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Choline appears to be a neglected nutrient. It is essential for healthy brain functioning, yet researchers of a recent study say the great majority of us do not get the recommended daily intake of choline in our diet. They suggest that this could be causing harm to our health, including the brain.

They also pointed out that since eggs and meat are the best dietary source, people on restricted or vegan diets are especially at risk of a choline deficiency. It is not found in most multivitamins.

The  Arizona State Univ. researchers found that choline deficiency is involved with multiple health problems throughout the body (e.g., inflammation, insulin production, cardiovascular disease, brain function) and even Alzheimer's disease. Their study was conducted on mice, but they felt similar processes occurred in humans.

Good dietary sources of choline: eggs, meat, dairy products, poultry, and fish. Lower amounts are in nuts, beans, potatoes, and cruciferous vegetables (e.g., broccoli).

Related to all this is that one should also try to lower intake of anti-cholinergic medications, if possible. Studies find that their use is linked to cognitive decline and dementia - they block the action of the brain neurotransmitter acetylcholine (which is produced by choline).

Excerpts from Science Daily: Study explores effects of dietary choline deficiency on neurologic and system-wide health

Choline, an essential nutrient produced in small amounts in the liver and found in foods including eggs, broccoli, beans, meat and poultry, is a vital ingredient for human health. A new study explores deficiency in dietary choline adversely affects the body and may be a missing piece in the puzzle of Alzheimer's disease.  ...continue reading "The Nutrient Choline Is Necessary For Brain Health"

Fabulous news for those persons wanting to reduce their risk of Alzheimer's disease as they age - get a flu vaccine, especially annually. A recent large study found that with each annual vaccine received in adults 65 years and older, the protective effect increases. That's it! So simple.

The study authors compared 935,887 flu-vaccinated patients and 935,887 non-vaccinated patients. At the start of the study, no one had an Alzheimer's diagnosis. They found a 40% lower risk of an Alzheimer's diagnosis in those receiving flu vaccines compared to individuals not receiving a flu vaccine in the following 4 years.

Other studies have had similar findings, as well as that getting other vaccines in adulthood also reduce the risk of dementia, such as pneumonia, tetanus, polio, and herpes vaccines. Current thinking is that this protective effect from vaccines is due to their immunological effects - that they boost the immune system in a good way.

From Science Daily: Flu vaccination linked to 40% reduced risk of Alzheimer's disease

People who received at least one influenza vaccine were 40% less likely than their non-vaccinated peers to develop Alzheimer's disease over the course of four years, according to a new study from UTHealth Houston. ...continue reading "The Flu Vaccine is Linked to a Lower Risk of Developing Alzheimer’s Disease"

Something surprising - having cancer is linked to a lower risk of Alzheimer's disease and a lower risk of neurodegenerative symptoms (e.g., memory loss) during their lifetimes.

One big analysis and review of 22 studies (representing more then 9.6 million people!) calculated that cancer diagnoses are associated with 11% reduction in Alzheimer's disease occurrence. However, this relationship does not hold true for melanoma. [Also, there is a strong positive correlation between melanoma and Parkinson's disease - which is a neurodegenerative condition.]

There are some theories, but it is still unknown why this lower risk of Alzheimer's disease occurs in persons with cancer.

Excerpts from The Scientist: Cancer Tied to Reduced Risk of Alzheimer’s Disease

In recent years, scientists around the world have been probing an unexpected trend: The risk of developing cancer seems to have an inverse relationship with the risk of developing Alzheimer’s disease.  ...continue reading "Reduced Risk of Alzheimer’s Disease In Those With Cancer"

A recent study found that eating higher levels of foods with flavonoids (e.g. berries, apples, and tea) may lower the risk of later development of Alzheimer's disease and other age-related dementias.

Since currently there are no effective drugs that prevent or actual medical treatments for dementia, it is great that what a person eats (the dietary pattern) long-term may be protective. Something we can do to lower our risk for Alzheimer's disease and other dementias!

Tufts University researchers followed 2801 persons (50 years and older) for 20 years and found that those with the lowest intake of flavonoid rich foods (especially 3 flavonoid classes: flavonols, anthocyanins, and flavonoid polymers) had a 20 to 40% higher chance of developing Alzheimer's disease and other dementias, when compared to those eating the most flavonoid rich foods. [Note: The lowest intake group averaged  about 1 1/2 apples, but no berries or tea per month.]

