The Possible End to Increasing Life Expectancy

One of the more controversial papers ever to be published in the prestigious New England Journal of Medicine projected that “the steady rise in life expectancy which had occurred over the past 2 centuries may soon come to an end.”  They ended the conclusion commenting that the youth of today may live less healthy and shorter lives than their parents.   As would be expected this paper sparked a large volume of letters to the editor criticizing this projection.  

While the authors based their projection on some very sound data, the real validation could only come with time.  As my favorite philosopher, Yogi Berra once said when asked to predict on Thursday who would win a golf tournament which ended Sunday, “ask me Sunday night.  I am a lot better at predicting the past than I am the future.”

While “Sunday night” is not here on this striking prediction about our children’s longevity, the preliminary data appears to be supporting this grim projection.  The primary basis of this projection was the ever growing rate of obesity and its relationship to increased rates of the chronic diseases such as diabetes, heart disease, cancer and many others.

As projected, overweight and obesity trends have continued upward across all population groups.  Currently about 9% of children 5 years of age and under are obese, and this rises to 20.5% between 12 and 19 years.  The increasing trend continues throughout adulthood.  Currently 38% of U.S. adults are obese and 74% are overweight.

Diabetes is perhaps the best leading edge indicator of the disease trends that may accompany the overweight and obesity change.  It is now projected that the 14.3% of the U.S. population have diabetes an increase of approximately 300% since 1990.  The real emphasis comes from the fact that fully 38%, or about 1 of every 3 persons in the U.S., is pre-diabetic with a high percentage expected to convert to full diabetes over time.

Pre-diabetes is a misleading term in some ways. Normal fasting blood glucose is 70-99 mg/dL.  Diabetes is a fasting glucose of 140 or greater.  Pre-diabetes is that zone of abnormal glucose from 100-139.  My take on pre-diabetes is that just as the first trimester of pregnancy is not “pre-pregnant” but is early pregnancy, the better term is early diabetes.

These trends are fueled by the general belief by most that no matter what they do to themselves, some medical innovation will bail them out.  At least some knowledgeable healthcare scientists seem to accept that the rate at which we can become diseased is beginning to outpace the ability to maintain chronic disease.  One trend that supports this concept is another important statistic, healthy longevity.  It is defined as age of onset of the first chronic disease.

Even as longevity has increased over the past 60 years, healthy longevity has decreased more dramatically.  This is what the authors of the NEJM paper referred to as “our children living less healthy lives than their parents”. Many treatments for chronic disease do not completely prevent the complications that often shorten life but rather they delay them.  The diabetic today has their disease longer than previous generations.

The average onset of type II diabetes was 52 years of age 40 years ago.  It is now 41 years of age.  While improvements in diabetes treatment have delayed the onset of complications, the earlier ages of onset may begin to override treatment based complication delays. 

One of the most striking papers I have read was a commentary by an endocrinologist at the University of Texas.  He had been in practice 30 years and commented that in his early years they would see perhaps only a couple of new onset cases of type II diabetes in adolescents each year.  Now they see several new cases every week.  This phenomenon was why the terminology when I was in graduate school, adult onset diabetes, was changed to type II diabetes.

This paper making these projections that received so much criticism in 2005 is being looked at as evolving reality in 2017.  Sad but true.

There is little disagreement that the primary driver of the chronic disease epidemic is diet based.  Likewise, the most effective solution will also be diet based.  Perhaps one of the best health investments we can make is to get some help from a nutritional health professional in understanding and optimizing our diet as well as that of our families.

Olshansky et al.  A Potential Decline in Life Expectancy in the United States in the 21st Century.  New England Journal of Medicine, 2005:352;11.

