Wednesday, December 14, 2016

The Post I Never Wanted to Write…but here I am!

A very controversial paper was published 11 years ago in one of our most prestigious medical journals by a group of prominent epidemiologists.  In this thought provoking paper in the New England Journal of Medicine the authors predicted a decline in life expectancy in the United States in this century.  Their words were disturbing, “…the steady rise in life expectancy observed in the modern era may soon come to an end and the youth of today may, on average, live less healthy and possibly shorter lives than their parents”.

These projections were based on the continuing increase in diseases driven mainly by lifestyle factors such as nutrition and exercise.  The most glaring example is the explosion in type 2 diabetes with the percentage of the population with it doubling about every 15 years.  The part of this iceberg not well seen as it is “below the water line” is prediabetes which now affects 1 in 3 U.S. adults and 15% of adolescents.

So back to the part I never wanted to have to post.  The purpose of that controversial paper was to enlighten us about the dead end that lay at the other end of the route through the maze that society was taking with lifestyle.  The enlightenment was, of course, to push our lifestyle route through this maze in another direction. 

Unfortunately, this message got ignored perhaps based on two other misleading messages.  These are that high carb, sugar loaded, chemical laden manufactured diets that the U.S. consumes couldn’t be that bad and that no matter what we do to ourselves, there are drugs and medical procedures that will serve as the wild card to negate the risk.  We now know the message the prominent epidemiologists gave us 11 years ago was accurate and that these other two competing messages are largely untrue.

The National Center for Health Statistics which tracts statistics on most aspects of our nation’s health revealed some sobering data earlier this month.  For the first time since 1993 during the peak of the AIDs epidemic life expectancy in the U.S. declined.  The current youngest children will have a life expectancy less that of the parents and grandparents. 

The primary reasons for the developing decline are the increasing rates of deaths from diseases including:

  • Heart disease
  •  Stroke
  • Diabetes
  • Alzheimer’s disease
  • Kidney disease

These statistics are in spite of ever growing numbers of adults being treated with drugs such as statins which are assumed to be preventing this outcome.  Telling of this disconnect was shown in a study published this year in the Journal of the American Heart Association.  The study looked at the ability of statin treatment to prevent or improve plaque build-up in the carotid artery, a factor that is known to increase the risk of both stroke and heart disease. 

While non-obese subjects had an average plaque reduction of -4.2% after one year of statin treatment, obese subjects had an average +4.8% increase with the same treatment. 

It seems arterial disease is driven by the interaction of several factors not just the levels of LDL cholesterol.  One noticeable associated factor was an inflammatory marker called C-reactive protein (CRP).  Central body fat (belly, waist, hips) generates pronounced inflammation which increases the risk of all 5 diseases mentioned in the list above.  Elevated CRP increased the risk of plaque progression 156% in 1 year.

Before the mind goes to just add an anti-inflammatory drug, a couple of things should be considered.  Their long-term use is associated with substantial increased risk of renal failure which is one of the cited diseases driving the downturn in longevity.  In contrast for every hour of sedentary time replaced by moderate physical activity there is a 24% reduction in the inflammatory marker CRP.

There are many more examples of the inferiority of the treatment of lifestyle driven abnormalities with drugs versus corrective lifestyle.  I talk to several prediabetics each month who are not aware that they have prediabetes in spite of lab studies demonstrating it for a couple of years.  I also talk to diabetics who have been told their blood HA1C levels are good at 7.0% because the medication has lowered it from 9.5%.  The normal range is <5.7% and the increased vascular disease risk at 9.5%, or poorly controlled diabetes, is +130%.  While the risk is lower at an HA1C of 7.0% it is still 40-60% higher than if it was in the normal range.

So why is 6.5%-7.0% which is the upper prediabetic range “good control” with medication? Studies have shown that pushing it lower with that type of treatment will cause episodes of intermittent hypoglycemia and actually increases overall death risk.  The only way to safely improve more in that circumstance is with intense lifestyle management including dietary change, exercise and weight loss.

Another example of how these diseases interrelate was discussed in the scientific section of the European Association for the Study of Diabetes.  Dutch researchers reported their study of brain changes associated both with diabetes and with prediabetes.  The reason for looking at this is that diabetes is a strong risk factor for developing some form of dementia such as Alzheimer’s disease. 

Two imaging findings are associated with the brain changes driving dementia in diabetes.  The first is diminished brain volume which represents actual loss of large numbers of neurons or brain cells.  The second is white matter lesions (WMLs) which represent small areas of damage caused by altered blood flow. 

