Six common beliefs addressed, Part 42

1. All fasting is the same.

Actually, it is not. "Fasting" is a term that's being used as an umbrella definition to describe a wide range of practices. This is confusing, as it makes people believe they are getting the same benefits, while following very different protocols. Each protocol has a different and specific effect on metabolism.

• A 12 - 18 hour "fast" is best described as time restricted eating.
• A 24 - 72 hour "fast" is fasting. People have now coined this 'intermittent fasting', but if you want to be precise, all fasting is technically intermittent, as only the dead can fast permanently.
• Any "fast" beyond 72 hours is not true fasting, but starving. People have coined this 'extended fasting', but that's not even a real term. I know the word "starving" makes people think of concentration camps, but starving, in this context, is used to describe the metabolic effect this practice causes.

On this blog, I don't get caught up in semantics or technical terminology, as I want to make sure that people understand the material using everyday, familiar language. So, for simplicity's sake, we use "fasting" to describe all three practices and only differentiate them by length. But, I absolutely can appreciate how it would give people a false impression to the benefits each method would have.

2. Does fasted exercise make you more insulin sensitive?

All exercise makes you more insulin sensitive. This effect is not exclusive to fasted exercise, as it produces no added "insulin sensitivity".

I have discussed before how exercise causes non-insulin mediated glucose uptake. This means that the benefit of exercise comes from the ability to clear glucose, from the bloodstream, without the need for insulin. This is fantastic for people who are insulin resistant. Requiring no insulin to facilitate glucose uptake, improves insulin sensitivity, over time, for the insulin resistant. It also helps maintain insulin sensitivity for those that aren't resistant. Circulating insulin can now be put to better use, like building muscle, as diet burns fat and exercise builds muscle. This is why exercise routines must be followed consistently, so that this effect occurs often. This effect has nothing to do with being fasted or not. It is simply exclusive of exercise, period.

So, even if all exercise makes you more insulin sensitive, in the context of obesity, when you exercise fasted, you are causing cortisol rhythm disruption, which can affect Dawn Phenomenon (DP). These spikes in blood glucose caused by DP only further deteriorate blood glucose regulation and that is pathological for obtaining better insulin sensitivity. Fasted exercise just produced you a negative and counteracted the positive you would have otherwise had.

Studies have shown diabetics have better postprandial glucose control, when a meal is consumed pre-workout, instead of post-workout. This is completely counter to what the entire fitness industry has always believed, since it's a known fact that insulin sensitivity is greater post-workout than pre-workout. This is why many athletes like to "carb up" after a workout. But, this is only true of healthy people.

People with metabolic syndrome/diabetes do not benefit from more "insulin sensitivity" post-workout, since they are chronically insulin resistant and the only tissue they have, which is very insulin sensitive, is their fat tissue. So, they should be more concerned about how their glucose regulation is improved by eating before their workout, because ultimately, it's this better glucose regulation that will result in truly improved insulin sensitivity.

3. Does exercising in a fasted state, corrects high morning blood glucose?

Everyone's Dawn Phenomenon (DP) is different. Many people who have metabolic syndrome develop an abnormal insulin to cortisol interaction and so they see their DP get worse over time, if their body is under a chronic stressor. This is why certain practices like ketogenic diets, fasting, exercise or a combination of all three, cause a deterioration in blood glucose regulation for some people.

It's a biological fact that stressing the body causes a rise of glucocorticoids. This process is already dysregulated in people with metabolic syndrome/diabetes. Just Google 'exercise and stress hormones' and you will get a lot of information about this. Fasting is another stressor on the body, so compounding the two only causes even more stress.

Lowering blood glucose, after exercise, is just lowered blood glucose at that moment. It does not mean that blood glucose regulation is being obtained. If there was proper blood glucose regulation, blood glucose would not need to be lowered, because it would already be low in a fasted state. There is no reason to have high blood glucose in a fasted state if it's being regulated properly.

So, as long as your blood glucose regulation is getting better with time, then you are managing your disease well. But, if your blood glucose regulation is staying the same or getting worse, then you would need to modify your regimen.

4. Low carbohydrate and ketogenic diets do not affect cholesterol.

Cholesterol discussions tend to bring out the crazies, so I am going to try and get to the point, with this question, so there's no doubt on my stance when it comes to cholesterol. I have talked about cholesterol, in depth, many times before, so I will try to avoid repetition. I wrote a general article on cholesterol that can be found here.

The reality is that if you are scared of cholesterol, then this may not be the right diet for you. There's really no other way around it because:

• Total cholesterol will go up on carbohydrate restriction, for many individuals, regardless of what low carb advocates say. Yes, it is related to the diet. 100%. The people who say it's not, are misinformed and are serving you some BS to save face.
• Specifically, LDL cholesterol will go up on carbohydrate restriction, for some individuals, regardless of what low carb advocates say.
• Specifically small, dense LDL cholesterol will go up on carbohydrate restriction, for some individuals, regardless of what low carb advocates say.

I know that low carb advocates will swear up and down that cholesterol is not affected by carbohydrate restriction. It is. There are multiple reasons for this and I am not going to get into them all, because it will cause for this post to become too long and I know people's attention spans run very thin, especially when it comes to reading. So, forget why cholesterol is affected. You only need to know that it is.

