However, if I consume 3% of calories daily as trans fat am I at increased risk of heart disease? What about 5%? In other words, is there a graded increase in risk above 1%? More than that, who in their right mind has a clue what % of calories they consume daily as trans fat; moreover, if I somehow manage to find out I consume 3 grams of trans fat, unless I do a caloric analysis of all I eat, how would I know what % of total daily calories that 3 grams represents? I understand the dilemma, the AHA wants to give the public advice in the language of panel findings; however, it’s useless, impractical information that the public can’t really digest. Not just that, physicians and dieticians on the front line, have the added burden of translating the advice to an undereducated public. The question then is: How do we give the public advice with a measure that’s useful? I’ll address that concern later. First the evidence.


The Evidence(Clinical and Basic Science Studies)
A very nice review of some of the clinical evidence showing the effects of dietary trans fats was published in Nutrition Research by J. Edward Hunter in 2005. I won’t review all the important information he presented, but will offer a bulleted list of some important numbers:

• Frying oils used in restaurants and other food dispensing operations range in trans fat content from 0 to 35% of total fats.
  
• Most current tub and stick margarines contain very little to no trans fat (however, check the nutrition label)
  
• Baking shortenings (still a bad player) contain approximately 15% to 30% fat as trans fat
  
• Beef and dairy fat contains approximately 3% trans fat
  
• On average Americans consume 2.6% of daily energy as trans fat or 5.3 g per person (Allison et al J. Am. Dietetics Assoc 1999;99(2):166-74). That percent has most likely dropped due to the campaign against trans fat and the new labeling initiative-.
  
• Europeans consume less at 2.1% of daily energy.

A large number of studies have analyzed just how trans fat intake might impact normal physiology. A fairly consistent finding reveals that as someone consumes an increasing amount of trans fat, the following happens:

• High Density Lipoprotein cholesterol (HDL-C) decreases
• Low Density Lipoprotein cholesterol (LDL-C) increases

Increased LDL-C and decreased HDL-C increases the risk over time of developing atherosclerosis or coronary heart disease. Eating saturated fatty acids increases both LDL-C and HDL-C, thus total cholesterol is elevated to a greater extent with saturated fatty acid consumption than trans fat.

According to a study conducted by Ascherio et al, in 1999, pooling the data from 17 other clinical studies found that LDL and HDL were significantly altered at the following % intake of trans fat;

• LDL was statistically elevated at 4% trans fat (of total calories)
• HDL was statistically decreased at 5-6% of total calories

Therefore putting the above information together, the average American and European consumes somewhere in the range of 2% of calories as trans fat (and probably less in the current market), but a statistically significant elevation of markers for increased risk of heart disease is roughly twice that value at 4-5%.

The dilemma addressed at the beginning of this presentation is what should the AHA tell the average individual about trans fat? What advice should they give? That's a problem not properly addressed or even considered by the AHA, because the answer is more than they are willing to take on. The bottom line, in my opinion, is to choose your fats carefully. Knowing the science of trans fatty acids is without question a starting point for anyone interested in the association between the foods we eat and our long-term health.

My advice: Learn what you can and make informed choices. That might sound trite and worn, and possibly even evasive, but without reading and understanding the science, we are doomed to the wisdom of concensus statements and what someone else has decided for us. That said, to substitute butter (or saturated fat) for margarine to avoid trans fat, is apparently a bad idea.

Trans Fatty Acids: Unhealthy or Undebated

Chronic disease as part of the aging process appears to some to be nothing more than the spin of a roulette wheel. Choose the wrong parents, wind up with the wrong genetic material, grow up in the wrong neighborhood, unknowingly eat the wrong foods, and the roulette wheel stops on your number. The counter to that rather arbitrary perspective on life and health is that good health and longevity are self-determined. And the personification of that perspective is the health-conscious, nearly panic-stricken individual who reads every health food article and takes to heart nearly all health claims.

