making the connection between nutrition & health

Sugars, Artificial Sweeteners and the Diabetes Epidemic

It has been an uphill battle to raise public awareness about the true impact of the Western sweet addiction.  About 75% of all manufactured food products are “enhanced” with sweetener.  The enhancing is for one purpose; it increases the drive in the brain to consume.  Tomato soup with sugar in it excites the brain better than just plain tomato soup. 

The problem is that sugar works its enticement in the same area of the brain that cocaine and other addictive substances do triggering the release of dopamine, a neurotransmitter that gives the sensation of pleasure.  Dopamine is responsible for what neuroscientists call “reward-driven learning” that drives repeating what triggered it.

If any broad public attempt has been made to curb the sugar problem, it has been substituting artificial sweeteners to prevent the associated health problems but allowing the habitual sweet rush to continue.  Unfortunately, a wealth of new data is showing that this has been a failed concept.

A 14-year study of over 66,000 women looked at the impact of sugar sweetened and artificially sweetened beverages (ASB) on diabetes risk.  The findings provide a stark reality.

                                                                                         Diabetes risk

Sugar sweetened beverage users                                      +34%

Artificially sweetened beverage users                              +121%

The problem comes from the body’s preparation to handle increased blood sugar.  The first warning seems to be the tripping of the sweet receptors (nerve endings) in the tongue that tell the brain to start the release of insulin.  These receptors don’t differentiate between real and perceived sugar, they only respond to sweet.  With time, insulin levels remain elevated causing the first step in the transition to diabetes, insulin resistance.

The study found that those who drank ASBs drank about twice as much as their SSB consuming counterparts.  The false security of artificial sweeteners likely allowed them to flog the sweet receptors to a greater extent causing greater ongoing insulin responses.  In a way, it appears to have led to greater addiction and the ensuing consequences.

Fagherazzi et al.  Consumption of artificially and sugar-sweetened beverages and incident type 2 diabetes in the Etude Epidémiologique auprès des femmes de la Mutuelle Générale de l’Education Nationale–European Prospective Investigation into Cancer and Nutrition cohort.  Am J Clin Nutr,  2013;97:517-523.


Best Health Tip for 2013 to Prevent Metabolic Disease

The new year always is a time to reflect and try to introduce habits that will result in a better year.  Health is often a primary area that individuals realize should be one of top focus.  Perhaps the top health tip for 2013 is to understand and control the glycemic load of one’s diet.

The discussion of this should start with simply understanding what glycemic load is.  It is simply the degree of “stress” that the metabolism of carbohydrates and sugars creates on our system.  Care should be taken not to confuse glycemic load with glycemic index.  Glycemic index is simply the rate at which sugars that are in a serving of any carbohydrate are digested and absorbed into the circulation. 

Two whole carbohydrates can have the exact same grams of inherent sugars and yet release them during digestion into the system at much different rates.  The one that releases the sugars faster causes greater metabolic stress to manage.  This may or may not be a problem.  If the sugars are released quickly but the total sugars per serving are low, the stress is reduced. 

Glycemic load combines both variables, the rate at which the sugars are released but also the total amount of carbohydrate/sugars in a serving of that particular food.  Foods are not covered in the Declaration of Independence so, no, not all foods are created equal.

While both glycemic index and glycemic load correlate with metabolic disease risk such as with diabetes, heart disease and some cancers, glycemic load has greater correlation or predictive value.

Generally the per serving glycemic load of a given carbohydrate is classified as high or low by these values:

It is better from a disease risk standpoint to look at the total daily glycemic load.  One snack of high glycemic load creates short-term metabolic stress.  Eating all high glycemic load carbohydrates during a day creates sustained metabolic stress.  A total daily glycemic load (sum of the GLs of all carbs eaten) generally should be below 140.  Total daily GL above 140 progressively raises blood triglyceride levels and depresses HDL or good cholesterol.  Both of these blood lipid changes have been correlated with heart disease risk.

In the above study the highest daily glycemic load group had a doubling of their 10-year coronary artery disease risk compared to those eating the lowest glycemic load.

                  

 

 

 

 

 

 

From a practical perspective, it is difficult to keep track of the glycemic load of everything eaten and totaling it for the day.  A simple alternative is to build the “pattern” of carbohydrate sources.  Most carbohydrates in the western diet come from added sugars, grain products and starches.  Ironically, these foods are all high glycemic load.  Other carbohydrates such as fruits and vegetables have low glycemic loads.

