Wednesday, January 25, 2012

What to drink?

There's probably no other thought that pops into our heads more often than "what should I eat?"  The answer should be simple, but the question has become frustratingly complex.  Should we eat for taste, or for health?  What about convenience?  And what about the more nebulous, but vitally important, question of the ecological impact of the food we are eating?

A corollary of the mealtime question, of course, is "what should I drink?"  We can again ask many questions about our liquid refreshments, and fortunately, a couple studies from the recent issue of The American Journal of Clinical Nutrition provide us with some answers.

One of these is not like the others...

The first study, by a group in Denmark, indicates what not to drink.  Designed as an experiment with their subjects freely roaming the world, the researchers gave groups of participants a different liter of fluid to drink each day for six months.  The experimental drink was good ole' Coca-Cola (made with sucrose rather than high fructose corn syrup in Europe), and the control drinks were reduced fat milk, diet-Coke, and water.  Drinks were delivered to the subjects homes at the start of the study, and empty bottles were collected afterwords; as such, it's likely that at least some of the daily allotments made it down the drain instead of the gullet.  But regardless of the precise amount consumed, the results are telling.

The regular cola, or as the Danish-scientists fondly called them, sucrose-sweetend soft drinks (SSSDs), but none of the other drinks, drove fat to accumulate in all of the wrong places.  The regular soda caused a 135% increase in liver fat, a 120% increase in intramuscular fat (think marbling in a corn-fed steak), and a 25% increase in visceral fat, which is the particularly deleterious fat that surrounds the organs within the abdomen.  Together, the liver and muscles comprise the greatest amount of insulin-sensitive tissue in the body.  When fat infiltrates these organs, they have trouble following insulin's orders, so the pancreas has to squeeze out more insulin to compensate.  This is insulin resistance.  But while none of the subjects showed compromised insulin function in the first 6 months, ectopic, or out of place, fat deposits are paramount to insulin resistance and the associated metabolic syndrome.

And the relative non-effects of the other drinks are equally interesting.

Despite a similar caloric content to the SSSBs, daily milk intake decreased the ratio of visceral fat to subcutaneous fat, meaning that milk helped carve people into a "pear" rather than an "apple" shape.  A calorie is a calorie, indeed.

Surprisingly, both diet soda and milk lead to a decrease in blood pressure.  What's more, the diet soda didn't cause any fat gain.  Diet soda is thought, at least by some, to contribute to weight gain because the sweet taste of diet soda is sufficient for the pancreas to secrete some insulin.  This study clearly argues against an "obesogenic" effect of artificial sweeteners, both directly, or indirectly by encouraging a sweet tooth.

But what shall we order at Happy Hour?

Red wine has become famous for being "heart healthy."  After all, the Mediterraneans are famous for drinking wine and having a relative absence of heart disease.  Additionally,  the grape-derived compound resveratrol has been shown to extend life... in metabolically compromised mice, anyway.  But really pinning down the benefit of red wine as been a challenge.

There isn't actually a whole lot of resveratrol in wine, and most animal studies employ pharmacological doses extracted from grapes.  So is it some other compound in wine?  Is it a combination of some?

And epidemiological evidence on red wine must be taken with a grain of salt.  Prospective cohort studies - like the Nurse's Health Study - are the best form of observational epidemiology, but they cannot exclude selection bias, that is, people who tend to drink red wine also tend to be wealthier, healthier, or live more moderate lives.  Selection bias prohibits researchers from truly knowing if it's the red wine or if it's simply the people who choose to drink red wine, that's the determinant of health.  Fortunately, researchers conducted an experiment.

This study examined the impact of red wine on heart disease risk factors, specifically the abundance of inflammatory proteins and immune cells in the blood.  Heart disease is characterized by systemic inflammation and the accumulation of immune cells, like macrophages and lymphocytes, within the blood vessel walls.  There's good reason to think that it's this inflammation, rather than cholesterol per se, that contributes to cardiovascular disease.  Any modality that can reduce inflammation likely protects the heart.

Each subject in the experiment participated in each of three four-week trials where they got to enjoy a couple of daily servings of red wine, gin, or de-alcoholized red wine.  The gin allowed the researchers to examine the impact of the alcohol, while the de-alcoholized wine isolated the multitude of polyphenols unique to fermented grape juice.  The results are intriguing, if not a bit complex.