Diabetics had 167% greater numbers of WMLs than healthy controls.  Most surprisingly, prediabetics demonstrated considerable increased WMLs with 66% more than age comparable healthy adults.
Brain volume reductions showed similar patterns with diabetics having the greatest but prediabetics having abnormal amounts as well.  The structural brain changes associated with eventual dementia are present in prediabetes but just not as advanced as in diabetes.

So the circumstances at the time I wrote newsletter articles about the New England Journal of Medicine paper 11 years ago have changed.  That alarming projection has become an alarming reality.  What is the same is two-fold.  First is the 11-year old projection should serve as a dramatic wake-up call.  The second is the solution remains the same although more urgent.

In the developing years of 20th century healthcare infectious disease was a major cause of death, and it could be effectively treated with a single drug.  That idea has persisted as the main tenent of health care.  The 21st century finds very different challenges, complex multi-system diseases highly related to several interacting lifestyle errors.  These diseases are not well managed with the one disease/one drug approach we have seemed to carry over.  They are also not ideally managed with the common 6-10 drugs that are trying to get at late effects of chronic lifestyle neglect.  We are working only in the right side of first diagram above.  The solution really lies in working predominantly on the left side of it.



Olshansky et al.  A POTENTIAL DECLINE IN LIFE EXPECTANCY IN THE UNITED STATES IN THE 21ST CENTURY.  New England Journal of Medicine, 2007;352:1138-1144.
Sandfort et al.  OBESITY IS ASSOCIATED WITH PROGRESSION OF ATHEROSCLEROSIS DURING STATIN TREATMENT.  J Amer Heart Assoc, 2016;5:e003621.
Perneger et al.  RISK OF KIDNEY FAILURE ASSOCIATED WITH THE USE OF ACETAMINOPHEN, ASPRIN, AND NONSTERIODAL ANTIINFLAMMATORY DRUGS.  New England Journal of Medicine, 1994;331:1675-1679.
Falconer et al.  SEDENTARY TIME AND MARKERS OF INFLAMMATION IN PEOPLE WITH NEWLY DIAGNOSED TYPE 2 DIABETES.  Nutrition, Metabolism & Cardiovascular Disease, 2014;24:956-962.

Sullivan MG.  BRAIN ATROPHY IS ALREADY EVIDENT IN PATIENTS WITH PREDIABETES.  Clinical Endocrinology News, Sept 14, 2016.

Thursday, November 10, 2016

How Hunger Games Bolster Brain Function


 Part 6 of “What Six Months of Soup Can Teach Me”

In many ways this installment of the blog on the benefits of modified intermittent fasting is the most fascinating.  It deals with the idea that the cognitive function of our brains actually improves during the times of sustained caloric reduction.  This interval refers to at least 12 hours where energy or caloric intake is substantially less than immediate needs.  Perhaps the easiest way to get to this state is the modified, intermittent fasting we have been discussing in this blog.

In this modified fasting state, the body shifts to an alternative energy mode of burning stored energy from body fat stores.  To do so it alters a diverse group of hormones and signaling molecules that actually help several of our systems, including the brain, actually function more efficiently.

While this may seem surprising, this trait was essential for man’s survival for most of our existence as we faced a constant challenge to regularly find/catch enough food up until approximately the past 200 years.  We are genetically wired to have heightened function during times of caloric restriction. 

The following quote from a Dr. Mark P. Mattson at the Laboratory of Neurosciences, National Institute on Aging in the medical journal, Aging Research Review explains this apparent dilemma:

Because it evolved, in part, for success in seeking and acquiring food, the brain functions best when the individual is hungry and physically active, as typified by the hungry lion stalking and chasing its prey. Indeed, studies of animal models and human subjects demonstrate robust beneficial effects of regular exercise and intermittent energy restriction/fasting on cognitive function and mood, particularly in the contexts of aging and associated neurodegenerative disorders.”

Both animals and humans have required intense mental focus in the fasting state when they were in pursuit of food.  The linking of fasting to better brain function was inherent to survival.




The metabolic changes during the fasting state were thought to impart an advantage to the success of finding subsequent food either through hunting of gathering.  It appears this fasting state increases mental alertness that would be needed pursuing wild game.  This interesting video about Dr. Mattson’s research is about how mice who have an increased genetic pattern towards developing memory impairment and dementia can greatly reduce this tendency with periodic fasting. 