The bulk of us live somewhere in the middle, between the roulette wheel and the spooked health-consumer; that is to say, most of us watch for important health and diet discoveries from reliable sources, take the proper steps to fit those new discoveries into our lifestyles, and hopefully live longer, more disease-free lives. And as a society, we take for granted that the intellectualization and distillation of scientific hypotheses turned scientific theories turned scientific facts, is a specialization which can be summed up by the consensus statements of highly respected academicians and or policymakers. And really, we should live in a time where no further consideration is necessary.

The case under consideration, as the title suggests, is the consumption of trans fatty acids. The designation trans fatty acid is actually a family of fats with oddly placed double bonds in the geometric "trans" configuration at various locations along the fatty acid molecule. The whole process began back in the butter versus margarine wars, when a butter substitute was sought by those chasing the butter market. The Federal Margarine Act of 1886 halted the process and forbid the sale of margarine after years of campaigning by the dairy lobby. With the color added laws, margarine had to be sold in its native state as the law prohibited adding any artificially coloring. As market forces are want to do, a color additive was sold separately and mixed into the sheepish colored margarine by the consumer, giving a yellow colored butter substitute.

Liquid oils at room temperature are hardened by exposing them to heat and pressure, a process we've all heard of called partial hydrogenation. The native vegetable or fish oils with numerous double bonds in the "cis" configuration are “hydrogenated” or water is added across the double bond to create a single bond. Fully hydrogenating a fatty acid with native double bonds results in a saturated fatty acid, absent of any double bonds. In the case of partial hydrogenation, some double bonds remain intact, thus “partial” hydrogenation results in molecules being shuffled like a deck of cards to create novel fatty acids not usually found in nature.


Some of the molecules created by the process remain in the native or “cis” configuration (a) while others result in flipped double bonds giving some a “trans” configuration (b) as depicted above. Chemically, trans fats behave like saturated fats. In some cases two trans bonds are created, referred to as trans-trans fat. Some fatty acids come with one cis and one trans double bond in a variety of locations. Therefore, the term trans fat is a global term, usually referring to the 18 carbon 1 double bond trans variety; however, like the term saturated fat, trans fat can refer to any of a number of molecules, including 16 and 14 carbon trans fat, or 18 carbon trans-trans fat or 18 carbon cis-trans fat.

The real surprise, whether you believe trans fat may or may not impact your health, is a simple review of the scope and variety of foods that contain trans fat. That review is illustrative to say the least. The foods containing trans fat range from gravies to cookies. Breaded chicken dishes may or may not contain trans fat. Some commercial varieties may contain a shockingly high percentage of fat as trans fat, while others may contain virtually none. Deep-fried anything is a notorious source of trans fats. Donuts and French fries are in fact a roulette wheel spin of trans fat; again, they may be high in trans fat or may contain just a small amount. And without a label, as a consumer you really have no idea which ones will be high in trans fat and which ones are low in trans fat—they all look and taste the same.

Popcorn either microwave or commercially bought at movies or county fairs may or may not contain trans fat. Most commercially available cookies are either bad for you or . . . bad for you. They’re either high in saturated fat or high in trans fat. A complete inventory of foods that contain trans fat and those that don’t isn’t really as simple as it might seem. As I’ll discuss later, even if you decided to avoid all trans fat, the places you’ll find it are in many cases in foods without a nutrition label--comercially processed and served at restaurants, fast food establishments or diners. And in those with a nutrition label, watch out for the new labeling system, there are hazards to navigate. More later . . .

Glycemic Index 3

The strength of any measure, such as the glycemic index (GI), is the accuracy and precision in which the values reflect the real world. Call up the GI of foods on Google and you’ll get a host of websites with a variety of values as if those values were written on stone tablets and delivered from the mountain top. So, where do most of those internet and diet book values come from? I’ll get to that.

Focusing for a second on the GI of foods presented in the last blog, a reader asked,

“Why the difference between the GI for Coca Cola in Australia and Atlanta?”