Does this mean that my birthday celebration was good for my heart?
I'd like to think so.
Red wine, and not the individual components, lowered several pro inflammatory molecules in the blood.  Collectively called "chemokines," CD40a, IL-16, MCP-1, and VCAM-1 were all reduced.  These molecules help immune cells cling and penetrate into blood vessel walls, where they form fatty plaques.  Other effects were specifically attributed to the components of the wine.

Two daily shots of gin made immune cells less sticky, while also increasing IL-10, a potent anti-inflammatory molecule that mellows-out aggressive immune cells.

And the polyphenols themselves lowered IL-6, an acute-phase protein that stimulates the liver to secrete C-reactive protein, which is routinely measured by doctors to assess heart disease risk.  Grape juice also contains polyphenols, but all of the sugar without the fiber likely makes the teetotaling drink more harmful than helpful.

Of course, the participants probably didn't drink every last drop; some of the soda, although perhaps not the wine, surely went right down the sink.  And we don't know exactly how important it is to decrease esoteric molecules like IL-16 from 478pg/ml to 450pg/ml.  But we do have a certain degree of confidence in deciding what we should drink.

We can say that soda consumption does indeed cause fat to be deposited throughout the body.  And the benefits of drinking wine could very well be attributable to the wine itself; and at the very least, some merlot doesn't appear harmful to the heart.

It looks like the cherry-brandy diet Coke highball I made the other weekend was an even better idea that I originally thought!

Sunday, December 25, 2011

Chicken Liver Mousse, not Moose


I've had a pound of chicken livers from the farmers market locked away in the freezer for quite some time.  The girlfriend isn't exactly dying to eat them, so I needed to wait until she was out of town.  But I still had to figure out what to do with them.  Fortunately, one of my colleagues is a former  chef, and when I told him about my stash of offal, he eagerly offered me a recipe.  Chicken liver mousse makes the medicine go down smooth.

Liver is the original multi-vitamin.  I'm generally cautious about parsing foods based on their vitamin, mineral, or other micronutrient content.  After all, it's hard to be nutrient deficient, or insufficient, when your main foods are vegetables, meat, and dairy.  So looking at nutrient content is almost a moot point.  But liver is worth talking about.  

Either cherished or despised, this vital organ provides compounds that are hard to squeeze out of standard muscle meat, such as choline and vitamin A, and provides more B vitamins than anything else.  

The graphs below show the vitamin content of 3.5 ounces of chicken liver, 1.75 ounces of chicken liver (an amount that could reasonably be eaten in a night's worth of pâté), and 3.5 ounces of chicken breast tenders, all cooked.  Vitamins are measured in different units, such as international units, milligrams, or micrograms, so it's only valid to compare the vitamin contents between the foods, and not between the different vitamins.  Two graphs are shown since some vitamins simply come in higher numbers (vitamin A) than others (choline), and I didn't want to do any crazy graph standardizing on Christmas Day.  A quick glance shows that the amount of choline and vitamins A and B12 in liver compared to breast meat is remarkable.  Whether you're an obligate carnivore, or mostly vegetarian, the occasional liver dish would be a nice way to round out a diet.  

Fig. 1  Vitamins with smaller numbers
Fig 2. Vitamins with larger numbers

But enough with the lecture.  The mousse is rich, slightly sweat from the Madiera, and a way to use up the somewhat obscure chicken livers that might otherwise be discarded before roasting a whole bird.  There isn't a lot of liver taste, I promise. But I still have to see if the girlfriend approves.  Merry Christmas!

Chicken Liver Mousse

Here's what you need.  And yes, it's essentially a 1:1 ratio of butter to liver, by weight.

Ingredients:  1/2 pound chicken livers, 1/2 pound butter, Madiera, water, salt and pepper.

1.  Poach the chicken livers in a 50:50 mix of Madiera and water,  or 1 cup of each, over medium-high heat.  Cook for no more than 3 minutes.  You want the livers cooked to rare or medium-rare, as overcooking them will negatively affect the puree.  


2.  Set the livers aside.  Reduce the cooking liquid to just under 1/4 cup.  In the mean time, cut cold butter into 3/4 inch cubes.

3.  As the cooking liquid approaches the right volume, puree the livers in a food processor using small pulses.  Then, turn the processor ON, and add butter, one cube at a time.  Hit it with a few splashes of fresh Madiera as you go. 