When the research is examined on caloric volume/intake the conclusions appear to be that a balance is needed.  There is a wealth of research correlating chronic caloric excess with chronic disease.  Obesity and diabetes, two well established diseases linked to chronic caloric excess are both important risk factors for dementia and Alzheimer’s disease.

Dr. Mattson summarized this best in his Aging Research Review paper:

“In addition to disengaging beneficial adaptive responses in the brain, sedentary overindulgent lifestyles promote obesity, diabetes and cardiovascular disease, all of which may increase the risk of cognitive impairment and Alzheimer’s disease.”




In contrast, there is a growing body of research finding that regular, intermittent negative energy balance or caloric deficit increases brain functioning and cognition.  Prominent brain researchers are now advocating intermittent fasting as an important therapy for cognitive decline.

The moral of this relationship between periodic fasting and better cognitive functioning is not that it is needed now to pursue food successfully.  Spending an afternoon observing the legions regularly gorging in fast food establishments would testify to that point.  For most of us we need only to think about the sleepy, foggy brain status after some feasting event such as a thanksgiving meal where we over-indulged.


The current value of periodic fasting is not survival by better food obtainment but rather better brain functioning by its ability to “re-set” metabolic functioning that is so critical for optimal brain health and function.  While ongoing caloric restriction can effectively improve a wide array of chronic health challenges including brain health and cognitive functioning, few will adopt that long-term behavior.  The intermittent modified fasting as described in this series results in much the same long-term benefit but in a much more lifestyle friendly manner for most.

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.


Thursday, September 8, 2016

How to Tell If Diet Mismatches Genetic Determined Metabolic Ability

Part 4 of “What Six Months of Soup Can Teach Me”

A few practical tips on doing this modified fasting diet are in order.  Timing this around what is going on in life can be helpful.  It gets harder during stressful times.  This made me appreciate how “stress eating” is a problem in the first place.  In contrast, this gets easier during times of high constructive activity.  It seems if we are meaningfully engaged, we don’t get as preoccupied with eating.  The moral is that controlling stress and being busy with meaningful activity is a poorly appreciated part of good dietary behavior.

On to the issues of what is happening with our eating behavior and why a modified fasting diet can be so helpful.  The real issue with the current Western diet for the majority of the U.S. population is that its composition places maximum stress on the portion of our metabolic machinery that is least adept at handling it.  Maximum stress on a weak area typically will cause failure, which in this case, is chronic metabolic disease.

That weak area is the broad group of enzymes used to manage a main end product of carbohydrate digestion - sugars.  There are many dozens of different enzymes involved in the process of trying to convert sugars into energy.  As we previously discussed, when the amounts of sugars exceed the need at the moment, it goes to the liver to be converted to the fat, triglyceride.  The triglycerides are then circulated destined for fat storage in the central (abdomen) portion of the body.  If carbohydrate/sugar intake chronically exceeds the need of the moment, triglyceride is increasingly produced and fat stores increase.

One of the primary features of the Paleo period genetic pattern is multiple SNPs of the genes involved in processing sugars to energy.  The 75-80% of westerners who have this pattern just cannot manage high amounts of carbohydrate/sugar under normal circumstances.

A great question to answer might be how much carbohydrate/sugar does one consume? 



The chart shows estimates of both the amount of energy or calories from carbohydrate as well as the factors regarding its quality.  The more refined the carbohydrate, the faster the sugars become available generating more metabolic stress.  Added refined sugars require no digestion before absorption so all of their energy is immediately available whether it is needed at that instant or not.

By all measures the amount of carbohydrate in the western diet has increased from 200-600%, yet the genetic ability to manage it has literally not changed.  The second and equally troublesome factor is the “glycemic load” of the western diet.  Glycemic load is a combination of how much and how fast a given carbohydrate will raise blood sugar.  Not all carbs are created equal.  Simple sugars and grains have a disproportionately high glycemic load compared to fruits and vegetables.  Simply put, they generate far more stress per gram on metabolism than other carb sources.

A great analogy might be a worker who can process 50 files very accurately in a 40-hour work week.  If you want to make this good worker make a lot of mistakes you can do it one or both of two ways. Have them try to process 200 files in the same week (increased amount of carbohydrate), or have them try to process the same 50 files but only working 2 hours a day for the 5 days (high glycemic load).  The western diet is like having that worker try to do both!

So how do we tell if we are in metabolic stress trying to manage carbohydrates?  The first sign is white adipose tissue or belly fat which is stored triglyceride. 