The answer is one of the keys to understanding why I contend the GI--as a clinical tool--is useless. I’ll soften that a bit: it’s a very crude tool at best, and may be useless. There are a number of reasons for that contention which I’ll touch on. However, criticism of the GI hasn’t stopped research interests from using it.

Case in point, a recent study published in the NEJM titled, Low-carbohydrate-diet score and the risk of coronary heart disease in women, the authors contended low carbohydrate diets (similar to Atkins and South Beach) were not associated with an increased risk of heart disease in a group of 88,000 nurses (the Nurses Health Study). Based upon a food frequency questionnaire, individual carbohydrate intake was coded for all study participants, and based upon the GI values of the foods reported from that questionnaire (Harvard has their own database for GI values), the Glycemic Load (that’s the GI multiplied by the amount of a particular food eaten) was also reported. The absolute carbohydrate intake and the calculated Glycemic Load was used to categorize women into both carbohydrate intake groupings, low to high, and Glycemic Load values. The authors found no relationship between absolute carbohydrate intake and heart disease, but that those with higher glycemic loads were found to be more likely to develop heart disease.

The reference I listed in yesterdays blog: Kaye Foster-Powell, et al. International table of glycemic index and glycemic load values is a compilation of numerous studies on a variety of foods which gives a crude database for the GI values of a number of foods. Pulling that reference and looking at something simple like rice, reveals that the values are all over the board depending upon the kind of rice, the method of testing, the country of origin, the study subjects used to arrive at the value—and potentially, the method of cooking the rice. As an example, Kellogg’s Corn Flakes is reported as follows:

Kellogg’s Corn Flakes ( USA) Study subjects: Diabetics GI = 92
Kellogg’s Corn Flakes (Canada) Study subjects: Diabetics GI = 86
Kellogg’s Corn Flakes (Australia) Study subjects: Healthy GI = 77
Kellogg’s Corn Flakes (Auckland) Study Subjects: Healthy GI = 72

Therefore, conducting a clinical research study, which of those values do you use to calculate the Glycemic Load? Usually the values are averaged to come up with some middle-of-the-road average value. But what does that do to accuracy? In addition to the database issue, and most problematic, foods are not eaten alone (as are the test foods listed). Most foods are part of what we call a “mixed meal” where a number of different foods are eaten simultaneously. Are the GI values valid for mixed meals? The answer is an unequivocal no. Eat Kellogg’s Corn Flakes from anywhere, put milk and part of a banana on it with some table sugar and all bets are off. The milk fat slows gastric emptying, thus changing the GI for corn flakes, the banana has fiber which again changes the value. And not to mention, what if you eat in a hurry, will that change the GI of the food? The answer is, it most likely will.

The bottom line is trust. Visit any old website and read an essay on the GI with a table of typical values. Find out where the author(s) derived the numbers. If they were from the International Table of Glycemic Index and Glycemic Load Values, trust them even less. Most values are averages from either healthy or diabetic subjects, some with glucose as a reference and some with white bread as a reference. Some evaluated test subjects for two hours and some for three hours. Conclusions in science drawn from such scattered and inhomogeneous sources build a foundation for junk science. The answer in the context of nutritional and food science, and in my humble opinion, is to remain skeptical.

Glycemic Index 2

The glycemic index was developed by David JA Jenkins who introduced it in 1981 as a tool to help manage type 1 diabetes. To better define the glycemic index of a food the following simple formula describes how a number is generated:

Glycemic Index (test food) =
Blood sugar change (Averaged) over two hours (of a test food) divided by the
Blood sugar change (Averaged) over two hours (of a reference food)


Therefore a test food, say an apple, is consumed with the resulting blood glucose measured frequently over two hours following consumption. In the same test subjects (to be able to compare the apple to something) a reference food is later consumed and blood glucose is again measured over a two hour period following consumption. The food used for the reference is usually 50 grams of pure glucose or 50 grams of available carbohydrate from white bread. Typically the number reported for the glycemic index of a food is a fraction. The blood sugar change over two hours with a reference food such as 50 grams of pure dextrose results in a higher blood sugar level than most all foods, including the apple. The larger the reported number, the higher the blood sugar from a test food compared to the reference. A glycemic index of 1.0 means the food in quesiton releases the same amount of glucose as a test meal of 50 grams of pure glucose. For the apple, the result is the following:

Glycemic Index (Apple) = 0.66


Rather than report a percentage or fraction, the number is usually just reported as 66.

