General information about Alzheimer’s Disease:
Before I start answering the “can mold cause Alzheimer’s” question, let’s first review some general information about this dreaded disease. Statistics from the Alzheimer’s Association cite over 5 million Americans have Alzheimer’s disease (AD), which accounts for 60 to 80 percent of all cases of dementia. That number includes 11 percent of individuals age 65 and older and one-third of those age 85 and older. Alzheimer’s disease impacts families more than you would think. If you have a family member with this disease (as I do—my mom), you will understand the statistics I’m about to cite are likely on the “low end.” Research reveals this disease impacts more than 15 million family members, friends, and caregivers. Per the Alzheimer’s Association, an estimated 16 million Americans and 106 million people worldwide will be diagnosed with Alzheimer’s disease by 2050 unless greater strides are made.
After cardiovascular disease and cancer, Alzheimer’s disease is now the third leading cause of death in the United States. Just as we have biomarkers which allow us to predict who will develop heart disease and some cancers so too do we have a genetic marker for some Alzheimer’s- susceptible people. Based upon a genetic evaluation of risk for all types of what is called the ApoE gene, the projections for disease change. You have a lifetime risk of approximately 15% when you factor in all of the ApoE genotypes.
Then the statistics are more staggering. As many as 45 million of the 318 million Americans now alive may develop AD during their lifetimes without taking preventive measures. While this article is not about brain diets, the best brain supplements or even overall brain health, let me mention that we are making great strides in the non-drug world towards the prevention of Alzheimer’s disease and even treatment.
While there is no actual effective treatment of Alzheimer’s disease, some clinical trials which include dietary intervention, exercise, and supplementation—all called “metabolic enhancement” (MEND)—have yielded promising results. In fact, I personally am conducting a small clinical trial where we expand upon MEND, with positive results thus far. The basics are an anti-inflammatory diet plan with intermittent fasting, daily exercise, lots of brain boosting supplements and bioidentical hormones.
One of the latest strategies put forth by the UCLA group is to identify specific sub-types of Alzheimer’s disease which are likely to respond to different treatment options. Their metabolic profiling in Alzheimer’s patients has revealed three distinguishable types of Alzheimer’s disease.
Three Types of Alzheimer’s
Type 1 is described as being high for systemic inflammation, reflected in laboratory tests such as a high CRP (also a marker for coronary artery placquing), a low albumin:globulin ratio, and high inflammatory cytokine levels such as interleukin-1 and interleukin-6.
Type 2 Alzheimer’s is characterized by marked reductions in hormonal levels such as progesterone, estradiol, testosterone, and vitamin D. This type often shows labwork revealing an increased homocysteine level as well as insulin resistance.
Type 3 Alzheimer’s is quite different from the other two categories, and a different pathological brain process may be the cause. Of interest, all of the Type 3’s had a genetic predisposition for “mold toxicity” per HLA testing. Approximately 24% of the population has an immune system which doesn’t “clear” biotoxins such as mold toxins properly. Again, all of the Type 3’s fell into one of these genetic sub-types. The onset of cognitive dysfunction in Type 3’s is typically younger (late 40s to early 60s). Also, the ApoE genotype is usually 3/3 instead of 4/4 or 3/4.
Their family history is negative (or only positive at much higher age). Their onset of symptoms usually follows a period of great stress and/or loss of quality sleep. Anesthesia or hormonal changes such as menopause or andropause may trigger onset as well. Presenting symptoms focus less on memory and more on “executive function” (judgment) deficits. Depression is also often an associated symptom.
Brain imaging studies on the Type 3 patients as well as neuropsychological studies also tend to be markedly different. Laboratory studies often reveal low levels of zinc (common in CIRS–see below), and some patients have labs suggestive of adrenal fatigue with reduced pregnenolone, DHEA-S and/or an increased AM cortisol.
What caused researchers to wonder “can mold cause Alzheimer’s?”
I’ll answer this directly at the end of this section. Let’s first review some “brain facts” about Alzheimer’s. We know Alzheimer’s disease causes deficits in memory, ability to think clearly, behavioral issues and more. The most common (but certainly not the only) early symptom of Alzheimer’s is difficulty remembering newly learned information. The reason for this is that Alzheimer’s changes generally begin in the part of the brain that affects learning. In addition, the notable changes in the brain of AD patients are:
Loss of nerve cells (neurons).
The presence of neuritic amyloid plaques (protein deposits that collect between nerve cells, or neurons) with a little sidebar from me on this. All of the current research is a race toward a drug to dissolve these plaques. However, one of the amazing benefits of curcumin is that it dissolves amyloid plaques likely better than any drug ever will. In my educated opinion, amyloid is not the chicken—it’s the egg.
I strongly feel that amyloid and tau proteins are formed in the brain as the brain is injured. Sure, it’s a great idea to start getting rid of plaque build up when you are in your 30’s. However, this is not, again, in my opinion, the solution for Alzheimer’s disease.