4.  Add the reduced cooking liquid (it should be a rich brown color) to the processor.  Salt and pepper to taste.  Process to incorporate.

5.  Spread the mousse into a shallow ramekin.  Cover tightly as you would guacamole, and remember that all of the iron in the liver will oxidize and brown when exposed to air, so make sure you keep it covered when it is stored.  Let it set-up in fridge for one hour.  The dish can easily be made the morning or night before, and stored in the fridge.

Serve over toasted baguette with thinly sliced blanched asparagus, along with a nice glass of Pinot Noir.  

This post was shared on Traditional Tuesdays.

Saturday, December 10, 2011

Coming to understand the bugs in our yogurt and in our guts

In many ways, medicine is remarkably similar to farming.  The ancient Romans and Chinese, for example, knew that rotating crops and spreading manure in their fields would vastly improve yields.  These farmers didn’t know the underlying biology, and it didn’t matter: these practices worked, and they worked well.  Often, medicine is little different.  Insulin was given before knowing that it spurred the movement of glucose transporters to the edge of muscle cells, and exactly how acetaminophen relieves headaches has remained elusive.  The bacteria that thrive in yogurt and kefir, otherwise known as probiotics, are the modern day equivalent of manure.  But researchers are beginning to get a grasp of the microbial world in our tummies.   

In a paper published last month, Jeffrey Gordon’s team at Washington University in St. Louis identified how probiotics may influence gut health.  The scientists inoculated a sterile mouse model with 15 strains of bacteria that normally reside within the human colon.  The mice were then given probiotics and studied for changes in gut function.

Source: Wikipedia.  The model bacteria e. coli viewed by electron microscopy
The most interesting finding was that the probiotics hardly changed the composition of the bugs in the gut.  That is, the beneficial bacteria didn’t simply displace the ones already residing in the animals’ intestines.  And this makes sense to Gordon, who when interviewed said that the bacterial-colonization idea was analogous to “pouring a gallon of Kool-Aid into your swimming pool and expecting it to turn red.”

Instead, the new bacteria apparently vary the gene expression of the native ones.

Human cells and all of the microbes that inhabit the body have individual sets of genes.  A combination of spontaneity, interactions with other genes, and environmental triggers causes the genome to produce chains of messenger ribonucleic acid (mRNA). The “expressed” mRNA, in turn, is converted, or “translated,” into chains of amino acids (proteins) that do all the wonderful things that cells – or bacteria – do.  If genes were sheet music, the mRNA would be the specific keys, or group of keys, that produce the distinct musical notes or chords.  Probiotics changed the frequency that the bacteria’s genes produced mRNA, like a pianist using fewer C’s and more major scales.  Different levels of gene expression, like different musical composition, produce different effects.

Source:  Wikipedia.  Gene coding a protein.

The most noticeable shift in expression was seen in genes that dictate carbohydrate metabolism, specifically molecules known as xylooligosaccharides that are commonly found in plants.  Importantly, the probiotics manipulated the same genes in the bacterial community of human subjects.  It’s these sudden manipulations that may explain the known benefits of friendly microbes.

Gut bacteria influence the entire body.  Clinical trials have consistently shown improved gut function in people taking probiotics, where the benefits are especially pronounced in those afflicted with diarrhea.  When mice are fed probiotics, the brain produces chemical critical for regulating anxiety.  Conversely, eliminating native bacteria can be detrimental.  Some scientists are considering the over-use of antibiotics as a contributor to the rising incidence of allergies, asthma, and inflammatory bowel disease because the drugs indiscriminately wipe out the pathogenic and helpful bugs.  And eating bacteria isn’t the only way to get them into the gut.

Fecal transplant is the most remarkable bacterial therapy, if not the grossest.  As the name makes obvious, the treatment takes feces and the billions of resident bacteria from one person and transplants it into someone else.  It has been used in several different conditions, but the most dramatic results have been shown in c. difficile infections, a relentless hospital acquired bug that is rapidly resisting more antibiotics.  The stomach-churning therapy resolves a whopping 9 out of 10 c. difficile cases with virtually no side effects, and apparently, no smell.  What this frontier of probiotics will evolve into, though, is still an open question. 

Both scientists and marketers are pushing the frontier of probiotics.  “Contains live active cultures” is plastered on every dairy product from yogurt to ranch dressing.  Unfortunately, promise before understanding is a simple recipe for bad nutrition.  Bacteria could become the new snake oil, like high-dose antioxidant supplements.  But microbiologist Jeffrey Gordon’s experiments offer a model to begin rigorously investigating how probiotics work, optimal combinations of bacterial strains, and appropriate doses. 

