Metabolical: The truth about processed food and how it poisons people and the planet

by Robert H. Lustig

Nutrition is not the same as food science. Nutrition is what happens to food between the mouth and the cell.

1) protect the liver, 2) feed the gut.

Seed oils are high in omega-6 fatty acids, which are highly pro-inflammatory;

1) protect the liver, 2) feed the gut.

the incidence of obesity-related cancers (e.g., colon, liver, pancreas, kidney) has continued to grow at annual rates of 2 to 6 percent a year for

Autoimmune diseases (like Crohn’s disease) are thought to attack randomly, but we now know that intestinal bacterial pathogens are frequently the target of a disordered immune response to the consumption of processed foods.

The holy grail of Modern Medicine is you can’t fix healthcare until you fix health; and you can’t fix health until you fix the food. Everyone is talking about healthcare, few people are talking about health, and nobody is talking about the food.

Leptin is a satiety hormone

released from your adipocytes that tells your brain, “I have enough energy on board;

can stop e...

Ghrelin is a hunger hormone released from your stomach that tells your brai...

Normally, insulin does double duty—it tells your body to “store,” while it tells you...

Therefore, the prime directive of metabolic therapy is “get the insulin down.” And that’s true, regardless of your weight.

Metabolic syndrome is the inappropriate storage of energy in the wrong form in cells that shouldn’t store it.

There are only three types of cells in the body that should store energy:

subcut...

vis...

adipose ...

muscle tissue and liver tissue are supposed to store excess energy as glycog...

How about the other 80 percent who are overweight and sick? They were sick first—they had metabolic syndrome—and that caused insulin resistance, which led to high insulin levels.

Fat cells responiding to insulin,and therefore,they get bigger!

But because their fat cells still responded to insulin, and that extra insulin allowed the fat cells to accumulate more energy, they got bigger.

normal weight population,

metabolic syndrome—meaning they have metabolic dysfunction, insulin resistance, and high insulin levels

But for whatever reason, they’re just not obese. In some of them, their fat cells are insulin resistant, too, so energy doesn’t accumulate in the subcutaneous tissue. Instead they put it in other organs that shouldn’t have fat, such as muscle and the liver.

Fat Liver!

TOFI, or thin on the outside, fat on the inside.

And then there are the 20 percent of people who are overweight but not sick. Because the subcutaneous fat tissue can actually be protective, giving excess energy a nontoxic place to go. Just because they’re obese does not automatically mean that they harbor the egregious and deadly forms of fat in other organs where it shouldn’t be. Rather, it’s the ectopic fat that determines if they’ll develop diabetes or heart disease.

ectopic fat:diabetes or heart disease (subcutaneous fat)

In fact, my group at UCSF and others have shown that fat in the liver is the most predictive of whether someone will get diabetes in the future—which

if your pancreas has fat in it, no wonder you can’t make enough insulin for your body’s needs.

Pancreatic fat

Each of these conditions occurs in normal weight people, too! Obesity is just another symptom of the problem, not the problem itself.

But the RR is not the important factor.

Their insulin didn’t go down because their weight went down—their weight went down because their insulin went down.

What they lost as a result was liver fat, which then made them insulin sensitive.

cholesterol

it’s an integral part of membranes and the precursor of steroid hormones.

statins

But when the data were analyzed, unless LDL-C was very high (over 200), it wasn’t a risk factor.

LDL over 200 is a risc factor!

Your LDL-C level is for the most part genetically determined.

Conversely, those with LDL-C levels less than 70 develop relatively little heart disease.

Yes, there seems to be a genetic protection at the low end, and r...

But for the rest of the population, LDL-C is not a great predictor of who will suffer a heart attack. It’s true that the HR ratio (hazard risk ratio; a measure of difference in risk versus the general population) of LDL-C is 1.3, which means that if your LDL-...

But correlation doesn’t mean...

then...

(greater than sixt...

do high LDL-C levels correlate wi...

Or maybe we’re measuring the wrong biomarker.

While fewer are dying of heart attacks, more people are suffering them.

There are two different LDLs, but the lipid profile test measures them together. The majority (80 percent) of circulating LDL species are called large buoyant or type A LDL, which are increased by dietary fat consumption. This is the species reduced by eating low-fat or by taking statins.

However, large buoyant LDL is cardiovascularly neutral—meaning it’s not the particle driving the accumulation of plaque in the arteries leading to heart disease. Then there’s a second, less common (only 20 percent) LDL species called small dense or type B LDL.

small dense LDL is predictive of risk for a heart attack.

but they’re not doing anything to the type B LDL, which is the problematic particle.