Generally, grains and starches have a per serving glycemic load of 12-30. Grain products are one of the most likely foods to have added sugar which further increases their value.  Fruits have intermediate glycemic loads of between 3 and 10.  Vegetables have glycemic loads of 1-3.

A typical day where 40-45% of the calories come from carbohydrate will contain about 10 servings.  If those 10 servings are built with vegetables>fruits>grain and no added sugars, the total daily glycemic load cannot exceed 110.  Below is an example of such a day:

Carbohydrate servings                               Glycemic load

5 vegetables (GL of 1-3 each)                   5-15

3 fruits (GL of 3-10 each)                            9-30

2 grains or starches (GL of 10-30              20-60

                                        Total GL         34-105

The typical western diet contains on 1.5 vegetable servings, 1 fruit, 6 grain and starch servings, and 2 to 4 “pure sugar” carbs such as ice cream, juice or soft drink.  This yields a much different glycemic load picture:

Carbohydrate servings                               Glycemic load

1.5 vegetables (GL of 1-3 each)                1-5

1 fruit (GL of 3-10 each)                              3-10

6 grains or starches (GL of 10-30)            60-180

3 “sugar” carbs                                        60-90

                                        Total GL         124-285

With this typical pattern, the average glycemic load is about 200-210, well within the highest coronary artery disease risk group found in the above study.  Heart disease risk is just one of several increased by high glycemic load eating.  Perhaps diabetes risk is the greatest.  The percentage of the population with diabetes is doubling about every 15 years.  This rise almost parallels the increasing glycemic load pattern of the western diet.

Perhaps the best health tip for 2013 is to control dietary glycemic load.  Keep it simple:

  • ·         Remove the added sugars from the diet
  • ·         Carbohydrate sources should be  –  vegetables>fruits>grains

Natural Reflux Disease Relief May Actually Work Better

GERD, or gastroesophageal reflux disease, is becoming one of the most common problems in modern society.  It is estimated to have increased 50% in the last decade alone.  The most commonly prescribed drug for GERD was the third largest selling drug in 2011 at $6.2 billion.

The explosive increase in GERD strongly suggests that it is being driven by environmental factors rather than genetics.  The dominant environmental factor is diet.  A very high percentage of GERD patients associate worsening of their symptoms directly with eating certain foods.  Given this nutritional connection, it only seems natural to investigate the use of nutrition to resolve GERD symptoms.

A study was undertaken in 350 persons with GERD.  They were randomized to receive either one of the commonly used drugs for GERD or a supplement of nutrients.  All symptoms were recorded in a diary over 40 days and the percentage of change was also recorded.  The drug treatment group reported similar results to many previous studies testing the effect of these drugs with many patients reporting some relief, but complete relief being obtained in only between a half to two thirds of users.

At the end of the 40 days, the improvements strongly favored the nutritional supplement group.

 

 

 

 

 

 

 

 

There were no subjects in the nutrient supplement group that had any adverse effects.  Nutrients heal without offsetting harm so that was to be expected; however, the researchers are used to commenting on that “outcome” as most of what they research are drugs which all carry some risk.

The risks with the drugs used for GERD are significant.  Normal secretion of acid in the stomach is imperative for digestion and absorption of nutrients from food, and for the the lower digestive tract to function properly.  Without it, nutrients such as calcium, B12 and several others are poorly absorbed from food.  Combine this with the fact that the foods that commonly cause GERD are typically low in these nutrients as well, and it will result in deficiency.

There is a growing association between long-term use of drugs for GERD and osteoporosis and metabolic bone disease.  This is speculated to result from poor calcium absorption but may also be related to poor absorption of other nutrients such as vitamin D and K, both needed for bone metabolism.  Anemia and peripheral neuropathy, both disorders associated with low vitamin B12 status have also been associated with long-term GERD medication. 

The nutrients used in the study included vitamins B6, folic acid, B12, betaine, amino acids methionine and tryptophan and melatonin.  It is ironic that some of them are the very nutrients that become deficient with long-term GERD drug use.  Perhaps the incomplete and poor long-term response to these drugs in some people actually relates to their reducing the very nutrients that are needed to naturally control digestive balance in the stomach in the first place.

de Souza Pereira .  Regression of gastroesophageal reflux disease symptoms using dietary supplementation with melatonin, vitamins and amino acids: comparison with omeprazole.  J Pineal Res. 2006 Oct;41(3):195-200.


When GMO Grains Raise Bad Cholesterol

We seem to be in an epidemic of high LDL or bad cholesterol.  It seems that very few adults reach age 50 without being afflicted with this plague.  How far away can laws be requiring beginning a statin drug before qualifying for Medicare?

