Indoor Cycling and Insulin Resistance

by Joan Kent | Apr 14, 2014 | Health and Wellness, Master Instructor Blog

By Joan Kent

ICI/PRO readers know that exercise can reduce the risk of heart disease, type 2 diabetes, hypertension, cholesterol problems, cancer, and more. Underlying those diseases is insulin resistance. Exercise reduces health risks by making skeletal muscle more sensitive to insulin, effectively reducing the resistance.

Insulin is a hormone that’s produced by the pancreas and allows glucose to enter cells for metabolism. It has several other functions, as well.

Under certain circumstances, someone might become insulin resistant, and the cells no longer respond to insulin’s cues. To get the job done, the body’s first line of defense is to produce more insulin. This may work, and can continue to work until the production of insulin no longer outpaces the degree of resistance. (That’s an extremely oversimplified description of the onset of type 2 diabetes.)

Along the way, the high levels of insulin are likely to cause a variety of health issues. So it’s not insulin resistance per se that causes disease, but the extra insulin that’s released to compensate. This is associated with Series 2 prostaglandins and inflammation, a topic covered in a previous post (An Important Key to Health).

What we typically learn about insulin resistance (IR) is that it’s a result of overweight. That’s a true enough statement, but not the whole picture. For example, IR can be caused by genetic factors. Over 40 genetic mutations can result in someone’s being born with insulin resistance or with a predisposition to it.

IR can also be the result of lifestyle factors. Lack of exercise is one obvious cause, along with diet. A high-fat diet can cause resistance to insulin through a specific mechanism, a high-carb diet through a different mechanism, and a high-fructose diet through yet another.

Insulin resistance isn’t always a result of overweight/obesity. It can also be a cause. Cells differ in their sensitivity to insulin. The primary site of IR is skeletal muscle. How does insulin-resistant skeletal muscle behave? It doesn’t allow glucose to enter the cell. The glucose ends up being transported to fat cells.

Another important site is the liver. How does an insulin-resistant liver behave? It doesn’t respond to the feedback loop that tells it to stop releasing glucose, so glucose levels remain high.

An interesting connection with depression exists, as well.

You recall from 7th grade biology that amino acids are “the building blocks of protein.” One of insulin’s functions is to transport amino acids to skeletal muscle, where they can be used for a variety of functions. Those functions include immune support, formation of hormones and enzymes, insulin receptor site turnover, pH and fluid balances, wound healing, tissue growth and repair, blood protein formation, energy use, and more.

The most important function is the formation of specific brain chemicals from specific amino acids. One amino acid, tryptophan, is the precursor of serotonin. The brain chemical serotonin has become commonly known, due to the anti-depressant medications that have been on the market for years.

Insulin resistance interferes with the transport of tryptophan to the brain and can therefore contribute to depression.

To the degree that indoor cycling can help reduce the incidence of insulin resistance, it can therefore help reduce the incidence of depression. This isn’t as far-fetched as it sounds. In the research for my dissertation, participants completed tests for depression and anxiety, both before and after they had gone through the 8-week study. Consistently, the participants who were exercising regularly had lower scores for depression and anxiety.

It’s kinda cool to realize that what we love to do helps our riders reduce their risk for health problems — along with their risk for mood issues.

Sugar Addiction Now Recognized As Mainstream Science

by Joan Kent | Apr 7, 2014 | Health and Wellness, Master Instructor Blog

By Joan Kent

The good news is things have moved forward with respect to food addictions. For one thing, food addictions are now acknowledged as real. (When I started doing this work, they were not — I remember how people would argue against the idea.) Now we know that food addictions are based in neurochemistry, making them physiologically real.

Those who claim they’re something else tend to be unaware, either of the neurochemistry and physiology of addiction OR of the neurochemical effects of foods.

Sugar addiction is still the most common food addiction I see in my practice.
But other common addictive foods, such as saturated fats and processed white flour, are not always recognized as such.

Genetic factors may predispose someone to a given food addiction. These can include a family history of alcoholism, diabetes, hypoglycemia, hypertension, depression, and more. There are also non-genetic predisposing factors, including, but not limited to, post-traumatic stress disorder (which alters neurochemistry) and body type.

The brain response to sugar, saturated fats or other foods is often as genetic as eye color. We each got what we got. What’s great is we can do something about it. Changes in diet can alter neurochemical levels and modify cravings, appetite, mood and food preferences in a beneficial way. My dissertation was on the treatment of women with binge-eating disorder. Eliminating sugar was found to bring a significant decrease in bingeing and craving.

It helps no one to ignore an addictive response to certain foods and treat it as if it were not an addiction. Treating an addictive response as an emotional problem misses the point. (Amazingly, there are still people in the weight-loss field who do that.) And it never gets to the underlying issue. Worst of all, it could very likely make the addicted individual feel like a failure if she or he couldn’t control the addictive response to sugar emotionally. How unnerving, when the response is physiological.

