An un-solvable medical disease?

You know what befuddles me?

Clinical nutrition confuses the heck out of me. The adjective ‘clinical’ implies that I’m talking about the medical aspects, the science of nutrition, not the basics.

Of course, you know what constitutes basic nutrition. Everyone does. The simple rules seem well…so simple. (With JMM-to-patient commentary in italics.)

  • Consume fewer calories. It’s amazing how little food our bodies need.
  • Drink fewer calories. Nothing helps create a negative calorie balance like limiting liquid calories–beer, wine, spirits, soda and sweetened sports drinks. My rule on drinking Coca-Cola: one can is allowed after a bike race or 60 mile-training ride. My rule on beer and wine: I don’t have one. Use an obvious meter here.
  • Eat less stuff that comes in packages or from the middle aisles of the grocery. Potato chips, Fritos, cookies, Pop-Tarts. Well, you get the picture. Need a rule: If a caveman ate it, then it’s probably good for you. Caveman didn’t order up PapaJohns or stop in for donuts or snack on Doritos. (Plus, they chased down (or gathered) their food. But that’s another post.)
  • Eat no trans-fat. These man-made conveniences are worthless and inflammatory. They seem silly to put in the body.
  • When eating, try to eat more plants, nuts, and fish. Not only do these foods provide valuable nutrients but they are also filling, slowly digested and associated with less insulin release. (Insulin is a hormone released to metabolize calories. Excess insulin creates trouble because it fosters fat storage and enhances atherosclerosis.)
  • Eat slow and enjoy the food. I just made that one up because it makes sense.

So what’s so confusing about clinical nutrition? What’s my problem?

Why do clinical people make the root cause of obesity so complex?

PEB = positive energy balance. Or, consuming more calories than burned seems the simple issue with obesity. Eat more than the body needs and the excess gets stored as fat. Even the prestigious medical journal, JAMA says so. Researchers from LSU overfed 25 volunteers and guess what happened: the overfed study subjects gained weight. The first sentence of their commentary says it all:

The key finding of [our] study is that calories are more important than protein while consuming excess amounts of energy with respect to increases in body fat.

Maybe it’s hopeless for me? I do not see McDonalds as a problem. I like McDonalds, that is, once in a while and without the biggie fries and coke. Did you know McDs has a grilled chicken sandwich? Did you know a hamburger without cheese and special sauce isn’t that high in calories? Likewise, a slice of pizza isn’t problematic; eating the whole pizza is. Same with cookies, and pie, and beer, and wine, and yes…even exercise can cause problems when consumed in excess.

I’m so dumb; I don’t even see the evil in having junk food in the hospital. One time, long ago, I wrote about the nutritionist who showed that he could lose weight, lower body fat and improve his cholesterol numbers by eating only junk food. He simply restricted calorie intake. (No, I am not advocating the Twinkie diet.)

Dumb. Un-nuanced. Uninformed. Crass.

These describers are often invoked when someone attempts to simplify obesity.

I know obesity is a struggle. It’s hard to eat well. Our societal success has created a near constant buffet. The US is not Europe, where stores close after dinner and quickie marts don’t exist on every corner.

I can’t offer my over-eating patients easy solutions. There are none. I over-eat too. Perhaps we medical people could offer a clearer explanation of the root cause.

The (positive energy balance) problem is dire; wasting energy on futile strategies, like banning junk food, and recommending complete abstinence from tasty treats seems nonsensical.

Successful people, particularly doctors, all have one trait in common: their ability to identify the problem.

Let’s start with simplifying the problem. It’s about PEB. Right?

JMM

Full disclosure: My family enjoys riding on a bike team sponsored by a pizza company. As a cardiologist, I don’t feel conflicted.

Penance: The other night I ordered (online) a PapaJohns pizza–did you know you can specify less cheese and extra green veggies? (Wait, now I am sounding conflicted.)

3 comments

  1. Excess insulin creates trouble because it fosters fat storage and enhances atherosclerosis.

    Would you please expand on this statement? Admittedly, it’s been decades since I took biochem, but I thought I learned that insulin release was proportional to sugars ingested. Where does excess insulin come from? If one eats the entire pie, then one would have significant insulin release, but is it “excess” or just proportional to the size of the pie?

    1. Alison,

      You are right about insulin secretion and calories.

      It’s over-simplistic, my attempt at an answer to your question: Over time, constant exposure to high calories causes high insulin levels to be secreted. This causes two bad things:fat deposition and down-regulation of insulin receptors (ie insulin resistance.) Thus starts the cycle that is sometimes called the metabolic syndrome (review here), where more insulin is needed to stimulate the now less-sensitive cells. What’s additionally worse about insulin is its growth factor properties, which have been implicated in causing irritable plaques inside of arteries–the reason why diabetics get more vascular disease.

      In case you have to be a registered user of Medscape, here are a couple of paragraphs that may explain:

      Insulin sensitivity and secretion are reciprocally related; thus, insulin resistance results in increased insulin secretion to maintain normal glucose and lipid homeostasis.[1, 2] The mathematical relation between sensitivity and secretion is curvilinear or hyperbolic. Several mediators are thought to signal the pancreatic B cells to respond to insulin resistance; failure of the signals or of the B cells to adapt adequately in relation to insulin sensitivity results in inappropriate insulin levels, impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and type 2 diabetes.

      These potential signaling mediators include glucose, free fatty acids, autonomic nerves, fat-derived hormones (eg, adiponectin), and the gut hormone glucagonlike peptide 1 (GLP-1). GLP-1 is an incretin hormone that stimulates insulin secretion, causes B-cell mitosis while inhibiting apoptosis, inhibits glucagon secretion, and delays gastric emptying with overall antidiabetic effects.

      The mechanisms responsible for insulin resistance syndromes include genetic or primary target cell defects, autoantibodies to insulin, and accelerated insulin degradation.[3] Given that glucose and lipid metabolism largely depend on mitochondria to generate energy in cells, mitochondrial dysfunction may play an important role in the development of insulin resistance and associated complications.[4]

      Obesity, the most common cause of insulin resistance, is associated with a decreased number of receptors and with postreceptor failure to activate tyrosine kinase. While adiposity and insulin resistance are related, they are not necessarily synonymous, and each may make independent and different contributions to increasing the risk of cardiovascular disease.[5]

      Thanks very much for stimulating me to review some basic biochem.

      1. Thanks! Good response. I had to look up a few words, I’d forgotten kinases. However, I think my brain has had a good anti-Alzheimer’s workout today.

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