If We Had This Drug, I Would Be on It

One of the largest studies on the reduction of chronic disease risk and mortality was recently published in The Lancet.  The study looked at the use of a particular treatment and the reduction of cardiovascular disease risk, stroke risk, as well as the risks of cardiovascular, non-cardiovascular and overall mortality.  The study was very comprehensive involving 135,335 individuals aged 35 to 70 years without cardiovascular disease from 613 communities in 18 low-income, middle-income, and high-income countries in seven geographical regions: North America and Europe, South America, The Middle East, South Asia, China, Southeast Asia, and Africa.

The results shown to the left were fairly striking with the treatment reducing the risks uniformly for all of the followed measures.  The vertical black line is the risk in the non-treatment group.  That is arbitrarily called “1” in a comparative study.

The graphic shows the risk reductions circled in red compared to those not taking the treatment regularly.  The red line shows the risk reduction to 0.7 which means a 30% reduction.  For cardiovascular events (CV disease) the reductions were all about 20%.  The mortality reductions were more dramatic, all being more than 30%.

The conclusion is that this treatment resulted in broad reductions in disease rates and deaths for the leading cause in developed and less developed countries.  The results occurred regardless of age, income status or country of residence.

Participation in this treatment would not take much persuasion if this drug existed, was widely available and relatively inexpensive.  While it meets all of those criteria, it has been and continues to be a hard sell to the population at large.  This is because the “drug” used in the study was actually “more than 3 servings per day of fruits, vegetables and legumes”. 

To give some perspective on these results, the results of similar clinical trials using statin drugs on total cardiovascular mortality have found risk reductions varying between 0 and 12%.  Seems like one could do twice as much just by eating enough fruits and vegetables daily.

The irony of all of this is that virtually every guideline out there supports this “therapy”, yet the minority of the population follow this in practice.  The breakdown seems to occur for many reasons.  Medical practice has become largely “this drug for that problem” with insufficient time spent or emphasis on implementing this very effective prevention.  This is driven by time restraints in patient care, patients preferring a pill over lifestyle change, and intense pharmaceutical advertising biasing opinions.

The bottom line is that you can’t fight data and in this case, it is convincing.  We are in the era of chronic lifestyle related disease and the biggest piece of lifestyle appears to be diet.

How Are Food Sensitivities and Depression Linked?

Food sensitivities or immune reactions to food have been linked to triggering several neurologic and psychiatric disorders.  This is caused by a couple of different mechanisms involving activation of the immune system.  The first is activation of a portion of the immune system called the innate immune system.  The system is the first part of the immune system to respond to challenge, and it activates systemic inflammation.  Much of how bad someone feels when they have the flu is inflammatory activation by the innate immune system.

About 1 in 10 persons will develop an innate immune response against a particular peptide in food, a problem called a foodsensitivity.  The immune system initiates an inflammatory response each time it detects the presence of that particular food peptide. 

Messengers called cytokines that activate inflammation also activate the more specialized part of the immune system called the acquired immune system.  One of its primary jobs is to produce antibodies against whatever has been perceived to be triggering the immune reaction.  Often this reaction can begin to make mistakes when it is chronically activated generating “cross-reactivity” where antibodies made against food molecules such as gluten begin to cause an attack against similarly appearing structures in the brain.

Studies have linked gluten triggered antibody reactions against brain structures in some seizures, neuropathy, migraine and cognitive impairment.  More recently the expanded knowledge of these reactions has suggested links between food reactions and two of the most common brain/mood disorders, anxiety and depression.

Typically, celiac disease is used as the model to test cross-reactivity between a food peptide and molecules in the nervous system.  Celiac disease is a cross-reactivity where antibodies against gluten begin to react with a peptide in the small intestinal lining destroying that structure.  This cross-reactivity can expand to structures in skin, glands and other areas including the nervous system.

A new study used this celiac disease model to look at nervous system involvement that may be associated with depression.  Patients with established celiac disease were examined with transcranial magnetic stimulation (TMS) which allows accurate measurement of the excitability of the brain.  All patients also completed a standardized test for depression, the Hamilton Depression Rating Scale (HDRS).  At the beginning of the trial 60% of the patients had positive depression scales.