So what does the number mean? In essence, it means if you compare equal amounts of carbohydrate from an apple and a reference food, the carbohydrate from the apple converted to glucose in the gut, leads to 66% of the blood glucose one would experience by eating the same amount of carbohydrate found in pure glucose.

Seems pretty straightforward. A food high in fiber would release very little digestable carbohydrate thus resulting in a lower glycemic index compared to a readily digestable carbohydrate like a potato. Some typical glycemic index values are as follows:

Reference: Kaye Foster-Powell, et al. International table of glycemic index and glycemic load values: 2002 American Journal of Clinical Nutrition 2002;76:5-56

Rice (white) studied in Canada = 72
Kelloggs All Bran Cereal studied at Battle Creek, MI = 38
Bagel (white) studied in Canada = 72
Coca Cola studied in Australia = 53
Coca Cola studied in Atlanta = 63

The Glycemic Index

With carbohydrate calories making up on average 65% of most Americans total daily caloric intake, any modification in the variety and volume of carbohydrate intake might have a profound impact on long-term health and weight management. Numerous popular diets have targeted the lowly carbohydrate, leading the charge in what will surely be remembered as the “low carb” diet era.

However, without a deeper understanding of the role carbohydrates play in normal physiology, in gut physiology, in the prevention of heart disease and cancer, and more globally, the role they play in long-term health promotion—cutting carbs may or may not be a desirable goal depending on which carbs are being eliminated. This series will attempt to demystify and unravel the popular notions of carbohydrate intake as well as the glycemic index and glycemic load and add insight into the relationship between carbohydrate intake and health.

A basic presentation of carbohydrate terminology will be presented first—which is an admittedly dry subject—but will naturally lead into some current controversies related to carbohydrate intake. The basic science and vocabulary of carbohydrates is critical to understanding not just the glycemic index and glycemic load, but numerous other aspects of carbohydrate physiology. Ultimately, the distillation of the following sections is the impact carbohydrates may have on weight management, health, and longevity.

The glycemic index and glycemic load are measures of glucose absorption and the concomitant blood glucose level resulting. In very basic terms, glucose is the fundamental building block of most carbohydrate molecules. The basic sugars are broken down into

monosaccharides

1. Glucose (glue-kose) Grape sugar
2. Fructose (frook-tose) Fruit sugar
3. Galactose (Galak-tose) Component of Milk Sugar

And disaccharides . . .

4. Sucrose (Sue-krose) Table sugar
5. Lactose (Lak-tose) Milk sugar
6. Maltose (Mall-tose) Malt sugar

The glycemic index asks the question: if I eat a food containing carbohydrates, how will it impact my blood sugar over the next two to three hours? Thus taking that approach, the disaccharides cannot be absorbed until broken down in the gut to allow the glucose (and fructose and galactose) to travel through the intestinal mucsoa into the blood.

Honey is primarily fructose and since we don't measure blood fructose levels, the glycemic index of honey is low. Again, when blood sugar is measured, we measure glucose, not fructose. Honey is gram for gram sweeter than table sugar, but the resulting glycemic index is lower. Confused? Don't be, fructose triggers those papillary taste buds with waves of sweetness and the resulting blood glucose elevation is minimal. Fructose is absorbed from the intestine and taken up by cells, with some being metabolized for the energy needs of cells, and some fructose is altered (metabolized) in reverse to produce glucose and enter the blood stream. Thus fructose containing foods have a low glycemic index. Numerous foods are flavored with fructose and high fructose corn syrup (HFCS). It hardly seems fair, but Cola drinks usually have a lower glycemic index than certain vegetables because they're sweetened with HFCS. More tomorrow.