The great 20th century physicist Richard Feynman once said that “what I cannot create, I do understand.”  It looks like the science of probiotics is taking a step in the right direction.

Monday, November 14, 2011

Weight loss in a pill

Source: Wikipedia.  Butter (fat) melting away...

What if you could take a pill that would simply melt your fat away?  The dream has become reality, but you have to be a chubby monkey to get your hands on it.

Barnhart and colleagues performed a placebo-controlled trial on adipotide, an experimental new drug to combat obesity, in obese rhesus monkeys.  Adipotide acts to slowly destroy the blood vessels that feed fat tissue.  By starving fat cells nutrients and oxygen, the cells eventually die, and fat loss ensues.  The compound has shown considerable success in rodents, but in order for the drug to progress into human trials, the experiments had to be replicated in non-human primates.  Indeed, the results are promising.

Spontaneously obese monkeys were given daily injections of adipotide, or placebo, for 28 days, followed by a 28 day recovery period.  The treatment group enjoyed a 15% weight loss, on average, by the end of the eight weeks – equivalent to a 275 pound person losing 40 pounds.  The bulk of the fat loss was visceral fat, which is the most deleterious region to carry body fat.

There is still plenty of time until it could be use to treat human obesity, but until then, the drug’s actions on fat tissue are interesting to ponder.

Souce:  Wikipedia.  Adipose (fat) tissue. 
The yellow fat cells are usually supplied by the red blood vessels.

Adipotide is a protein-based compound that binds to the endothelial cells that line the vasculature of fat tissue.  The protein enters the cells and causes them to commit planned suicide, or “apoptosis” in biology-speak.  Deprived of blood, the fat cells progressively die-off as they starve of oxygen and nutrients.  The fatty acids and triglycerides within the cells are released into the circulation and the body cleans-up the debris, leaving the monkeys svelte.  But where does the fat go?

One would expect a flood of triglycerides into the blood stream.  This is called hypertriglyceridemia and is a component of the metabolic syndrome and is a risk factor for heart disease.  However, this doesn’t appear to be the case.  The animals’ blood lipids improved throughout their weight loss.  What’s more, the animals became considerably more insulin sensitive – an important improvement that prevents diabetes and other complications of obesity.  Together, these data suggest that the freed fat was successfully oxidized, or “burned”, by the body for energy.

Throughout the treatment period, the monkeys receiving adipotide consumed fewer “biscuits” than their overweight controls.  The authors attribute the poor appetite to enhanced satiety, rather than nausea, which in turn led to weight loss.

However, adipotide did not cause lean monkeys to eat less.  The selective effect on appetite suggests that eating less isn’t the primary effect.  And after all, the drug targets the fat cells, not the brain.  Rather, it seems plausible that the dying fat cells free up an abundance of fat to be used for fuel.  With plenty of fuel available to the body, there’s little reason to stock up on biscuits.

There isn’t any data measuring the type of fuel – carbohydrate or fat – metabolized by the monkeys, so the mechanism requires a bit of speculation. 

The monkeys lose fat mass into the circulation, which gets oxidized for energy.  Fat loss improves insulin sensitivity, so the animals don’t have to secrete as much insulin in order to compensate for insulin resistance.  Plenty of fat for energy in the presence of lower insulin – remember, insulin drives fat storage – allows the monkeys to get by with eating less.  It’s like a drug-induced low carb diet, but instead of a bun-less cheeseburger, the monkeys are able to dine on their fat stores.  Although the cheeseburger would have one less side effect.

Source: Wikipedia.  A lean (and wild) rhesus macaque

The experimental monkeys showed transient problems with their kidneys, as indicated by elevated creatnine levels and slight microscopic damage to the tissue.  It’s unclear from this study whether the problem stems from the drug itself or a complication from the dying fat cells.  Side effects are especially problematic if adipotide needs to be taken chronically.

The monkeys started to show some regain of weight by the end of the four week recovery period, but the amount was minimal.  This could be an inherent problem to the drug, or it could be because they stuck to their low-fat junk food diet - monkey chow composed of 59% carbohydrate, 28% protein, and 12% fat – that made them fat in the first place.