A previous study performed by these researchers using TMS demonstrated that the celiac patients had abnormal balance between brain activation and inhibition.  The “balance” in brain response comes from the signal from one neuron to the next being “toned” by both inhibitory and excitatory interneurons.  These interneurons express neurotransmitters that turn up (excitatory) or turn down (inhibitory) the amount of signaling between neurons much like dimmer switches.

Normal information processing in the brain involves excitatory signals involved in the desired process at any moment combined with the inhibition of others that would take the desired function “off track”.

All subjects were asked to follow a gluten free diet.  Sixteen months later the TMS and the HDRS were redone.  There was actually a small reduction in the imbalance in brain activation.  In contrast, the depression scale showed active depression in only 8%, down from the original 60%.

The altered pattern of brain activation was the result of improved control of the inhibiting neurons that used the neurotransmitter GABA to produce the inhibition.  Research has indicated a high rate of cross-reactivity between gluten and casein, a peptide in dairy, antibodies with the enzyme GAD which is responsible for the production of GABA in the brain.  The antibody destruction of that enzyme appears to result in the abnormal pattern of brain activation.

This study brings up several points about the relationship between food sensitivities and depression.  The first is that once the food sensitivity is diagnosed, avoiding the triggering food improves the depression.  The second point is that the brain does not recover a normal activation pattern simply from avoiding the initial food trigger. 

The researchers discussed the failure of the brain to completely normalize its activation pattern.  The subjects were an average of 39 years of age.  Their immune reaction against gluten had been present for many years.  While the chemical stimulus to the brain which altered its activation pattern was removed, the abnormal brain pattern had likely become “learned”.

All learning comes through repeated stimuli to the brain resulting in neurons developing preferred connections and activation patterns.  We now know that when this has occurred with an abnormal activation pattern such as stress, the brain eventually “learns” that preferred pattern.  At this point in time techniques such as neurofeedback which is EEG guided brain training must be used to re-train the brain back into a more normal pattern.

For many the best outcome with depression will result from finding the original trigger such as a food sensitivity but then restoring normal brain activation patterns with neurofeedback.

Irritable Bowel Syndrome

The What, Why and How

Irritable bowel syndrome, or IBS, is the most common functional digestive disorder.  Generally, digestive problems fall under two categories, functional and pathological.  Pathological disorders are basically those that can be seen and/or measured such as tumors, ulcers and others.  The vast majority of testing that is done for digestive complaints is done to look for pathologies.

Functional disorders, in contrast, are diagnosed by the presence of symptoms combined with the absence of pathology.  Generally, they can be described as some phase of the digestive process simply not “functioning correctly”.  They are often diagnosed by ruling out pathology in the presence of symptoms rather than demonstrating some abnormality.  As with many “rule out” diagnoses, the patient is often left only knowing that they have no pathology but without getting answers about what needs to be done to resolve the symptoms.

It is estimated that 80% of digestive disorders are functional and only 20% are pathologic. IBS is the most common functional digestive disorder.  Between 10-15% of the population experiences IBS.  The typical symptoms include abdominal pain, bloating, and often constipation and/or diarrhea. They may vary from episode to episode. 

The most important point to appreciate regarding IBS is that it is a heterogeneous disorder.  This simply means that it is not caused by one thing but rather can be caused by several problems.  The most important point in resolving any individual case is to find all of the triggers in that circumstance.  IBS is also typically “multifactorial” which means it is caused by several contributing factors.

Occasionally, it will be just one factor such as a food sensitivity.  Most often, however, it results from the co-existence of multiple factors in the same person. Appreciating this relationship is the most important factor in obtaining resolution of the problem.

The two diagrams show the concepts of multifactorial and heterogeneous. Patient "A" has 4 contributing factors causing their IBS. While different ones are contributing more or less to the problem, resolution is unlikely to occur unless all are addressed.