 There are several qualifications about cholesterol’s “plague” status that cholesterol has obtained.  Research has shown the relationship between elevated cholesterol is very clouded after age 60, and it may have an opposite correlation at that stage of life.

 

 

 

 

 

 

 

Another qualification that should be appreciated in the “plague” designation is that not all LDL or bad cholesterol is risky from a heart disease perspective.

 Those issues aside, there is some relationship between LDL cholesterol levels and heart disease risk.  Inappropriately elevating cholesterol can relate to several lifestyle factors, although these factors may not be what most people assume.  One factor has emerged from newer study; consuming GMO grains.

It seems that one of the ways our cells can be triggered to do or not do something is by signaling from a small molecule called microRNA, or mRNA for short.  These are small segments of genetic code the cell produces to change the behavior of an enzyme or protein.  What we have only begun to appreciate is that mRNAs from the genetic material of the plants and animals we consume have the ability to alter the behavior of an enzyme or protein in our bodies.

Since mRNAs originate from the genetic material in a cell, the mRNAs we are exposed to eating genetically modified food are “different”.  Regrettably, we have not required enough long-term testing before allowing the introduction of GMO into our diet to find out if this altered cell signaling by altered plant genetic material has any ill effects.  Now that the research is being done, the response could most appropriately be “oops”!

Researchers have found a particular mRNA called “MIR168a” in adults who consume GMO rice.  To evaluate the impact of the presence of this altered mRNA, a study looked at MIR168a blood levels in animals fed GMO rice, their levels of LDL cholesterol receptors in the liver and their LDL cholesterol levels.

The first conclusion was straight forward; all animals who consume the GMO rice have the altered mRNA MIR168a present in their blood.  The second conclusion was that the presence of MIR168a correlated with reduced LDL cholesterol receptors in the liver.  These receptors are how we remove excess, unused LDL from the blood to be broken down by the liver.  The blood LDL cholesterol level is not simply a result of its production but also the ability of the liver by the LDL receptor to remove the excess from the circulation.  LDL cholesterol receptor levels were reduced about a third in the GMO fed animals.

 

 

 

 

 

 

 

 

Since the job of the LDL receptor is to remove excess LDL and normalize blood levels, it would be expected that LDL cholesterol would go up with the GMO feeding.  The data was no surprise.

 

 

 

 

 

 

 

 

The researchers comment that while previous studies have demonstrated that genetic material from one species can transfer to another within its kingdom (plant to plant), this is the first to demonstrate that genetic material can be transferred from one kingdom to another (plant to animal) through consumption of the plant.  In addition, the effects of this genetic material transfer were not favorable, lowering the liver receptor that helps clean excess LDL from the blood and raising LDL cholesterol 48%.

Too often, we intervene in nature for a short-sighted purpose only to find out the negative effects later.  This was the case with DDT, dumping pollutants into the ocean because it was big enough to hide them, and many more.  As with most cases where man has altered nature with too little thought about outcome, the results have not been good.  20 years of evolving problems will likely convince all that GMO foods are “un-natural”.

Does it sound like a stretch that eating GMO food could raise LDL cholesterol?  Not any more!

Zhang et al.  Exogenous plant MIR168a specifically targets mammalian

LDLRAP1: evidence of cross-kingdom regulation by

microRNA.  Cell Research (2012) 22:107-126.


Chronic Migraine Headaches?

It Could Be Gluten Sensitivity

Chronic migraine headaches are common and can be very disabling.  Some new data has found a rather striking relationship between gluten sensitivity and these headaches suggesting that this relationship should be explored in anyone with these headaches.

A study done jointly at Columbia University and Mount Sinai School of Medicine looked at the rates of migraine headache in 324 subjects with some form of gluten sensitivity or other inflammatory bowel disease such as Crohn’s Disease.  They compared the rates of migraine in these subjects with 178 subjects without any of these disorders.  The results demonstrated a strong relationship between gluten sensitivity or inflammatory bowel disease and migraine.  The RR is the relative risk which is the number in the control group with migraine.

 

 

 

 

 

 

 

 

Perhaps the most fascinating finding was that gluten sensitivity actually created a much higher risk than did celiac disease.  In celiac disease, gluten causes a severe inflammatory reaction in the lining of the small intestine to the point that the lining demonstrates damage.  Gluten sensitivity is an immune inflammatory reaction to gluten but with less pronounced intestinal findings and more systemic findings such as joint pain, swelling, headache, etc.