In some ways, food addictions may actually be more difficult to conquer than other addictions. Obviously, abstinence is not an option. We can decide to give up alcohol or any other drug and only be the better for it, even if going through the rehabilitation is tough. But food is something we have to deal with several times a day, every day, for the rest of our lives, so the problem is insidious.

Virtually any food can result in addiction for people who are susceptible. That can occur due to various food sensitivities (sometimes called “allergies”, a controversial term with respect to foods). The sensitivity may result in a neurochemical cascade that can trigger an addictive response. So, interestingly, some people with food sensitivities end up addicted to the very foods that make them feel worst.

Elimination diets are sometimes used in such cases. I have used that approach at times for suspected food sensitivities. Most food addictions, though, seem to hinge on general neurochemical responses (by all) that are problematic for some due to predisposing factors, based on family history. That can often be determined via questionnaire. If more specific information is necessary (by blood test, for example), I refer to an M.D.

The bad news in this situation is that food addictions, especially sugar addiction, are disturbingly common and are contributing profoundly to obesity, diabetes, heart disease, and several types of cancer. But that’s a post for another week.

Sugar Addiction, Binge Eating, and Why You Shouldn’t Eat What You Crave

by Joan Kent | Mar 17, 2014 | Health and Wellness, Master Instructor Blog

By Joan Kent, Ph.D.

A looong time ago (1998), I wrote a doctoral dissertation that started with several observations about women with binge-eating disorder. One was their relationship with sugar. As I examined the DSM-IV criteria for substance dependence against the DSM-IV criteria for binge-eating disorder, it became obvious that addiction to sugar was very likely driving the binge eating. ‘No kidding,' you say, but this was radical thinking in 1998.

My research divided the participants, all screened for binge-eating disorder, into three groups. The low-sugar group was given low-sugar nutrition guidelines to follow. They logged their food intake, including any binge episodes and/or cravings, and came to weekly support meetings.

The low-fat group followed low-fat guidelines, logged their food, binges and cravings, and attended weekly meetings. The control group had no nutrition guidelines or support meetings and simply logged their food, binges and cravings.
All groups reported periodically for weigh-ins and measurements.

Bingeing and craving decreased most in the low-sugar group. Weight loss was greatest in that group, although the weight loss couldn’t be fully explained by comparing calorie intake among the groups.

What I find funny (okay, maybe a little irritating) is that people are now — in 2014 — finally — at long last — finding a connection between sugar addiction and the obesity epidemic. I guess the 1985-1999 low-fat craze — and a “craze” is what it was — had to die before people could see what was going on. (What can I say? My mother always told me I saw connections others didn’t.)

So how does sugar contribute to the obesity epidemic? Let’s take a look at what sugar does:

• Sugar triggers a “priming” reaction — even a little makes us want more. This is due to a specific dopamine receptor in the brain. Some people experience this more acutely than others. I consider this effect of sugar the main argument against eating “a small amount” of what we crave. Priming can turn that into a very large amount.
• It’s addictive, so it definitely makes us want lots of sugary food and encourages over-consumption.
• Sugar addiction is physiologically real. It may cause withdrawal symptoms (cravings, agitation, restlessness, inability to focus, and more) when it’s not available. Seeking and eating sugar frequently to end the discomfort of withdrawal can lead to overeating and weight gain.
• Sugar may be responsible for what I named “secondary fat consumption”. None of the study participants got cravings for fats. Almost all got cravings for sugar. But! In response to the sugar cravings, they’d often eat foods that contained lots of fat. For example, a craving for sweet was likely to be answered with a bowl of ice cream — high in both sugar and fat. Why? Research shows that fat makes sugar taste sweeter. The added calories and fat were significant in all groups.
• It triggers the release of beta-endorphin in the brain. Beta-endorphin inhibits the brain’s primary satiety center (the VMH). That may increase appetite, increase food consumption at a given meal — and lead to more frequent meals.
• Beta-endorphin changes food preferences toward other beta-endorphin triggers: fats or more sugar. The preference for healthful fare, such as vegetables, shrinks in comparison to those foods. Calorie intake can easily rise. Also, meals that are high in fat can trigger ghrelin, a hormone that tends to increase appetite as it slows metabolism — a potentially dangerous combination for weight and health.

It’s clear from this list that sugar makes it all too easy to over-consume food and calories, especially empty calories. We can see the role it plays in binge eating and overweight. I stress that this connection was crystal clear to me in 1998 when I wrote my dissertation, and still in 1999 when it was completed.
So thanks for indulging me. I just needed to take credit for this, since credit is now being claimed by others some 15-plus years later.