In contrast to patient "A" the second example, patient "B" has a different grouping of factors causing their IBS (multifactorial), and they are not the same as patient "A's" triggers (heterogeneous).

These different triggers of IBS are not equally common.  Food sensitivities, or immune inflammatory food reactions, are perhaps the most common.  These are delayed food immune reactions with symptoms beginning from several hours to 1-2 days after the food exposure.  Typically, the person has eaten multiple times in between obscuring the relationship.

Dysbiosis is another common contributing trigger to IBS.  This is an imbalance in the bacterial population living in the digestive tract.  Certain species help with the regulation of inflammation in the digestive tract.  These species should make up the dominance of the population of the 100 trillion bacteria in the human microbiome.  Many factors may cause the favored species to diminish allowing less desirable “opportunistic” bacteria to populate.  This often causes a low grade inflammatory response instead of the inflammatory preventing response created by the preferred bacterial population.

Stress often is the most difficult for most to understand the relationship with IBS.  The autonomic nervous system that governs all function in the digestive tract has two divisions, the sympathetic which controls “fight or flight” and the parasympathetic which controls “rest and repair”.  Digestive function is shut down during fight or flight and activated when in rest and repair. 

Ongoing stress tends to train the nervous system to stay in sympathetic dominance inhibiting function in the digestive tract.  IBS cannot be fully understood without a look at the balance in the autonomic nervous system.  This can be done with a test called heart rate variability which shows the sympathetic/parasympathetic balance.  Once the problem is understood, autonomic training can be successfully used to retrain balance in sympathetic/parasympathetic tone.

IBS is truly multifactorial, heterogeneous.  Only approaching its diagnosis and treatment with this understanding will consistently yield good results.

Are Herbs All the Same?

I get asked some version of this question frequently.  A recent interaction triggered this blog post.  A patient had chosen to use an herb product she bought online versus the one that I recommended from the Standard Process herb line, MediHerb.  The follow-up test didn’t look any better, and there wasn’t much change in symptoms.  The dilemma it presented was that there could be 2 reasons.  The first is that the protocol we arrived at wasn’t what was needed, and the second was that the product she took wasn’t adequate to produce good clinical effect.

Shortly after that interaction information arrived from Standard Process with a detailed analysis comparing the content of several Echinacea products.  There are different forms of Echinacea, and different companies also use different qualities of herbal material. 

Echinacea is noted for its immune enhancing properties.  The effect comes from constituents in the herb called alkylmides and there are two types of these, 2-ene and 2,4-diene.  They must appear together for the herb to have good clinical effect.  The 2,4-diene alkymides generate much of the clinical effect, but they tend to be broken down quickly by human liver enzymes.  When they occur together with the 2-ene alkymides, they prevent the excessively quick liver breakdown and generate the good immune enhancing effect.

So what difference does which Echinacea used make?  Plenty.  It seems that Echinacea augustifolia doesn’t contain much of the 2-ene alkymides so the 2,4-diene alkymides get broken down too fast to generate much effect.  Echinacea purpurea contains a lot of the 2-ene form allowing better clinical effect.

MediHerb goes to great length to balance the two forms of Echinacea to generate optimal effect.  In an independent lab study MediHerb Echinacea Premium alkymide content was compared to 9 other commercial products. The chart shows the results.  The MediHerb product contained about 2 1/2 times as much alkymides as the next highest product and many times greater than most of the others.  The comparison chart at the bottom of how many tablets of each other product would have to be taken to equal the alkymides in a single Echinacea Premium.  So, are all herbs the same?  No, not at all.  As Paul Harvey used to say, “now you know the rest of the story”.

PS  -  As I was correcting the final proof of this post, I received a new 6-minute video from MediHerb showing the extent of their efforts to produce the best quality herbs.  So fitting!!
Click Here To See The MediHerb Video!

What is Non-Celiac Gluten Sensitivity?