Typically, when triglyceride production stays high, more will be produced in the liver than can be quickly transferred to belly fat causing blood triglyceride levels to rise.  As fat stores become high, belly fat begins to produce inflammation which begins to injure insulin receptors which are needed to signal cells to take in and use blood sugar.  This fuels the whole triglyceride production cycle even further.

Additionally, when liver triglyceride production is high,  the production of HDL or “good cholesterol” drops and the production of a very small cholesterol molecule, VLDL, increases.  These VLDL particles are particularly worrisome as they become very small dense LDL which is the most dangerous regarding vascular disease risk.

The last step in this metabolic dysfunction cascade is that the insulin resistance so impairs the ability of cells to take in sugars to burn or convert to triglyceride that blood sugar rises.  At the first sign of this the diagnosis of “pre-diabetes” is made, and as it progresses it is eventually called diabetes.  Pre-diabetes is like calling the first trimester of pregnancy “pre-pregnancy”.  I think it should more appropriately be called simply early diabetes.

That was a lot so I’ll summarize.  The common order of problems showing up suggesting metabolic distress in handling carbohydrates is:
1)    Belly fat – excess triglyceride
2)    Increasing blood triglyceride - >125 mild concern, >150 real concern
3)    Decreased HDL - < 40-50.  A triglyceride/HDL >3 is a real concern
4)    VLDL cholesterol >30
5)    Increased small LDL particles – requires specialized testing called an NMR profile
6)    Increased blood sugar

The small LDL particle size needs a little explanation.  We generally make two sizes of LDL or “bad cholesterol”.  The size of the particles determines their ability to cause vascular disease with small, dense particles being more dangerous than large, fluffy ones.  We all make some of each but in varying ratios.  Genetics influence this ratio some, but diet also highly affects it.

The diagram shows 2 persons (“S” and “L”) with an identical LDL cholesterol value of 130 mg/dL.  This is the total weight of LDL in a fixed volume of blood. The small, dense particles are called apo B and the large, fluffy ones are apo A. 

While person “S” and person “L” have the same total weight of LDL, person “S” on the left side has many more small particles and therefore greater risk.

Some persons with “normal” LDL cholesterol levels develop vascular disease while others with relatively high LDL cholesterol never will.  The particle size and number variable is thought to be an important determinant of this contradictory risk.

The point of all of this is that before blood sugar inches up into abnormal range, the body has been firing warning shots across the bow for many years with the above changes in body and blood profile.  Diabetes is a late effect of chronic metabolic chaos. 

A minority in western populations can tolerate a greater percentage of carbohydrate and a somewhat higher glycemic load.  This is like the uncle someone has who smoked a pack of cigarettes and drank a quart of whiskey each day living to be relatively healthy until killed in a skydiving accident on his 90th birthday.  We all assume we are “that guy”, but they are very rare.  Most of us will need to give careful attention to matching our diet chemistry to our true metabolic ability.  Not doing so has led to the epidemic of metabolic disease which we are trying to beat down with drugs.  The food got us there, and it is the foundation for an effective solution.


So I continue with the modified, intermittent fasting to help reset my metabolism.  Starting with a normal body fat I still lost 7 lbs the first 2 weeks and 1 inch off my waist.  If you take the list of the problems that show up early indicating some metabolic stress, the modified, intermittent fasting does a “system restore” on it all.  The first indicator that that is happening is pulling triglycerides out of belly fat to burn for energy.  I choose not to curse my genetics but rather cheer the knowledge of a solution.

Thursday, August 25, 2016

What Six Months of Soup Can Teach Me

Part 3 – How Genetics and Lifestyle Interact, Good or Bad

The big question for all of us to address is how much of our health and disease outcomes will be determined by genetics and how much will be determined by lifestyle, particularly diet.  If you accept that genetics is largely responsible, you will be absolved of most responsibility for the outcome.  Your only hope is medical breakthroughs if you drew poor genetic cards.

If you accept that lifestyle is primarily determinant, it puts the control of your health fate squarely on you.  To my thinking, this is the best case scenario.  What science has shown us since the completion of the analysis of the entire human genome in 2000, the reality is that our health fate is a mixture of both genetics and lifestyle. 

There are approximately 23,000 genes in each of us that our responsible for the design of the proteins, enzymes and other things that form are makeup and function.  Each gene can have many little variations called single nucleotide polymorphisms, or SNPs, with “many” being defined as 40-60.  Some 3.5 million SNPs have been identified in the human genome so we all have thousands of them.