Flavonoids are naturally occurring bioactive pigments, of which there are 7 types, that are found in plant-based foods. Some good sources of different types of flavonoids include berries & red wine (anthocyanin rich), onions & apples, pears (flavonol rich), citrus fruits and juices, teas, dark chocolate, parsley, celery,and soy products.

Eating a variety of fruits and vegetables appears to be best for health benefits. There is no one super-food. Other studies also find that the Mediterranean diet, which emphasizes fruits and vegetables (thus flavonoid rich), may reduce the risk of cognitive decline and dementia, including Alzheimer's disease.

Why are flavonoid containing foods protective, specifically "neuroprotective"? Studies suggest that they do the following: antioxidant effects, protect neurons from neurotoxins and combat neuroinflammation, and favorable changes in brain blood flow,

Excerpts from Science Daily: More berries, apples and tea may have protective benefits against Alzheimer's

Older adults who consumed small amounts of flavonoid-rich foods, such as berries, apples and tea, were two to four times more likely to develop Alzheimer's disease and related dementias over 20 years compared with people whose intake was higher, according to a new study led by scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University.  ...continue reading "Eating More Fruits and Berries Lowers Risk of Dementia"

In the last few years a number of researchers have suggested that microbes may be triggering or somehow causing Alzheimer's disease. Various microbes have been suggested, and research is finding links with herpes viruses, fungi, other microbes, and gum disease (periodontal disease) microbes. Now another study proposes that the common bacteria Porphyromonas gingivalis - which causes chronic periodontal disease, is linked to the development of Alzheimer's disease.

Researchers have suggested that during an initial infection, the "infectious agent" (viruses, etc.) reaches the central nervous system and brain, then stays there in latent form (inactive) for years. And then when the immune system declines with age (which is a normal part of aging) - the microbes (virus, fungi, etc.) become reactivated and cause inflammation and the chain of events leading to Alzheimer's disease.

Note that in the recent study implicating P. gingivalis - the Cortexyme, Inc. company is doing the research and they, of course, are developing a product - so beware of bias. Also, the research done so far is in the earliest stages. But...it is exciting to see if further research (from them and from others) supports some sort of microbe, or several types of microbes, behind the development of Alzheimer's disease. Will we find that there is an "infectious cause" of Alzheimer's disease ("infection-induced neuroinflammation")? Because this means that there is a way to prevent or treat Alzheimer's disease - some sort of antimicrobial, antibiotic, antiviral, or antifungal. Stay tuned for further research.... From Medical Xpress:

Bacterial pathogen Porphyromonas gingivalis may contribute to Alzheimer's disease: Study

Cortexyme, Inc., a privately held, clinical-stage pharmaceutical company developing therapeutics to alter the course of Alzheimer's disease (AD) and other degenerative disorders, today announced publication of a foundational paper supporting its approach in Science Advances. In the paper, an international team of researchers led by Cortexyme co-founders Stephen Dominy, M.D. and Casey Lynch detail the role of a common bacterium, Porphyromonas gingivalis (Pg), in driving Alzheimer's disease pathology, and demonstrate the potential for small molecule inhibitors to block the pathogen.  ...continue reading "Periodontal Disease Link to Alzheimer’s Disease?"

New research is published every day, but only some studies are big research stories or game-changers. The following are what I consider some of the most memorable studies of 2018 – some in a good way, but some of the others have left me with a sense of horror. I think there will be follow-up research, so keep an eye out for more on these important topics.

Are we heading toward a time in the not so distant future when all men are infertile? (Due to exposure to all the endocrine disruptors around us.) Will All Men Eventually Be Infertile? This was posted September 5, 2018.

Researchers are now seriously investigating and finding evidence that microbes may be causing Alzheimer’s disease. This approach is rapidly finding support in the medical field, and may lead to possible ways to treat or prevent the disease. Possible Herpes Virus Link to Alzheimer’s Disease was posted July 13, 2018, and Herpes Viruses and Alzheimer's Disease on  June 22, 2018.

Type 2 Diabetes May Be Reversed With Weight Loss was posted August 10, 2018. This study and an earlier similar study from 2016 found that losing over 30 pounds over a short period can reverse type 2 diabetes - 46% in the 2018 study and 60% (in people who had it less than 10 years) in the earlier study.