The most noted gluten related disorder is celiac disease which is an autoimmune disease where the immune system reacts against gluten making antibodies to destroy it but then eventually confuses self-tissue with gluten.  The self-tissue that the immune system confuses with gluten is an enzyme in the lining of the small intestine called tissue transglutaminase (tTG).  Once the immune system mistakes tTG for gluten, it makes antibodies against that enzyme which destroy the lining of the small intestine.

The symptoms of celiac disease had been talked about by various healers for centuries, but the first accurate description of the cause of the abdominal disease was given by British physician Samuel Gee in 1888 who developed an all-banana diet to cure it.  While he attributed much of the effect of this diet to something in the banana, it actually proved later to be that it removed all gluten.

Celiac disease was thought for most of the 20^th century to be the only gluten related disorder.  However, over the past 30 years many individuals with symptoms of IBS but with negative testing for celiac disease obtained marked relief from a gluten free diet.  This has more recently led to the appreciation that immune gluten sensitivity commonly exists but without the cross reactivity to tTG and the autoimmune reaction to the small intestinal wall.  This disorder has been termed non-celiac gluten sensitivity (NCGS).

Two consensus conferences were held in 2011 and 2012 establishing NCGS as an accepted entity and establishing a scientific consensus of the diagnosis.  This has been a particularly important step in the

understanding of digestive and related immune disorders given that it appears to be far more common than celiac disease.  While celiac disease occurs in approximately 1% of the population, NCGS occurs in 10%, or one in 10 individuals.

The symptoms of NCGS tend to be both digestive and systemic.  Most patients will have both, although they tend not to relate the systemic effects like brain fog or joint pain to their digestive symptoms. 

A recent analysis of the symptom patterns seen in NCGS found that they are broad and can vary from patient to patient.  Abdominal pain and bloating were the most common digestive symptoms occurring in over 80%.  Stomach/epigastric symptoms were not uncommon occurring in almost 50% of patients.

The systemic symptoms associated with NCGS tend to often not be recognized as related.  Common systemic symptoms include fatigue, headache, anxiety and joint/muscle pain.  Recent study has linked NCGS to be a common cause of fibromyalgia. In 20 patients diagnosed with chronic fibromyalgia, all had significant improvement,

while most had complete remission of the disorder. Eight patients also had chronic fatigue syndrome which commonly co-exists with fibromyalgia, and many had co-existing migraine, back pain and/or depression which also responded. These were noteworthy improvements given the average duration of symptoms in this group was 12 years. 

The systemic symptoms seen in NCGS are caused by the immune reaction triggered by gluten.  While the immune reaction to gluten is triggered in the digestive tract, these reactions are systemic turning up inflammation throughout the body.

NCGS is the most common food sensitivity but by no means the only one.  Several other food peptides may trigger immune reactions with dairy and legumes/beans also being fairly common triggers.  Some individuals have tried avoiding gluten but have had no improvement in symptoms.  This can occur for several reasons:

•       Leaky gut exists
•       Multiple food sensitivities co-exist
•       Avoidance is not complete or long enough

Leaky gut is the common term for gut barrier compromise.  The inflammation triggered by the primary food reaction causes the small intestinal lining to become too porous and many food peptides will leak in triggering immune reactions.  Often in this situation avoiding one food helps for a little while, but then other foods begin to also cause the reaction.  As food sensitivities are typically delayed reactions, it is very hard to tell which food or meal caused the symptom flare-up.

Biomeridian testing can be used to isolate immune food sensitivities but also to detect the presence of leaky gut which may prevent symptom improvement.  It can also isolate other causes of digestive symptoms which can mimic a food sensitivity. 

The study of the relationship between food sensitivity and fibromyalgia is telling.  The subjects had been symptomatic before considering that a food sensitivity could be triggering the symptoms.  As the awareness of food sensitivities increases, the mystery of many symptoms will be solved sooner.