It is likely that any food sensitivity may cause migraine given the increased rate in inflammatory bowel disease which is not classically related to gluten reaction but may be related to other food components such as dairy, eggs, nuts, etc.  Gluten sensitivity and other food sensitivities are the most challenging to diagnose.  Biopsy tests that are diagnostic for celiac disease and inflammatory bowel disease are not helpful in gluten and other food sensitivities.  Blood antibodies which are helpful in food allergies are not present in sensitivities.  They are caused by inflammatory chemicals called cytokines which are difficult to isolate and measure.

As an alternative, food sensitivities are best diagnosed with a test that looks at body reactions such as Biomeridian sensitivity testing.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

The test measures reactivity in allergy meridians during exposure to different substances. 

Given the strong relationship found between food sensitivities and migraine headache, investigation of this possible cause seems warranted in headache sufferers. 

Prevalence of Migraine in Patients With Celiac Disease and Inflammatory Bowel DiseaseThe Journal of Head and Face Pain, 2012


The Omega-3 Fatty Acid and Mercury Dilemma of Fish Oils

Omega-3 fatty acids impart significant health benefits from lowering blood triglycerides and raising good cholesterol to reducing inflammation.  The list of common diseases that higher omega-3 fatty acid (omega-3s) intake may help prevent is impressive.  Few in science question these relationships.

The dilemma regarding omega-3s seems to be rather how we can get enough of these helpful fats to reap the benefits.  This requires between 3 and 4 grams.  The current US dietary intake is about 0.3 grams, or only a tenth of what is needed for health benefit. Only a couple of hundred years ago they came exclusively from diet.  That has been disrupted by several alterations to the western diet. 

All omega-3s originate in the plant kingdom in a fatty acid called alpha linoleic acid (ALA).  Many animals can consume this plant source, and they have a series of enzymes that convert ALA into active omega-3s in their body.  Humans are included in this group and had consumed a diet which was rich in ALA allowing us to make perhaps up to half our needed omega-3s.  The other half came from animal product from animals consuming a diet rich in ALA and therefore rich in omega-3s in their fat.  The denser plant sources of humans such as green plants (vegetables) and certain seeds are now not a dominant portion of the diet.

 

 

 

 

The western diet has replaced much of our vegetable consumption of 75 years ago with grains which do not contain ALA.  Accordingly, we make very little omega-3s ourselves.  Beef used to contain considerable omega-3s because cattle consumed mostly grass which contains ALA.  They now consume mostly corn and soybeans which contain none.

All of this leaves us with the three common options:

  • Don’t get enough omega-3s
  • Eat wild fish 4-5 times each week
  • Use fish oil supplements

Wild is highlighted here as most of the fish consumed to “fix” the problem is farm raised.  Wild fish consume smaller fish and the chain backs all the way down to the smallest eating green algae, a dense source of ALA.  Farm raised fish consume grain and just as with their land based counterparts, make very little omega-3.

The worst choice above is to not get enough omega-3s.  The second two options (wild fish and fish oil supplements) have an added issue.  The fish that are dense omega-3 providers can tend to have problems with accumulating mercury and PCBs.  While we have studied the benefit of the omega-3s, any harm done by exposure to mercury has not been well understood.  A new study has shed some light on the issue.

The study examined 572 men from Scandinavia who consumed varying amounts of wild fish.  They looked at the myocardial infarction (MI) or heart attack rates of the different levels of consumption compared to age matched non-consumers.  As an additional twist, the study looked at mercury levels in participants to see if that also affected MI rates.  The general conclusions were that high omega-3 consumers had somewhat lower MI rates than lower level consumers.  When the two groups were also further split into groups reflecting both high omega-3, and high or low mercury groups, the results were quite different.



 

 

 

 

 

 

 

 

High omega-3 intake but with high mercury levels was no better than low omega-3 intake.  Higher mercury exposure appears to negate any benefit of intake of omega-3s.  The greatest reduction in MI risk was in those consuming high omega-3s with low mercury exposure.

The conclusions seem to be pretty straight forward:

  • Higher omega-3 fatty acid intakes lower MI risk
  • Higher coincidental mercury intake negates any benefit

Which solution each individual chooses is unique to their lifestyle.  For most it will be to take fish oil supplements.  Only a few companies have their oils independently tested to certify that they are free of significant levels of mercury and PCBs.  So if fish oil is your best solution, make sure it is a certified oil free of significant contamination.  Otherwise the solution may be no solution at all.


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