The presence of neurofibrillary tangles (twisted fibers in the nerve cells; theorized to contribute to cellular breakdown).
Brain inflammation (swelling).
Brain shrinkage (atrophy).
Experts who study and treat CIRS (mold and other biotoxin illness) report that some of the major symptoms of mold illness include manifestations of brain involvement that can be demonstrated on NeuroQuant testing.
CIRS can cause problems with memory, thinking, behavior, emotions, and even patterns of speech.
Let’s get more specific:
To sum up what you need to know if you’re reading this “for yourself” or “for a loved one” is that the individuals who have been treated by Dale Bredesen, M.D.-head Neurologist at UCLA for CIRS (inflammatory mold disease) are a sub-class of individuals who have been diagnosed with Alzheimer’s. According to his published research and some ongoing research, the “Type 3 Alzheimer’s” patients have all responded positively to a complex mycotoxin-binding protocol established for the treatment of CIRS.
Dr. Bredesen and his team tests all potential study patients for HLA typing. This allows them to see if they fall into the approximately 24% of the population who is sensitive to biotoxins. To clarify, this means their immune system can’t recognize and clear them the way that the other 75% of the population is able to do. The results: Yes. In fact, each and every one of them does. Is it possible that some “Type 2 and Type 1” patients are CIRS patients as well? In my opinion, there certainly is that distinct possibility, but there are no current studies. Because of that possibility, I personally am HLA testing all patients who are “presenting” with symptoms of Alzheimer’s and asking about potential mold exposure.
If toxic mold can cause Alzheimer’s how prevalent is this?
Estimates reveal Type 3 Alzheimer’s represents approximately 10% of the patients with Alzheimer’s disease, therefore potentially affecting hundreds of thousands of Americans. This potential epidemic may have gone unrecognized to date for the same reasons most doctors are not familiar with the diagnosis or treatment of mycotoxin illness. The reasons are: (1) The Type 3’s have been hidden beneath the large group of patients with Alzheimer’s disease without consideration of a metabolic analysis. (2) CIRS is neither widely recognized nor even considered in evaluations at neurological centers which specialize in dementia. (3) Standard assessments for patients presenting with mild cognitive impairment don’t include lab testing for the innate system immune over-stimulation which is the hallmark of CIRS.
There are tens of thousands of reported cases of CIRS without dementia. In addition, there are examples of Type 3 Alzheimer’s disease without CIRS. But, with the world of toxins we live in, that makes me personally wonder how many neuro-toxins have gone unaccounted. Is this just a coincidence you may ask? Well, hardly. Despite the fact that both Alzheimer’s disease and CIRS are relatively common illnesses, there is much supporting evidence to qualify Type 3 Alzheimer’s as being a predominantly mycotoxin-induced illness. Most patients with Type 3 Alzheimer’s disease also have laboratory abnormalities typical of CIRS. Then there are the repeated findings of biotoxin-sensitive HLA haplotypes in Type 3 Alzheimer’s disease patients. In addition, not mentioned previously, there has been the documentation of neurotoxin-producing mold in the homes of these individuals as well as their positive response to “mold detox treatment.”
As someone with an HLA haplotype which is biotoxin sensitive, a recent history you have likely read about in other posts, and with a mother diagnosed 15 years ago with what I now know is Type 3 Alzheimer’s disease, perhaps my view is a bit skewed to look carefully for cases of CIRS and now, cases of Type 3 Alzheimer’s. Despite my scrutiny of the literature linking mold to things like weight gain, auto-immune disease, metabolic syndrome and, now more than ever, Type 3 Alzheimer’s disease I think that the 10% estimate is low.
Let’s first consider that an estimated 50% of buildings in America are water-damaged and thus prone to toxic mold growth.
Then let’s take the statistic that 24% of Americans are genetically programmed to be unable to “clear” biotoxins. Next, consider the statistic that is low—the estimate that only 10% of Alzheimer’s diagnoses are Type 3’s. That means a bare minimum of 1.6 million Americans will be Type 3-CIRS Alzheimer’s cases by 2050 diagnosed properly or not. Note that doesn’t take into consideration all of the cases of CIRS which go un-diagnosed.
Instead, people are treated with biologics for auto-immune disease, drugs for high cholesterol, and their memory deficits are chalked up to getting older, being ill or being on drugs. The amount of people who might have some degree of CIRS is statistically about 80 million. That’s a whole lot of people! Of those, the research just hasn’t been done on how many Type 1’s or 2’s might be “out there.” Can mold cause Alzheimer’s? I hope you understand that indeed it can and that you share your new-found knowledge with friends and family.
My case for the need to test all “comers” with cognitive deficits is based on my CIRS statistics which show that 100 percent of those studied and diagnosed have some sort of “CIRS-footprint” on their brain NeuroQuant test. Who knows how deep this epidemic actually goes? Contact me if you think this applies to you or a loved one.
References: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586104/ and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4789584/