More and more evidence is accumulating that certain diets are anti-inflammatory. Especially beneficial are diets rich in fruits, vegetables, seeds, nuts, legumes (beans), and whole grains - which also have a lot of fiber. This is exciting research because chronic low-grade inflammation is linked to a number of chronic diseases (heart disease, cancer, etc.). Fruits, Vegetables, and Whole Grains Lower Inflammation – posted August 1, 2018.

[Related to this last topic is one of the most eye-opening studies I have ever read on how what one eats has a quick effect on gut microbes and health of the gut (including inflammation of the colon): Changing Diet Has Big Effect On Colon Cancer Risk – posted April 28, 2015.]

Over the last few decades, the mainstream theory of Alzheimer's disease (amyloid deposits build up in the brain) and medical treatments (drugs) just hasn't led anywhere. Nothing has worked to stop Alzheimer's disease. But evidence is building for an alternative view - that microbes in the brain are leading to the development of Alzheimer's disease (here and here). Now new compelling evidence from studies implicates several strains of herpes virus in Alzheimer's disease. At least one study has suggested herpes zoster, others the common herpes simplex, while other studies suggest other herpes strains. Which means that treatment could perhaps involve anti-viral drugs! (Wouldn't it be great if that works???)

In one study researchers found that human herpes virus DNA and RNA were more abundant in the brains of those diagnosed with Alzheimer's disease and that "abundance correlated with clinical dementia scores" - meaning the more of it, the sicker the person was. And the two viruses they found to be most strongly associated with Alzheimer's, HHV-6A and HHV-7, were not as abundant in the brains of those with other neurodegenerative disorders.

The article mentions another recently published study from Taiwan. This amazing study looked at more than 33,000 individuals in Taiwan and found that patients with herpes simplex infections (HSV) may have a 2.56-fold increased risk of developing dementia. And they found that the use of anti-herpetic (antiviral) medications in the treatment of HSV infections was associated with a decreased risk of dementia - that the risk dropped back down "to baseline". The conclusion was that the antiviral medication reduced the risk of Alzheimer’s by keeping the herpes infection in check. Yes! Finally, a way foreward in this horrible disease.

Scroll down and read what one group of researchers says: "Our model right now is that it’s not just a single microbe, but a disturbance in the brain microbiome that can lead to Alzheimer’s disease.”

From A. Azvolinsky's article at The Scientist: Herpes Viruses Implicated in Alzheimer’s Disease

The brains of Alzheimer’s disease patients have an abnormal build up of amyloid-β proteins and tau tangles, which, according to many researchers, drives the ultimately fatal cognitive disease. This theory is being amended to a newer one, which posits that microbes may trigger Alzheimer’s pathology ...continue reading "Herpes Viruses and Alzheimer’s Disease"

The last post dealt with the link between highly processed food and increased risk of cancer. Now an interesting article written by Dr. Lisa Mosconi (Associate Director of the Alzheimer’s Prevention Clinic at Weill Cornell Medical College/New York -Presbyterian Hospital) refers to that study when discussing research about lifestyles (and especially diet) and later Alzheimer's disease.

It'll be interesting to see how this research plays out - is her approach stressing diet (and avoiding ultra-processed food and trans fats) and lifestyle correct or not? Much of what she says definitely makes sense and is supported by research, such as the negative health effects of chronic inflammation, and how eating actual, real foods has beneficial health effects. On the other hand, vitamin, mineral, and fish oil supplements generally don't show those health benefits (as she discusses here).

Currently there are a number of theories about causes of Alzheimer's disease (including the role of microbes), as well as a number of drug treatments that so far have gone nowhere. If Dr. Mosconi's research interests you, then read the interview she did in 2017. [In the interview she talks about the importance of exercise, intellectual stimulation, social networks, and the benefits of eating real foods rather than supplements. She recommends: drink water, eat fish, eat vegetables and fruit, eat glucose rich foods, and don't eat highly processed and fast foods.]  From Quartz:

The road to Alzheimer’s disease is lined with processed foods

Dementia haunts the United States. There’s no one without a personal story about how dementia has touched someone they care for. But beyond personal stories, the broader narrative is staggering: By 2050, we are on track to have almost 15 million Alzheimer’s patients in the US alone. ... It’s an epidemic that’s already underway—but we don’t recognize it as such. The popular conception of Alzheimer’s is as an inevitable outcome of aging, bad genes, or both.  ...continue reading "Ultra-Processed Foods and Alzheimer’s?"