A SNP is a variation of just one nucleotide in a long genetic chain of code.  This is shown here in two variations where “G” or “T” are substituted for the more ideal “A”.

If a polymorphism of a gene that makes an important enzyme in carbohydrate and sugar management exists, the resulting enzyme will function more weakly than normal rendering that person less carbohydrate and sugar tolerant.  Another way of saying that is that they will get in metabolic trouble more quickly eating a higher carb/sugar diet. 

The reason I choose this example is that this pattern seems to exist in about 75-80% of the U.S. population including me.  My dominant genetic pattern comes from my mother’s side of the family, Irish transplants from the earlier 1900’s.  Diabetes and heart disease were the norm in the preceding two generations I knew.  A favorite uncle died of a second heart attack before the age of 40.

So what difference would this Irish/Western European genetic background have to do with carbohydrate tolerance?  It seems when our ancestors left Africa way back, they came to a fork in the road.  They must have listened to one of my favorite philosophers, Yogi Berra who was quoted saying, “if you come to a fork in the road, take it!”  My group turned left up into Europe, while others went to the middle east and beyond.


The theory goes that in Europe there were more animals which led to hunter- gathering type survival.  For those who took the right fork to the middle east, animals were more scarce so they ate more what they could gather which was more dominantly carbohydrate.  Once they figured out how to domesticate grain in Turkey in 9000 B.C., modern plant agriculture was born further increasing the percentage of dietary carbohydrate for those folks.

Two dominant gene patterns naturally occurred in these populations with implications about carbohydrate tolerance.  Those in the middle eastern group who genetically were favored to handle larger amounts of carbohydrate tended to be much healthier, while those who had the less able carbohydrate genetic pattern struggled.  One of the early victims of metabolic stress is fertility so each population became fairly uniform in genetic pattern suited to the food supply of the area. 

My tribe was Paleo-type diet suited.  Migrate us again to the U.S and put our genetic pattern into a 55% carbohydrate, refined sugar and high grain dietary environment and metabolic chaos has ensued.

Fortunately, those who have genetic mediated difficulty in managing carbs/sugars problems can largely be prevented with parts of two different strategies.  The first is keep yourself in a dietary environment that does not stress your metabolic weaknesses.  This is the lower carbohydrate (<40% of energy), very low sugar eating pattern.  Carbs should also come only from whole, complex carbohydrates and are dominantly from vegetables rather than grains.  Grains have a glycemic load (they raise blood sugar and sugar management stress) 8-10 times higher than the same grams of carbs from vegetables.

The second part to managing genetic weaknesses is a targeted nutrient program. 
The diagram shows an important enzyme reaction in converting a breakdown product of sugar, pyruvate, to acetyl CoA which becomes energy. 


The conversion of pyruvate to energy is begun by the enzyme, pyruvate dehydrogenase, When the gene responsible makes a copy of the enzyme, it is inactive.  It is activated by “cofactor” which in this case is vitamin B1 or thiamine.  Those with a gene pattern that causes them to make a weak version of the enzyme can increase its activity by adding higher amounts of co-factor or vitamin B1.

The best approach to our genetic weaknesses is to consume a diet that is compatible with our strengths and places little stress on the weaknesses as well as supplementing extra nutrients known to increase weak enzyme activities. 

But how can one tell what their pattern is?  There are a few ways.  First is family history, although that is not foolproof.  A lot of processed carbohydrate products didn’t exist when grandma was a kid, sugar wasn’t added to everything, nor was processed grain a staple as it is now.  She could have had a subtler carbohydrate intolerance that her diet didn’t not exploit, but ours will.

The second is “wait and see” which many are doing.  If we end up at 55 years old with diabetes and 2 or 3 other related diseases, it tells us more about our intolerances. I don’t think this “wish I had known sooner” approach is the right way to go for me.

The third approach is that different tests such as blood chemistry profiles show the stress of an imbalance between genetic mediated metabolic ability and our diet.  This allows the pre-empting of the potential bad outcome before it has done the damage.  I will talk about how to do that in the next post.


So what does all of this have to do with modified fasting and the chicken soup?  Everything!  If the body is saying we have a metabolic mismatch between fuel and the ability to manage it, modified fasting periodically helps perform a “system restore”.  I do it every so often to keep my computer healthy, why not for my health?

A Simple Step to Improve Diet, Weight and Mental Health

Human behavior can be a funny thing.  At times it is so complex, yet some very seemingly simple things can change it in positive ways.  A n...