Monday, October 10, 2011

A couple links to share

Over lunch today (chicken along with butternut squash topped with butter and cinnamon, in case you were wondering), I came across a couple of links that really hit the mark.  The first is a LA Times article on the current science of antioxidants.

Source:  Wikipedia.  Oxidized iron, or better known as rust.
Everyone wants to avoid oxidation, whether it's the browning of apples or one of the mechanisms behind aging.  The latter phenomenon is why everyone hunts down antioxidant rich foods.  Fortunately, it seems that every food has some sort of antioxidant (even butter has vitamin A!), but some foods are particularly high in certain antioxidants (think pomegranates).  So, the theory goes, oxidation is bad, foods have antioxidants, so let's eat a whole lot of selects foods - or squeeze the antioxidants out of them - to ward of oxidation and subsequent aging and disease.  Or maybe it's not so simple.

This article basically sums up my entire opinion of antioxidants.  Yes, we probably need antioxidants.  But we don't know nearly enough about biological oxidation and dietary antioxidants to be able to come up with a miracle diet or formula to prevent disease.  And it appears that our body even uses some oxidation to its advantage, as a previous study has shown that high doses of antioxidants can prevent the insulin sensitizing effect of exercise.  So my rule of thumb for antioxidants, avoid the foods that don't have them, which just so happen to be white flour, white rice, and sugar.  How convenient.

And if you have fifteen minutes, here is an excellent talk by a physician turned epidemiologist.  He discusses the major problems of epidemiology and newspaper headlines, and the serious ethical dilemmas we are encountering with large pharmaceutical trials.  He also mentions the publication bias problem that I mentioned in my meta-analysis post.

Thursday, October 6, 2011

A molecular biologist serving pizza and fatty liver

Source:  Wikipedia.  I would have had some if it looked this good...

There’s few things more ironic than walking into a lecture titled “the molecular biology of hepatic steatosis” and being met by a table stacked with pizza and soda.  Of course, the molecular biologists in the crowd weren’t the ones with non-alcoholic fatty-liver disease (or NAFLD), but it’s hard to ignore the dissonance.  Fortunately, the talk was better than the lunch offerings.

The lecture was by a medical researcher who investigates the molecular mechanisms behind fatty liver disease.  Today he was highlighting his group’s most recent work on the molecular mechanisms connecting obesity to liver fat deposition.

Source: Wikipedia.  Adipocytes (fat cells).

The researcher wanted to address several hypotheses.  The first hypothesis is that when people become obese, their fat cells enlarge (rather than multiply) to a point that induces cellular stress.  This stress then produces a cascade of intracellular signals that tell the fat cell (adipocyte) to begin apoptosis (intentional cell death).  The troubled fat tissue then secretes deleterious cytokines, or hormone-like chemicals.

Source:  Wikipedia.  A Macrophage.

The second hypothesis is that these cytokines recruit immune cells – specifically macrophages, an important cell of the innate immune system – that begin to engulf the fat cells.  The combination of dying fat cells and macrophages causes a big problem.

When fat cells become too large, and start dying off, they dump their fat content into the circulation – like an overstuffed cream-filled donut.  This results in a surplus of free fatty acids floating around the body.  And this is important because two-thirds of the fat in the livers of people with NAFLD are derived from the circulation.  And it isn’t just the adipocytes causing trouble.

Macrophages enjoy company, so they recruit more macrophages by secreting cytokines that have wonderful names such as Tumor Necrosis Factor alpha and Interleukin-6.  These chemicals, and many others, create a vicious cycle whereby inflammation produces more inflammation produces more information.  The inflammation in the fat then appears to spill out into the circulation and reach the liver.

Source: Wikipedia.  Not-alcoholic fatty liver disease.
Liver cells are pink,  the white is fat that shouldn't be there...

Inflammation in the liver leads to dysfunctional fat metabolism.  The liver then begins producing too much fat, which also accumulates in the liver.  The excessive free fatty acids in the circulation and the dysfunctional fat metabolism in the liver account for virtually all of the excess fat seen in NAFLD.  This fat then begets more inflammation.

The excessive fat and inflammation in the liver, and the fat from inflammation, generate a lot of oxidative stress in the liver.  This oxidative stress produces more inflammation, and causes the liver cells to dye off.  This can lead to a clinically inflamed liver (steatosis hepatitis) and even cirrhosis (think alcoholic).  At least, according to the researcher's hypothesis.