FDA News

Federal Trade Commission Steps Up to the Plate

Finally, the FTC stepped up to the plate and fined makers of four over the counter (OTC) weight reduction pills for making false claims. The makers of Cortislim, Cortistress, Xenadrine EFX, Trimspa and a Bayer multivitamin (which promised to increase metabolism) were named in the FTC fine. In total the fines were levied to the tune of $25 million dollars spread out over the various manufacturers of the above products. According to FTC Chairman Deborah Platt Majoras (as reported on MSNBC)

“What we challenge is the marketing of the claims,” she said. “The marketers are required to back up the claims with the science and if they can’t do that they can’t make the claim. But we don’t ban the products from the shelves.”

Finally, an FTC chairman mentioning science as a foundation backing up a manufacturers claim. Apparently the fines are going to be returned to the duped consumers. And how that might be accomplished for an OTC product would be interesting as no record of specific purchases are recorded unless the consumers kept their receipts.

Dieting: Success and Failure (Part 5, Final)

The urgent message that we are all gaining weight has gone out. The biology of eating is well described and the intake of too much food with too many calories leads to weight gain—that much we know. We haggle like fish mongers over which nutrient is causing all the damage. Billions of NIH grant dollars have been spent on the topic. Is the culprit too much carbohydrate, too much protein or too much fat? Without a nickel of NIH money, I’m here to report the culprit is simple: overeating.

We have segregated and compartmentalized what evolved as a hunger driven process into a process of daily routine and ritual not unlike brushing our teeth or walking the dog. Through our collective maturation from hunter-gatherer omnivores to agricultural based diets to an industrial/technology driven society, we have lost the connection with our food chain. We have lost track of what food is and where it comes from, relegating our food choices to a menu of prior taste experiences or an array of foods someone else grows or hunts or gathers for us, and in many cases, cooks for us. In the most liberal sense, we eat what we hunt and gather at the local market. We eat until satisfied based upon taste experiences, adaptation to a meal size, and of course, until the meal is over. In the process of converting a basic survival instinct into a daily routine, the ability to maintain connectivity between our state of hunger and the state of our body—got lost.

In the same sense, eating might be likened to other fundamental drives like sexual activity, thirst, the need to sleep, and the need to be social (a basic instinct of another variety, but still a basic instinct). What if sexual activity were relegated to a daily routine of morning and evening engagement? Day in, day out, rain or shine, headache or no headache, the routine of sex occurs daily at the same time—with few exceptions. The idea strikes us as untenable and the thought of it being regimented to that degree allows sex to lose its reckless verve, subjugated instead to a lower wrung on life’s ladder of important activities. By that description, it would be a daily grind—a daily routine. Using that analogy, has food intake and the concomitant taste and satiety experiences we expect daily been subjugated to a daily grind? Are we marching through the day marking time between meals?

As the final segment of Dieting: Success and Failure I’m ending on an uneasy note. Anyone looking for an easy answer to the grocery store checkout-line magazine header “Lose Belly Fat Easily” will leave unfulfilled. In the real world, losing belly (visceral) fat might seem easy to those reading this blog, but to the average individual, it’s nearly an impossible task. We assume with little curiosity that throughout life we can navigate effectively through a gauntlet of fine foods possessing indescribable flavors and tastes, and remain capable of picking and choosing the time and place we consume those foods. Of course, the counter to that quixotic proposal, and sitting at the opposite end of the self-control scale, is the notion that we have little to no control over any of it.

The painful truth is modern medicine is good at solving specific clinical issues and problems related to disease states like angina due to cardiovascular disease or helping diabetics manage hyperglycemia, but when someone wants to lose weight, Barnes and Noble is a better resource than The American Journal of Clinical Nutrition. Sadly, if you ask twenty experts in the field of nutrition how to solve a behavioral problem such as overeating, the responses (if they come) will be as varied as the available mass marketed foods.