Please join us  -  Learn about a very innovative program for the prevention and treatment of Alzheimer’s Disease

Banks Nutrition Center would like to invite you to an educational event about Alzheimer’s Disease. There are some very promising treatment programs evolving that for the first time are showing the ability to reverse the course of Alzheimer’s disease. The most striking is the Bredesen Protocol. Dr. Banks will be discussing this treatment protocol and will answer any questions you may have about Alzheimer’s prevention and treatment. Our goal is to help you have a better understanding of the disease and to know there is hope.

The Bredesen Protocol
Preventing & Treating Alzheimer’s Disease

Dr. Scott Banks, D.C., M.S. -Clinical Nutritionist

Event Date: Saturday, June 10th 2017
Time: 11:00AM to 1:00PM
Banks Nutrition Center

Does Nutrition Really Matter?

The Numbers Don’t Lie

The primary driving factor in the growing rates of and the costs associated with chronic disease is diet.  The solution to this problem would appear to be simple, change our diet, yet simple and clear is far from what the public sees.  There are so many special interests associated with this problem that many different solutions confuse the issue.

The best way to answer this question is to look at the actual research data we have regarding it.  While it has been very clear for quite some time, this is often not what the public sees.  A striking new study should bring the real answer into focus.

The study followed over 21,000 adults over 11 years.  Adherence to the Mediterranean and Paleo dietary patterns were assessed. 

Death rates from cancer, cardiovascular disease and from all causes were compared between those with the highest and lowest quintiles (highest 20% to the lowest 20%) of adherence to these two diets.  The results were striking with high adherence to the Paleo diet reducing deaths from 22-28%, while high adherence to the Mediterranean diet reduced risks 32-37%.

The comparable prevention rates of death from about any cause associated with chronic disease is very telling.  The tale is that bad diet drives the risk of death from a broad group of diseases, and good diet offers broad protection against this same spectrum. 

If these results could be produced from a single drug, it would be hailed as a great medical breakthrough and many would be standing in line to get it.  It would also be very expensive and would have its limitations as every drug has been found to. 

For example, improvements in delaying the complications of type two diabetes (TTDM) have been made with the ever-evolving group of medications targeting the disease.  The complications include diseases that diabetes drives such as stroke and heart disease.  While the advances in drug therapy have pushed back these complications by a decade or so, they are simply delayed and will eventually occur.  The problem is that while the complications can be delayed a decade or so, the age of onset of TTDM has plunged from 56 years of age to 40 years of age over the past 40 years.

It is simple math, if you push back the complications associated with a disease by a decade or so but the disease is occurring a decade and a half earlier in life, the battle is being lost.  The real elephant in the room here is that no medication has made any progress with preventing diabetes.  That can only be done with diet.

The only fail-safe solution can be as it always has been – to fix the factors that cause the disease in the first place.  Diet and exercise are the two factors that most associate with risk with diet being the strongest by a long-shot. So, does nutrition really matter?  In fact, as this study shows, it literally is a matter of life and death.

Whalen et al.  Paleolithic and Mediterranean Diet Pattern Scores Are Inversely Associated with All-Cause and Cause-Specific Mortality in Adults.  Journal Nutrition, 2017.

Helping You Eat Healthier Restaurant/Farm Review #17

Helping You Eat Healthier

                         Review #17

Welcome to our seventeenth review of restaurants and farm markets in our healthy eating series. This is a great restaurant that serves up creative delicious dishes showcasing local seasonal produce or seafood. They were listed on "13 Best Brunch Places in Virginia" in Virginia Is For Lovers Travel Blog. 

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Bay Local Eatery

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Bay Local Eatery was established with the local community in mind; everything they serve is made in-house using locally sourced produce, meats and seafood. They like to describe their culinary style as "Coastal Southern", taking advantage of everything that the region has to offer. Bay Local Eatery prides themselves in making everything fresh and in-house every day while never pulling anything out of a bag and putting it into a fryer. They love to be creative in the most delicious way possible.

