Stephanie Seneff: Why Low-Fat Diets And Statins May Cause Alzheimer's

MONDAY, JULY 21, 2014

APOE-4: THE CLUE TO WHY LOW-FAT DIET AND STATINS MAY CAUSE ALZHEIMER'S

ABSTRACT

Alzheimer's is a devastating disease whose incidence is clearly on the rise in America. Fortunately, a significant number of research dollars are currently being spent to try to understand what causes Alzheimer's. ApoE-4, a particular allele of the apolipoprotein apoE, is a known risk factor. Since apoE plays a critical role in the transport of cholesterol and fats to the brain, it can be hypothesized that insufficient fat and cholesterol in the brain play a critical role in the disease process. In a remarkable recent study, it was found that Alzheimer's patients have only 1/6 of the concentration of free fatty acids in the cerebrospinal fluid compared to individuals without Alzheimer's. In parallel, it is becoming very clear that cholesterol is pervasive in the brain, and that it plays a critical role both in nerve transport in the synapse and in maintaining the health of the myelin sheath coating nerve fibers. An extremely high-fat (ketogenic) diet has been found to improve cognitive ability in Alzheimer's patients. These and other observations described below lead me to conclude that both a low-fat diet and statin drug treatment increase susceptibility to Alzheimer's.

1. INTRODUCTION

Alzheimer's is a devastating disease that takes away the mind bit by bit over a period of decades. It begins as odd memory gaps but then steadily erodes your life to the point where around-the-clock care is the only option. With severe Alzheimer's, you can easily wander off and get lost, and may not even recognize your own daughter. Alzheimer's was a little known disease before 1960, but today it threatens to completely derail the health system in the United States.

Currently, over 5 million people in America have Alzheimer's. On average, a person over 65 with Alzheimer's costs three times as much for health care as one without Alzheimer's. More alarmingly, the incidence of Alzheimer's is on the rise. Dr. Murray Waldman has studied epidemiological data comparing Alzheimer's with femur fractures, looking back over the last fifty years [52]. Alarmingly, he has found that, while the incidence of femur fractures (another condition which typically increases with age) has gone up only at a linear rate, the increase in the incidence of Alzheimer's has gone up exponentially, between 1960 and 2010 Alzheimer's Epidemic [15]. Just between 2000 and 2006, US Alzheimer's deaths rose by 47%, while, by comparison, deaths from heart disease, breast cancer, prostate cancer, and stroke combined decreased by 11%. This increase goes far beyond people living longer: for people 85 and older, the percentage who died from Alzheimer's rose by 30% between 2000 and 2005 [2]. Finally, it's likely these are under-estimates, as many people suffering with Alzheimer's ultimately die of something else. You likely have a close friend or relative who is suffering from Alzheimer's.

Something in our current lifestyle is increasing the likelihood that we will succumb to Alzheimer's. My belief is that two major contributors are our current obsession with low-fat diet, combined with the ever expanding use of statin drugs. I have argued elsewhere that low-fat diet may be a major factor in the alarming increase in autism and adhd in children. I have also argued that the obesity epidemic and the associated metabolic syndrome can be traced to excessive low-fat diet. Statins are likely contributing to an increase in many serious health issues besides Alzheimer's, such as sepsis, heart failure, fetal damage, and cancer, as I have argued here. I believe the trends will only get worse in the future, unless we substantially alter our current view of "healthy living."

The ideas developed in this essay are the result of extensive on-line research I conducted to try to understand the process by which Alzheimer's develops. Fortunately, a great deal of research money is currently being spent on Alzheimer's, but a clearly articulated cause is still elusive. However, many exciting leads are fresh off the press, and the puzzle pieces are beginning to assemble themselves into a coherent story. Researchers are only recently discovering that both fat and cholesterol are severly deficient in the Alzheimer's brain. It turns out that fat and cholesterol are both vital nutrients in the brain. The brain contains only 2% of the body's mass, but 25% of the total cholesterol. Cholesterol is essential both in transmitting nerve signals and in fighting off infections.

A crucial piece of the puzzle is a genetic marker that predisposes people to Alzheimer's, termed "apoE-4." ApoE plays a central role in the transport of fats and cholesterol. There are currently five known distinct variants of apoE (properly termed "alleles"), with the ones labelled "2", "3" and "4" being the most prevalent. ApoE-2 has been shown to afford some protection against Alzheimer's; apoE-3 is the most common "default" allele, and apoE-4, present in 13-15% of the population, is the allele that is associated with increased risk to Alzheimer's. A person with apoE-4 allele inherited from both their mother and their father has up to a twenty-fold increased likelihood of developing Alzheimer's disease. However, only about 5% of the people with Alzheimer's actually have the apoE-4 allele, so clearly there is something else going on for the rest of them. Nonetheless, understanding apoE's many roles in the body was a key step leading to my proposed low fat/statin theory.

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Graham