Striking New Data on Sugar and Alzheimer’s

While the death rates from many chronic diseases have stabilized or declined over the past 2 decades, there have been 2 exceptions.  The rates of diabetes and Alzheimer’s have dramatically increased. Their parallel increase is not surprising as diabetes is a major risk factor for Alzheimer’s.  Newer research is now suggesting that the relationship may begin sooner than the appearance of the diabetes.

Type two or “adult onset” diabetes has one of the most established relationships to dietary patterns.  It is largely a disease of “carbohydrate intolerance” brought on by excessive simple sugars and refined carbohydrates in the diet.  This pattern of eating over time leads to insulin resistance where cells become poorly responsive to insulin.  In the early stages the body produces excessive insulin trying to force cells to respond to insulin.  Blood sugar is maintained at normal levels by the excessive insulin so without measuring blood insulin levels the problem remains hidden.

The importance of the insulin resistance/normal blood sugar phase is that it has now been demonstrated that changes in brain function representing “pre-Alzheimer’s” occur in this phase.(1)  Using functional MRI which shows the ability of brain areas to activate during memory tasks, this study showed that in those with insulin resistance the core brain areas that process memory were impaired in their functioning.  The ability to process recall memory was also examined with a memory test called “what, where, when” (WWW).  Subjects are shown successive diagrams briefly and then their ability to recall what was seen, where it was in a diagram and when in the series it appeared. As the diagram shows, the WWW memory was diminished 50% in those with insulin resistance.

The concern with this observation is that the abnormal brain functioning seen in Alzheimer’s disease begins to be seen long before its onset when insulin resistance is present. New study has now shown that the process appears to begin even before insulin resistance occurs with the behavior that eventually causes insulin to dysfunction, simply eating higher amounts of sugar!

This new data emerged as a new part of the famous Framingham Heart Study.(2)  This branch of the study followed over 4200 adults with standard testing used to evaluate the presence of either pre-Alzheimer’s called MCI, or Alzheimer’s.  Testing included neuropsychological testing and volumetric MRI which is a sensitive measure of actual brain loss that is the hallmark of Alzheimer’s.  The adults were also assessed for daily sugary beverage intake.  Sugary beverage intake has been found to be a stable marker reflecting general sugar intake levels.  The findings were striking. 

The volumetric MRI showed that those who consumed 1 or more sugary beverages daily had a significantly greater loss of total brain volume, and this was especially present in the hippocampus, a primary memory processing area.  Neuropsychologic testing revealed a similar pattern on memory testing with significant losses associated with 1 sugary beverage/day and even greater loss with 2 or more.  They concluded that the memory loss was equivalent to 3.5 – 13 years of brain aging.

The researchers conclusions tell it all, “Our results provide further evidence that sugary beverage consumption is associated with markers of preclinical Alzheimer’s in humans.”  So while the earliest understanding of the relationship between the whole sugar dynamic was that elevated blood sugar in the form of diabetes increased Alzheimer’s risk, the current understanding suggests that relationship begins much earlier.  The next understanding was that the damage to the brain which drives Alzheimer’s could be shown in the early phase of prediabetes, insulin resistance. 

The most recent understanding is the damage begins even before insulin resistance begins simply associated with eating high amounts of sugar which correlates both with brain volume loss and impaired memory testing.  This relationship had been demonstrated in animals for about a decade.  The caution cited in these studies has been that the result may not translate into a relationship between sugar consumption and Alzheimer’s in humans as it does in animals.  The translation has now been done.

Some of the other important points the researchers discussed include:

·         Fruit juice contains the same sugar content as soft drinks and produces the same effects.

·         Diet soft drink consumption was also associated with lower brain volumes and is a concern.  They also induce higher insulin levels and likely drive insulin resistance also.

·         A 6-ounce serving of 100% juice exceeds the new recommended daily intake of sugar for children.

To get ahead of the rapidly increasing rates of Alzheimer’s we need to start with the modifiable lifestyle factors that are associated with the disease.  Consuming the amount of sugar that has become typical in the Western diet is a major one.