Cholesterol is mostly determined by genetics and partly affected by diet. Many people go on carbohydrate restriction and see no effect to their cholesterol, whatsoever, and some see a lowering of cholesterol. But, for many, that's not the case. Cholesterol is extremely biodiverse for every individual and that's why not everyone is affected the same way. What these changes in your cholesterol mean, can only be determined on an individual basis and through lipid testing by a healthcare provider. This means that just because your total cholesterol rises, it's not necessarily indicative of a problem. Vice versa, if your total cholesterol lowers, it's not indicative that all is good.

Because cholesterol is so complex and individualized, you should never go by total cholesterol levels, alone, as it does not say much about your cardiovascular health or risk. You can have very low total cholesterol and still develop cardiovascular disease (CVD). You will have to discuss your particular, individual situation with your healthcare provider, because what your markers mean are affected by:

• Your current metabolic health.
• Your family history of CVD.
• Whether you currently have CVD or a history of it.
• Your genetically determined cholesterol profile. 

What to do about your cholesterol is a decision that you have to make, with your healthcare provider, by weighing the pros and cons of your dietary regimen, any recommended medications and your genetic risk factors. This is not a decision that should be made from information you found on the internet. I know that talking to your doctor, about these things can be difficult, but the internet cannot be a stand-in surrogate for a real doctor. So, if you can't talk to your doctor, fire him and hire one you can talk to.

For most people cholesterol can be controlled multiple ways, while continuing to follow carbohydrate restriction. The choice is not between high cholesterol or going back to pizza. There are ways to formulate your carbohydrate restricted diet to be more cholesterol friendly, if you are worried about your numbers.

• Do not consume fat in excess. Carbohydrate restriction is primarily carbohydrate restriction, not fat consumption.
• Switch saturated fats to monounsaturated fats.
• Stay away from coconut oil. The lauric acid in coconut oil is known for abnormally raising LDL levels in some individuals.
• Switch to leaner cuts of meats.
• Give your cholesterol some time to normalize. Markers tend to be wonky for the first few months/years and stabilize with time and fat loss. 

5. You must avoid insulin spikes.

Postprandial insulin spikes are necessary, not only for facilitating glucose from meals into cells, but also for halting the body's catabolic process properly. Halting catabolism takes a very different amount of insulin than just glucose facilitation into cells, as that's mostly done by various glucose transporters (GLUTs). So, insulin release occurs in stages.

• When you eat a protein meal, insulin spikes to stop catabolism and allow nutrients into cells. Then it returns to basal (fasting) levels. 
• When you a eat a carbohydrate meal, insulin spikes to stop catabolism and allow nutrients into cells, but now it also has a load of glucose to help clear from the bloodstream. This causes for insulin to remain in the bloodstream for longer than it should. This begins to interfere with fasting blood glucose, catabolic regulation and insulin's normal pulsatile function.

This is why the spiking of insulin is not what ultimately causes the problem. The problem is caused by prolonged insulin release/expression after the initial postprandial spike.

6. There is no difference in gaining weight, being overweight or being obese. All excess weight is the same. 

All weight gain is related, but not the same. I know that when obesity/weight gain/loss is discussed in groups, pages, blogs and by weight loss programs/coaches, they all tend to lump everything weight related into one category, but that's all BS. The mechanisms behind obesity and weight gain are very different. The dynamics between weight loss and gain are different depending on the context in which they occur. Obesity, weight gain and loss are all triggered by different things.

For instance, cancer patients lose weight for very different reasons than marathon runners. A Westerner eating pizza, gains weight for a very different reason than a hunter/gatherer who gains weight seasonally. All of these people cannot be given the same treatment for losing or gaining weight, as their neuroendocrine systems will respond very differently, since they are all in different metabolic states.

• Eating in excess always results in weight gain, but weight gain is not pathological. It’s completely normal.
• Eating less always results in weight loss, but simple weight loss does not correct obesity, as not enough weight from fat is ever lost and so this weight loss does not change body composition or corrects an exaggerated starvation response.

Obesity is pathological fat gain which appears to be most commonly caused by the excess consumption of a specific combination of macronutrients. In Western society those macronutrients are the combination of carbohydrates and fat. Both of these macronutrients are exceptionally toxic in Western societies, since the carbohydrates come with fructose and the fat comes in the form of vegetable oils. Both fructose and vegetable oils appear to be the leading culprits in the development of obesity.

Unlike weight gain, obesity includes several metabolic pathologies and it does not respond to "eating less”. This is because obesity affects the starvation response of the body, body composition and nutrient storage signaling pathways, all of which are not corrected by simply eating less and are not present in simple weight gain. Furthermore, obesity seems to affect the hypothalamic function of the brain.

Hyperinsulinemia is implicated in both weight gain and obesity, but it appears that with obesity it becomes chronic and insulin not only reaches much higher levels but it is chronically released/expressed and loses its pulsatile function. In weight gain insulin levels rise, but not as high or chronically and continue to retain their pulsatile function. Hyperinsulinemia is not always correlated with obesity. This is because serum insulin levels are not always indicative of poor insulin function.

So, the mechanisms behind insulin's involvement in obesity and metabolic dysfunction is not well understood and remains incomplete. But, we absolutely do know that insulin is involved, as there is no weight gain, of any sort, without insulin.