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.

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.

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.