Bay Local's menu was inspired from a collection of family recipes and local favorites. They have a brunch and dinner menu; on these menus you will find many deliciously creative items. The brunch menu includes items such as appetizers, house favorites, omelets, benedicts, burgers, sandwiches, lettuce wraps and salads. Their dinner menu includes items such as shareable appetizers, house favorites, tacos, fresh chowder of the day, lettuce wraps, burgers, sandwiches and salads. They do have some gluten-free and vegetarian items on their menu and you are also able to substitute your bun to a gluten free bun for a small extra charge. Their menus also offer a couple cold press juices such as the Exotica that consists of apple, orange, kiwi, carrot, melon, strawberry and mint. Some favorite dishes on the menu are any of the benedicts; the favorite benedicts are the garden bennie, crab cake bennie and the bay local bennie. Another favorite item on the menu is the Bay Three Way, an assorted platter or homemade chicken salad, tuna salad, hummus, arugula, mixed greens, vegetables and fruit with garlic toasted pita points. Their menu changes with the season and features "fresh-ials" which are fresh specials that showcase seasonal produce or seafood. You can find the "fresh-ials" on the chalkboard in the restaurant offering delicious specials for the day.

For a great delicious meal with a warm and welcoming vibe, be sure to check out Bay Local Eatery. Since the ambiance is charming, warm and inviting, it is usually pretty busy and can be a little loud from everyone's laughter, but it is still an enjoyable meal! They are located at 2917 Shore Drive in Virginia Beach. They serve brunch 7 days a week from 7:00am-3:00pm, and dinner Thursday through Saturday from 5:00pm-11:00pm. Also a second location will be opening up soon in the spring in the Linkhorn Shoppes on Laskin Road in Virginia Beach.

 For more information about Bay Local Eatery give them a call at 757-227-4389 or visit their website at http://baylocalvb.com/

Diet and Disease

State of the Art 2017

The hallmark of good healthcare is that it is “evidence-based”.  This simply means that decisions in care and preventative strategies are largely based on quality scientific evidence rather than empirical information.  This is not to say that empirically based knowledge, that based only on practical experience, is not important but that scientifically derived evidence tends to be more accurate in the long run.

Regarding diet, we are emerging from 3 to 4 decades of “this seems to make sense”, rather than evidence-based decision making.  Unfortunately, the common advice has proven quite inaccurate and somewhat contributory to the greatly increasing rates of some chronic diseases such as diabetes.

Given the above state, I thought it was appropriate to celebrate “National Nutrition Month” with a look at the evidence-based knowledge that we have concerning the relationship between diet and disease.  The most striking realization has been that the low fat focus of the past 30-40 years has not only been ineffective in preventing the chronic diseases it was touted to be a solution for, it actually has been contributing to the increased development of most of these very diseases.  There are several reasons for this:

·         Low fat means higher carbohydrate

·         A low fat diet has never been shown to lower blood lipids

·         The low fat/high carb diet causes greater weight gain than comparative diets

·         The low fat/high carb diet causes a greater shift to a disease-causing blood lipid pattern

A little background is necessary to understand this important error that cost Western Nations 30 years of good dietary understanding.  In the 1950’s a physiologist named Ancel Keys reported that in his study of seven western countries, a higher total and saturated fat diet was associated with greater heart disease risk. The problem was that Keys actually studied data from 29 countries but “proved” his theory only reporting that from 7 countries and omitting that from the 22 countries (76%) that found no relationship.  Extensive scientific review has now found this study inaccurate and misleading:

“There is now probably unanimous consensus in the scientific community about this study - it is faked, since Dr. Keys cherry picked just 7 countries. He had data of 22, and when statistical methods are applied - there is no significant relationship between dietary fat consumption and heart disease.”

The reasons why the medical community, which prides itself as being “evidence-based”, dispensed erroneous advice for 3-4 decades are complex.  They are generally looked at as the top source of nutritional advice for disease prevention, yet many studies examining their training and ability to do this suggest otherwise.