The researcher had plenty of data from cell cultures and mice, each experiment clearly showing an increase in relevant proteins and genes in response to diet-induced NAFLD.  He also cited a clinical trial that showed that vitamin E (an anti-oxidant) supplementation was more beneficial than the insulin-sensitizing drug metformin in patients with confirmed NAFLD.  Although, admittedly, the anti-oxidant treatment didn’t seem to be that much of a better treatment.  But perhaps oxidation is indeed the culprit, and Vitamin E just isn’t a strong enough anti-oxidant. 

The obesity to inflammation to fatty liver (and other problems) is a compelling hypothesis, and it has plenty of support in the research community.  If this hypothesis with stands the test of time, then it would support the notion that whatever makes us fat (sugar ‘cough’ and ‘cough’  white flour), probably also leads to insulin resistance, fatty liver, and all the other diseases associated with the Western diet.  But however it goes, I’m still glad that I brought tuna, broccoli, and buttered brown rice instead of chowing down on cheap pizza and soda.

Wednesday, October 5, 2011

You have the wrong guy...again.

"If one is going to make recommendations about how to optimize one's diet, one has to consider what kind of calories are going to take the place of those from saturated fat." - Ronald Krauss, M.D.

While few may characterize his research in such a way, Ronald Krauss has been investigating the law of unintended consequences as it applies to nutrition.  Krauss has demonstrated, in obese people and people with impaired metabolism, that replacing dietary saturated fat with carbohydrate, especially refined carbohydrate, will not improve the overall blood-lipid profile, and will actually make it worse.  Reducing one nutrient requires careful consideration of what it will be replaced with.

Denmark has introduced a tax on foods that are high in saturated fat.  The tax will be applied to foods that contain 2.3% saturated fat, although it is unclear whether this means 2.3% of calories or by weight.  Presumably, this tax is intended to reduce the production and consumption of foods that ostensibly lead to cardiovascular disease (CVD).  But there are a few problems with this.

As I've written on my blog, the reduction of dietary saturated fat does not necessarily lead to reduced risk of cardiovascular disease.  If you decrease a macronutrient, you must consume something in its place.  Replacing saturated fat with polyunsaturated fat reduces the risk of CVD, but does not lower the risk of CVD mortality or total mortality.  It is not certain whether replacing saturated fat with monounsaturated fat or unrefined carbohydrates will reduce CVD risk.  And replacing saturated fat with refined carbohydrates - white flour and sugar - likely increases the risk of CVD.  At the very least, a substitution with refined carbohydrates will expand the collective waist line of a population.  And this is a problem, as Denmark's strategy will almost assuredly increase the consumption of refined carbohydrates.

For the past forty years, Americans have experienced what happens when saturated fat is demonized.  Industry replaces saturated fat with either trans fats (because they mimic saturated fat) or  with sugar (because palatability leaves with the fat).  And how do home cooks replace saturated fat?  They don't simply use canola oil rather than butter.  Instead, they do what's easy:  eat more carbohydrates and buy foods that are nothing more than industrially produced oxymorons.  Besides, the most obvious problem with today's diet is the lack of whole foods.

One of the first tenants of the food movement is to de-emphasize individual nutrients.  Mark Bittman, a commentator for the New York Times, would likely agree.  Yet he readily deplores saturated fat.  What's more, Bittman conflates saturated fat with obesity.  No one thinks saturated fat has anything to do with obesity - not the low carb crowd, or the calories counters.  Public health authorities (and food policy commentators) need to get the facts straight about saturated fat, and then focus on the obvious.

The major problem facing nutrition and food is the processed carbohydrate, especially sugar.  Table sugar, or sucrose, like alcohol, does not need to be consumed in any amount.  It offers no nutrition and can (and likely does) only cause harm.  But it is a wonderful treat and is part of our food culture - there's nothing wrong with some birthday cake - so like alcohol, it's a reasonable candidate for taxation.  Saturated fat, on the other hand, comes from whole foods and is usually accompanied by important nutrients; not to mention that foods with saturated fat are delicious and also part of our food culture.

I'm not just stubborn about food taxes (see picture above), or a nihilist about food policy.  I want to go after the right target.  So if taxes will be employed to reduce the consumption of deleterious foods, or to generate revenue to combat the economic burden of diet-related diseases, then let's finally get over saturated fat, and start going after the obvious problem - the 32 oz. sodas that people regularly mainline.