Thursday, October 13, 2016

Modified Intermittent Fasting and Powerful Antioxidant Effects

Part 5 of “What Six Months of Soup Can Teach Me”

I had a couple of weeks off from posting updates here related to conference travel.  As it is hard to impossible to do the 2 days a week of the program during travel, add to that a hurricane power outage and that became a couple of weeks off.  First, that’s OK.  A short interruption around life’s requirements won’t undo the benefits.  It will, however, if “life’s requirements” become a frequent norm rather than the exception. 

The another observation over that time has been that some of the goals of the modified fasting program have become incorporated into my eating the other days.  These include less grains and lower carbohydrate consumption.  What the modified fasting helped my brain appreciate is that the benefits are many, and the “hardships” of doing so really aren’t hardships or difficult.  This is kind of like all of the worry about jumping into cold water that proves not to be that cold after all once we get in.

To summarize up to this point, modified intermittent fasting consists of only consuming a low carbohydrate, “paleo like” soup two non-consecutive days each week.  The first serving is eaten within 30 minutes of getting up.  The second is eaten 12 hours later. This would create a low energy meal at say 6 AM followed by 12 hours of fasting, a second low energy meal at 6 PM followed by another 12-hour fast until the next morning.  Normal eating occurs on the other 5 days. 

The fasting intervals move us from the fed mode where we build fat to the fasting mode where we burn fat for energy.  The important changes, however, are that in this fasting mode, blood sugar, insulin, inflammatory signaling and blood lipid profiles all occur.  With time these factors permanently shift from the disease causing pattern to a disease improving/preventing pattern.

We left off in the 4th post talking about the metabolic effects of this 2 day each week program, and they are many including changes that lower the risk of diabetes, heart disease and about all of the other common chronic metabolic related diseases that are all too prevalent.  While it may be easier to see how eating a very small amount of carbohydrate 2 days per week would help improve blood sugar levels as well as blood lipids such as cholesterol and triglycerides, it may be a little harder to understand how it may help the risk of many cancers and of degenerative brain diseases such as dementia and Alzheimer’s Disease.

Many of the positive effects of modified fasting do relate to spending time with lower energy intake, particularly of carbohydrates.  This moves us from the metabolic pattern of converting excess carbs/sugars to fat which is the American dietary induced norm and to one where we begin to covert stored fat back into energy.  Another very important one is that it upregulates our production of internal antioxidants which has broad benefit to reducing the risks of many types of disease.

We humans produce potentially harmful molecules called free radicals.  These are molecules that are generated by metabolism and can damage our own tissue if they are left active too long.  

They are notable in that they are missing one electron in the outer portion. 
Electrons have to be paired in even numbers to be stable.  The molecule in the left side of the diagram has 6 electrons in the outer ring.  Notice that each one has a paired electron opposite it.  The free radical on the left is simply one that has lost one electron and is unstable.  This loss could have been triggered by normal metabolism which makes a few mistakes or some stress exposure such as radiation or toxins.

The problem with a free radical is that it will aggressively seek to steal an electron form a molecule close to it to become stable.  Two locations that this may occur with important consequences are stealing a molecule from our cell DNA or from the cell membrane.  That area of the DNA is then damaged or mutated and often becomes a potent disease generator from heart disease to cancer.

The cell membrane is how the cell protects its inner components such as the DNA and also how the cell communicates with the environment outside the cell.  If the membrane becomes damaged, its communication is impaired.  For example, if insulin is trying to tell cells to take in glucose that may be impaired.  This process is termed “insulin resistance”, and it is an important early step in the development of diabetes.

As we would expect there is a potent system to neutralize free radicals, the antioxidant system.  Antioxidants can donate an electron to a free radical making it neutral and preventing it from damaging cell components to find this electron.

 While dietary antioxidants help to neutralize the free radicals that we generate continually, they are often sporadically supplied and are inadequate at fully neutralizing the average daily production of free radicals.  The majority of antioxidants are plant based in fruits and some vegetables that were sporadically available only during certain seasons. 

So how did humans survive for 5-6 million years with erratic availability of food based antioxidants?  We have another internal system of antioxidant enzymes.  The dominant members of this family include glutathione (GSH), super oxide dismutase (SOD), and catalase (CT).  These enzymes account for about 80% of the total antioxidant capacity on the body on any given day. 

On days where we have good food based antioxidant exposure we are at 100% antioxidant capacity.  If the dietary component is weak, we still have 80% of our total capacity.  This is why the majority of large longitudinal studies have failed to find strong links between dietary antioxidant supplements and strong disease preventative effect.  In contrast, studies that have looked at our internal levels of antioxidant enzymes and disease find that there is a strong correlation with protective effect.

This understanding brings up the important question, what increases our internal antioxidant enzyme production?  The first clues came from studies on ongoing caloric restriction.  Ongoing reductions of caloric intake of 40-50% have been associated with extensions of healthy lifespan (disease free) of about 20%.  The next step was to explore how sustained caloric restriction does that.  A major factor was that it causes a marked increase in the production of these protective antioxidant enzymes.

That’s where the difficulty came in.  Few adults will adhere to this daily dietary pattern from mid-life on.  This modified intermittent dietary pattern demonstrated many of the other benefits of caloric restriction including lowering blood glucose, insulin and improving blood lipid patterns.  Given this similar pattern of improvements to daily caloric restriction, the impact was then examined on antioxidant enzyme production.  Sure enough it also causes increases in these important disease preventing enzymes.  As modified intermittent fasting is much easier for most to follow compared to ongoing, heavy caloric restriction, it is a viable alternative to reap these benefits.

This relationship between modified intermittent fasting and improvement in internal antioxidant enzyme levels opens up understandings of how this pattern of dietary behavior may produce benefits such as cancer protection and anti-aging benefits rather than just fat loss. 
One of the most fascinating beneficial effects of modified intermittent fasting and disease prevention/modification is its ability to improve brain function.  Given the emerging epidemic of degenerative brain diseases such as dementia and Alzheimer’s Disease, the implications are immense.  We will discuss this area in the next post.

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