Tag Archives: Triglycerides

Leptin Resistance

What is Leptin?

Leptin is a hormone released by fat cells that helps regulate hunger. And it may hold the key to why a low carb / paleo diet works for so many people.

Role of Leptin in Hunger Signals
Leptin and Hunger
(Click Image to Enlarge)

Success on a low carb / paleo diet is often attributed to “never feeling hungry”, an effect not seen on other diets. People point to the satiating aspects of fat or protein in eliminating hunger, but dieters may be suffering from a rarely diagnosed condition called leptin resistance that is corrected by the low carb diet.

Leptin circulates through the bloodstream in an amount directly proportional to the amount of fat you have. In theory, the more leptin you have circulating the less you will eat, because it signals that you have enough stored energy for all your metabolic processes. When leptin levels dip, it signals the brain that you are hungry.

So, that means fat people should never be hungry, right? Not so fast, grasshopper.

Resistance is Futile

Most low carbers are familiar with the concept of insulin resistance in those with type two diabetes and metabolic syndrome. In a healthy individual, insulin signals the cells that glucose is available, and the cells respond and allow the glucose to enter the cell (if they need the energy). Insulin resistance is a condition where the cells become resistant to the effects of insulin, requiring more and more insulin to deal with blood sugar levels. If a regular cell opens the door to a gentle knock, the insulin resistant cells respond only to ferocious pounding on the door with a battering-ram’s worth of insulin. The pancreas, which produces insulin, cannot keep up with the demand for more and more insulin, and dangerously high levels of blood glucose result.

A similar thing happens with leptin resistance, but through a different mechanism. There’s no shortage of leptin in an otherwise healthy obese person, and the fat cells never grow tired of producing it. But the circulating leptin is blocked and cannot turn off the hunger signal. The fat person remains hungry. And hungry people eat.

What Causes Leptin Resistance?

Some have theorized that dietary fat and blood glucose levels interfere with leptin. While there is a link between leptin resistance and the levels of fat circulating in the blood (triglycerides), eating dietary fat doesn’t seem to have an effect. Recent evidence showing a diet high in fructose contributes to leptin resistance adds to the growing body of evidence against high levels of fructose in the diet. The amount of fat in the diet did not matter; leptin resistance peaked with the high fructose diet, and reversed itself to normal levels when the rats ate a sugar free diet, no matter how much fat they had. Lucky rats.

We know that leptin signals our brain that enough energy is present, and the body does not need any more food. Leptin is able to cross the “blood brain barrier” (BBB) to do this. The BBB is a protective system of small capillaries that protects the brain from most chemicals but allows the important ones through. It works like a filter. So what causes the curious case of leptin resistance, where this essential hormone is blocked by the BBB? As Dr. Mike Eades explains:

Research done a couple of years ago in St. Louis and in Japan pinpointed the problem. Triglycerides – fat circulating in the blood – interrupts the passage of leptin across the BBB. If trigylcerides are high, which they are in most obese people, then, basically, they block the movement of leptin into the brain. So, leptin levels are elevated in the blood, and triglycerides keep the leptin from getting to where it needs to get to shut off hunger.

One Solution

Controlling trigylceride levels can reverse leptin resistance. In my own experience, hunger evaporated on my low carb diet as my triglycerides fell from 344 to 105. Before that, I was often hungry, even after eating past the feeling of fullness and often to discomfort. On my low fat diet 15 years before, I was miserable because I was always hungry. But that, as they say, is a personal testimony and not a scientific finding. Too bad I’m not a rat.

The easiest way for most people to lower triglyceride levels is to adopt a very low carb diet (less than 50 grams of carbohydrate per day), then transition to a moderate carb diet devoid of most grains. Niacin and fish oil have also proven to be effective in many people, even those with genetic reasons for high triglycerides (familial hypertriglyceridemia). I combine all three approaches, and have found the eliminating any one of those results in my triglycerides rising again. Management of triglycerides in this way is done in concert with a physician and blood tests. Those with chronic health problems should check with their doctors first, of course, especially those with reduced liver or kidney function, or those suffering from conditions such as gout that require specific diets.

Resisting Resistance

Humans are adapted to eat a certain diet, and in terms of adaptation, the modern agricultural era is a blip on the radar screen. We simply haven’t had time to adapt to large quantities of grain and other carbohydrates in our diets. The inexpensive access to readily available carbohydrates is new, barely 10,000 years old, and our biological machinery is not able to handle it. That’s the philosophical framework under girding the modern low carb / paleo diet movement. The rise of leptin resistance is just one more metabolic condition that supports the effectiveness of a low carb / paleo lifestyle.

Other Resources

MegaSearch: Leptin Resistance

Heart Scan Blog: Niacin

Heart Scan Blog: Fish Oil

Twilight Zone of Diet Studies

Imagine if you will a diet study, a seemingly ordinary diet study. One that compares low carb and low fat diets. Now imagine that you are reading the results, and find the unequivocal superiority of the low carb diet.

Results:

Both the Low and Moderate Carbohydrate groups lost significantly more weight as well as inches from their waists and thighs than the Control group, while the Low Carbohydrate group lost a greater percentage of body fat. Although the Moderate Carbohydrate group showed significant reductions in serum cholesterol, the Low Carbohydrate group showed the greatest improvements in serum cholesterol, triglycerides, high-density lipoprotein, low-density lipoprotein, and very-low-density lipoprotein.

Consider, if you will, how you would write the conclusion to these findings. That all-important snippet of text that will be read by those too busy to read the full synopsis, the snippet that will be picked up in articles and future studies.