Dieting: Success and Failure (Part 4)

New Years Resolutions

One of the most persistent complications of weight control is the distraction and spot-fire stamping about used with New Year’s Resolutions. It’s not uncommon for one of the top ten most popular resolutions to be one of the big three:
1. Lose weight
2. Eat better
3. Eat healthier
But then, we already knew that, because we’ve all been there. The problem with vague notions like lose weight (How does one reliably do it? Where is there any insightful information on the subject without a lot of pseudoscience and crap?) or eat healthier (Who has the ultimate analysis of healthy versus unhealthy food?) is picking the science out of the background noise and marketing. The amount of insight and basic nutrition knowledge it takes to carry any of the above resolutions out, goes far beyond Atkins for Life and in reality may require more remedial nutrition education than most of us are willing to take on. Picking up a formulaic diet manual is about as resolution defining as attempting to empty Lake Michigan with a paper cup. You may start dishing the water, but folks, the lake isn’t dropping.

Adding to the confusion is the big-box bookstore approach to selling us mainstream weight loss advice. Enter any of the big stores around the first week of January and what does the curious pre-dieter find? A front table packed with the latest and greatest weight loss manuals espousing the one true method to finally take it off and leave it off. Nothing on that table offers insight into the process; rather, it represents a stack of desperate manuals with insecure formulas to follow for a defined period of time. And indeed, in time the manual seems foolish. I’ve never been to the South Beach and I have no idea what they eat there, but on good old mainstreet USA, we eat good food. We eat Phad Thai and roasted Tom turkey with stuffing (not together though). We drink Chateau Neuf du Pape and nibble on smoked brie and crackers. We order a pizza with stuffed crust and wash it down with Becks. We love the texture and mouth appeal of Cheetos. Now please, who on the South Beach doesn’t like nachos? In total, the average dieter (and count me in) finds the dietary changes artificial and contrived, returning us instead to what we know—the great taste of 21st century foods and to hell with abstinence. An orange never tasted quite the same as Philly cheesesteak sandwich. And celery never quite gave me the solace of Doritos.

So what measure of success do we use for the New Years Resolutions? Stand patiently by our bathroom scales waiting for the abstinence to be metered out in lost pounds? Wait patiently by the journals hoping a pill will come down the marketing pipeline that might kill those modern food cravings? No, the answer is knowledge and education. When the next weight loss corporation claims you might lose 7 lbs. in 7 days, realize it may not be fat you’re losing and it may not offer a permanent solution.

So what is the formula for weight loss? In the most extreme case, starvation, the formula for weight loss is well known. Weight loss in the initial days of fasting and early in starvation represents primarily the loss of water from glycogen utilization and the resulting diuresis (loss of fluid associated with burning glycogen). As the fast continues, the weight loss diminishes until glycogen stores are exhausted (usually just a day or two) and adaptation to metabolizing protein and fat stores occurs. Usually by three weeks of starvation, protein is being spared and fat stores become the sole source of energy. Weight loss has stabilized and seems to slow to a crawl. At this point roughly 4 pounds is lost per week of starvation (not dieting, but absolute fasting). Doing the math we can tabulate the loss as follows with a typical 5 foot 5 inch tall,150 pound individual. The following is a ballpark figure and depends on calories burned during activity and many other assumptions:
1. Fat Energy: 9 kcal per gram of fat (the amount of energy derived from fat tissue)
2. Daily Energy Needs: 2000 kcal’s needed for energy per day of normal activity
3. Fat Used: Using #1 and #2 above, 222 grams of fat per day is needed to meet energy needs
4. Weekly Loss: 222 grams x 7 days = 1554 grams (3.4 lbs)

So next time the weight loss purveyors advertise that you can lose 7 lbs. in 7 days, return to this blog and do the math.