A study published in 2006 of over 2300 medical students at 16 representative medical schools found that 72% beginning medical school thought that nutritional counseling was “highly relevant” to medical practice.(1)  By their final year the number had dropped almost in half to 46%.  Only 19% thought that they had been adequately trained to provide this advice, and only 17% reported to doing so with their patients.

A prior study examined the knowledge of internists and cardiologists about the impact of diet on blood lipids.  Eighty-four percent of cardiologists and 96% of internists did not know that a low fat/high carb diet would raise blood triglyceride levels.  Similarly, 70% of cardiologists and 77% of internists did not know that this diet would lower HDL, or good cholesterol.

The problem is that medical education is devoid of nutritional education instead focusing on other areas of concentration.  Nutrition science has not filtered into that training, yet the public perception is that this is where nutritional advice should be available. 

This domain should default to specifically trained individuals well versed in nutritional science, but many barriers to this remain in the system.

The thought process that has led to the standard low fat diet advice for the past 3-4 decades was an oversimplified assumption that the fat responsible for arterial plaque must be generated by dietary fat.  However, the higher carbohydrate dietary pattern that this assumption created actually causes a more risky shift in blood lipid patterns than does a higher fat, lower carbohydrate pattern.

In reality, any energy in excess of immediate need is sent to the liver to be converted to fats as that is the primary energy storage form that humans use.  The sugars from a higher carbohydrate diet have been shown to increase liver triglyceride production, lower HDL production, increase LDL or bad cholesterol production and cause a shift in the LDL particle size to a smaller, more plaque-forming variety.  This combination of changes is the one that causes the greatly increased vascular disease risk in diabetics.

The increase in LDL production associated with a higher carb diet occurs because this diet causes higher insulin levels.  Making cholesterol in the liver requires energy availability, and insulin is a potent signal of energy availability.

Most major bodies that set guidelines about dietary behavior have recently revised their positions stating that the dietary high fat hypothesis has not proven true.  They also suggest that the low fat diet preoccupation has pushed us to a higher carbohydrate diet that has been a potent driver of the obesity and diabetes epidemic. 

Diabetes is of particular concern as vascular complications remain the dominant cause of associated disease and deaths.  Fuel to this concern was added recently by a study that looked at carotid artery plaques in obese and non-obese subjects.  While high dose statin therapy lowers plaque volume by 4.2% in non-obese subjects, obese subjects had it increase 4.8% in 12 months despite lowering of LDL.(3)  Other factors besides LDL contribute to plaque formation including inflammation and glycation, or direct sugar damage to tissue.

The lesson to deduce from the evidence-based look at the current research on diet and disease is that we are generally ill suited to the dietary pattern of the last 30 to 40 years.  While humans thrived on a diet of about 30% protein, 40% fat and 30% complex carbohydrate for the first 6 million years, the current shift to 15% protein, 25% fat and 60% carbohydrate has resulted in growing rates of a number of chronic diseases that have a metabolic basis. The high percentage of total carbohydrate has been further complicated by the dominant amount being refined and with added simple sugars.

So the knowledge base we have concerning diet in 2017 looks very different from the commonly recommended dietary pattern of the last 40 years.  Now we face the difficult task of actually implementing that change, but the motivation is that the stakes are high.

1)    Spencer et al.  PREDICTORS OF NUTRITIONAL COUNSELING BEHAVIORS AND ATTITUDES IN U.S. MEDICAL STUDENTS.  Am J Clin Nutr, 2006;84:655-662.

2)    Flynn et al.  INADEQUATE PHYSICIAN KNOWLEDGE OF THE EFFECTS OF DIET ON BLOOD LIPIDS AND LIPOPROTEINS.  Nutri J, 2003;2:2-4.

3)    Sandfort et al.  OBESITY IS ASSOCIATED WITH PROGRESSION OF ATHEROSCLEROSIS DURING STATIN TREATMENT.  J Am Heart Assoc, 2016;5:e003621.