Perhaps you will write something that bears some resemblance to the words and phrases in the Conclusion. Something that recognizes the low carb diet as being at least equal in your test for weight loss, yet reducing more body fat than the low fat diet. Consider how you will sum up the findings, that the low carb diet provided significantly better results for cholesterol and triglycerides. But before you put your pen to paper, read the actual conclusion:

Moderate approaches to weight loss such as a moderate-carbohydrate low-fat diet may be prudent.

There is nothing wrong with your eyes. Those are the words the study authors penned. An example, perhaps of cognitive dissonance.

You are traveling through another dimension –a dimension not only of sight and sound but of mind. A journey into a wondrous land whose boundaries are that of imagination. That’s a signpost up ahead: your next stop: the Twilight Zone of Diet Studies!

Dieting for Risk Factors

With the usual caveat that I am not a medical professional, I want to propose an idea for your consideration. I would encourage you to discuss this idea with your doctor before embarking on any diet plan.

I think it makes sense to first identify your individual risk factors for the things that kill us. The Centers for Disease Control (CDC) publishes charts showing the leading causes of death for men and for women. Looking at the charts you see that heart disease is the leading cause of death at about 27% of all deaths. We tend to focus on those stats and work to minimize our chances of dying from heart disease. That’s certainly the approach taken on a society-wide level with the low-fat diet recommendations (the low fat diet is thought to reduce serum cholesterol levels leading to less heart disease, although many of us find that it increases cholesterol instead.) What I think we are ignoring is that our individual risk factors may be for something entirely different. Remember, that heart disease is not the cause of death for a majority of the people … 73% of them, in fact. Are we increasing our risk of dying early by trying to reduce our risk for heart disease?

The American Heart Association (AHA) identifies the risk factors for heart disease in two categories, those you can change and those you cannot. The categories are a mistake, in my view. It is the risk factors you cannot change that may be the most susceptible to changes in diet: age, sex and heredity. 83% of the deaths due to heart disease happen after age 65, so time is on your side if you are younger than that. Males are more susceptible to heart disease, and have a higher incidence of dying younger than that age 65 statistic. And family history, including race, plays a factor.

The factors you “can change”, according to the AHA, are things like tobacco use, obesity, high blood pressure, serum cholesterol levels, activity levels, and diabetes.

The standard treatment to reduce risk factors for heart disease is a low fat, relatively high carbohydrate diet and prescription drugs to lower cholesterol. The prescription drugs are necessary because many people find a low fat, high carbohydrate diet raises cholesterol (especially triglycerides). Low carb diet advocates challenge this view, and note that many people find a low carb diet improves their lipid profile without the use of prescription drugs (as well as improving weight, high blood pressure and other factors).

The problem is that there is no easy way to score these factors. Do you check off each factor, and if you have more than three, start to worry? Or is family history such an important factor that it, by itself, compels you to work to reduce your risk? Certainly, if your parents and all your siblings died of heart attacks, you probably realize it “runs in your family.” But for most of us, even getting the full list of risk factors isn’t enough to tell us if we, personally, are at risk.

The place to start is a doctor who knows your medical history. Ask him point blank: what do you think I’m going to die from? The answer will be about risk factors for the diseases on those CDC charts, and which one your history indicates the greatest risk for you. Heart disease and cancer are at the top, by a large margin. But as you read down the list, you see stroke, respiratory disease, and diabetes.

Its interesting that diabetes is a risk factor for heart disease, and diabetes itself is the 6th leading cause of death.

My largest risk factor, given my family history and age, sex and physical condition is diabetes. Several people in my family, a brother and my mother, have adult-onset diabetes. I’m male, over 50, and have more than two of the markers for “metabolic syndrome” (pdf file from CDC on metabolic syndrome). In contrast to that, I have very little heart disease in my immediate family.

My doctor recommended a low carb diet to reduce my high triglyceride level; success is shown by lowering triglycerides from 462 to 113 on my last blood test. I’m staying on it to lower my weight and blood glucose level, as well as meet the other cholesterol goals (HDL, LDL, etc., as shown on the About Page).

The term “diet” is often associated with a reduced calorie, temporary eating regimen that you abandon after reaching a weight goal. The problem with this approach is that it ignores the very real impact your diet has on your health. The real goal should be to live longer, not simply to lose weight and “look good”. A pretty corpse is still dead.

Your diet should reflect the best bet to protect against your individual risk factors, and not to fulfill a broad societal goal.

LDL – Measure it Directly

My medical history includes a high triglyceride level over 400, and my doctor asked for a direct measurement of my LDL. Usually, the labs calculate the LDL by using a formula rather than measuring it directly. As Dr. Michael Eades says in his blog:

… Friedewald substituted triglycerides (TGL) divided by 5 for VLDL in the above equations, giving us the so-called Friedewald equation for calculating LDL.

LDL = Total cholesterol – HDL – TGL/5

And this is how it is still done in labs all over the world 27 years after Friedewald’s paper. If you’ve had a lab report showing an LDL figure, I can guarantee it was calculated by the Freidewald equation and not measured directly.

It has long been recognized that if the triglycerides are over 400, the calculation does not work. So you have to measure the level directly. In that same blog post, Dr. Eades explains his experience that LDL calculations are inaccurate when the triglycerides are low as well. I have linked two articles Dr. Eades identifies as supporting that position in our new LDL Research Page.

Many studies show marked improvement in patients HDL, triglycerides and glucose levels with low carb diets. Often, the low carb dieter has a rise in total cholesterol and LDL. Researchers are not concerned with the higher total cholesterol number, but the LDL level increase does concern them. But most studies use the Friedewald calculation that may not give an accurate picture of the true LDL level.

If my LDL gets too high, I’ll be certain to ask for a direct measurement of it, rather than a calculation. The extra cost for the test is probably cheaper than taking statins.