1)     Cheke et al.  Obesity and insulin resistance are associated with reduced activity in core memory regions of the brain. Neuropsychologia, 2017;96:137–149.

2)     Pase et al.  SUGARY BEVERAGE INTAKE AND PRECLINICAL ALZHEIMER’S DISEASE IN THE COMMUNITY.  Alzheimer’s & Dementia, 2017 ePub, 1-10.

Why is There a Developing Epidemic of Alzheimer’s or Dementia?

The dementia is a group of specific disorders where different parts of the brain degenerate causing symptoms such as memory loss, difficulty with aspects of functioning such as speech or behavior and eventually difficulty with all life functions.  Alzheimer’s is the most common form of dementia accounting for approximately 70% of this population.  While the ability to prevent and treat many other chronic diseases is improving, this has not been the case with Alzheimer’s and other dementias.  Some of the facts include:

·         Alzheimer’s is the only disease in the list of the 10 most common disease associated deaths that there is no available treatment that may prevent, cure or slow its progression. 

·         Approximately 200,000 adults in U.S. under the age of 65 years are already diagnosed with the disease.

·         Most will die from the disease within 4 to 8 years. 

·         It is perhaps the most costly disease involving greatest direct medical costs combined with great costs for long-term care. 

·         One in five (20%) individuals > 65 years have MCI (pre-Alzheimer’s) and many will convert to Alzheimer’s within 5 years.

·         Currently there are approximately 5 million adults with Alzheimer’s. 

·         This will double within 15 years and triple within 35 years resulting in a staggering $21 trillion in direct costs over that interval.

Given the inability of treatment to modify the disease once it is well established, the focus of favorably impacting the epidemic is shifting to prevention and aggressive early treatment.  Up to this point there had been little progress as treatment has been almost entirely focused on drug interventions.  To date there have been 244 drug trials for Alzheimer’s, and 243 produced no positive results in altering the course of the disease.  Only two classes of drugs have been approved for treatment, but they only “soften” symptoms in the short term and do not alter the progression of the disease.

The reasons for the disappointing treatment results are thought to relate to the fact that Alzheimer’s origins are multifactorial.  Dale Bredesen, MD, the Director of Neurodegenerative Disease Research, David Geffen School of Medicine at UCLA, describes the disease process as being like water leaking through a barn roof that has 36 holes.  Drug therapies have targeted one hole which does little to stop the roof from leaking during a heavy rain. 

The 36 factors that Dr. Bredesen discusses include genetic predispositions, environmental factors, metabolic factors and lifestyle driven factors.  While some are non-modifiable such as genetics and population aging, the majority are modifiable and therefore can be targeted with treatment.  The lifestyle/metabolic related factors are diverse such as vitamin B12 deficiency, low cell omega-3 levels, pre-diabetes, chronic high insulin levels, high inflammation and many more.

Dr. Bredesen has developed the first treatment approach that has actually demonstrated effectiveness in preventing the conversion of MCI into full Alzheimer’s as well as reversing mild Alzheimer’s itself.  The process involves measuring extensive numbers of variables and finding the collection that are imbalanced and contributing to the disease process in that given person.  Once the “triggers” are identified a diverse treatment program specific to each individual’s imbalances is designed and implemented.

One of the most interesting findings in the first group of patients treated with this process was that those who had genetic predispositions such as the apoE4 variant had equally good outcomes with intensive lifestyle management.  This is a very important finding as 75 million Americans have the abnormal apoE4 genetic predisposition and without changes to how things are currently being done, 30 million are destined to develop Alzheimer’s disease.  While individuals with the genetic risk have a greater tendency to develop the disease, they appear to respond well to tight metabolic regulation.  The genetic factors simply appear to make them more susceptible to errors in metabolic/lifestyle factors.

The population is aging, and age is a major risk factor for Alzheimer’s.  Approximately one in six individuals have genetic variations that increase their risk.  However, a rapidly changing factor that appears to be driving a significant portion of the increase in Alzheimer’s are the increases in metabolic/lifestyle factors.  Genetics and age are non-modifiable.  Fortunately, a major part of this puzzle is highly modifiable, and strong changes in this area have shown great promise in preventing and helping this disease.