Another article was published this month raising the issue of whether Alzheimer's disease is caused by a microbe - which can explain why all the medicines and experimental drugs aimed at treating the "tangles" or amyloid plaques in the brain are not working as a treatment (because that's the wrong approach). The microbe theory of Alzheimer's disease has been around for decades, but only recently is it starting to be taken seriously. Some of the microbes found in patients with Alzheimer's disease (from analyses of both normal brains and Alzheimer patient brains after death): fungi, Borrelia burgdorferi (Lyme disease), herpes simplex virus Type 1 (HSV1), and Chlamydia pneumoniae.

The general hypotheses seem to be that Alzheimer’s disease is caused by infection, but it isn't linked to any one pathogenic microbe.  Instead, the evidence seems to support that "following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation". So the microbes act as "triggers" for Alzheimer's disease - the microbes get into the brain, and immune responses somehow eventually result in the amyloid plaques and Alzheimer's disease. From The Scientist:

Do Microbes Trigger Alzheimer’s Disease?

In late 2011, Drexel University dermatology professor Herbert Allen was astounded to read a new research paper documenting the presence of long, corkscrew-shape bacteria called spirochetes in postmortem brains of patients with Alzheimer’s disease. Combing data from published reports, the International Alzheimer Research Center’s Judith Miklossy and colleagues had found evidence of spirochetes in 451 of 495 Alzheimer’s brains. In 25 percent of cases, researchers had identified the spirochete as Borrelia burgdorferi, a causative agent of Lyme disease. Control brains did not contain the spirochetes.

Allen had recently proposed a novel role for biofilms—colonies of bacteria that adhere to surfaces and are largely resistant to immune attack or antibiotics—in eczema....  Allen knew of recent work showing that Lyme spirochetes form biofilms, which led him to wonder if biofilms might also play a role in Alzheimer’s disease. When Allen stained for biofilms in brains from deceased Alzheimer’s patients, he found them in the same hippocampal locations as amyloid plaquesToll-like receptor 2 (TLR2), a key player in innate immunity, was also present in the same region of the Alzheimer’s brains but not in the controls. He hypothesizes that TLR2 is activated by the presence of bacteria, but is locked out by the biofilm and damages the surrounding tissue instead.

Spirochetes, common members of the oral microbiome, belong to a small set of microbes that cross the blood-brain barrier when they’re circulating in the blood, as they are during active Lyme infections or after oral surgery. However, the bacteria are so slow to divide that it can take decades to grow a biofilm. This time line is consistent with Alzheimer’s being a disease of old age, Allen reasons, and is corroborated by syphilis cases in which the neuroinvasive effects of spirochetes might appear as long as 50 years after primary infection.

Allen’s work contributes to the revival of a long-standing hypothesis concerning the development of Alzheimer’s. For 30 years, a handful of researchers have been pursuing the idea that pathogenic microbes may serve as triggers for the disease’s neuropathology..... In light of continued failures to develop effective drugs, some researchers, such as Harvard neurobiologist Rudolph Tanzi, think it’s high time that more effort and funding go into alternative theories of the disease. “Any hypothesis about Alzheimer’s disease must include amyloid plaques, tangles, inflammation—and, I believe, infection.”

Herpes simplex virus type 1 (HSV1) can acutely infect the brain and cause a rare but very serious encephalitis. In the late 1980s, University of Manchester molecular virologist Ruth Itzhaki noticed that the areas of the brain affected in HSV1 patients were the same as those damaged in patients with Alzheimer’s disease. Knowing that herpes can lie latent in the body for long periods of time, she began to wonder if there was a causal connection between the infection and the neurodegenerative disorder.

Around the same time, neuropathologist Miklossy, then at the University of Lausanne in Switzerland, was detailing the brain damage caused by spirochetes—both in neurosyphilis and neuroborrelia, a syndrome caused by Lyme bacteria. She happened upon a head trauma case with evidence of bacterial invasion and plaque formation, and turned her attention to Alzheimer’s. She isolated spirochetes from brain tissue in 14 Alzheimer’s patients but detected none in 13 age-matched controls. In addition, monoclonal antibodies that target the amyloid precursor protein (APP)—which, when cleaved, forms amyloid-β—cross-reacted with the spirochete species found, suggesting the bacteria might be the source of the protein.

Meanwhile, in the U.S., a third line of evidence linking Alzheimer’s to microbial infection began to emerge. While serving on a fraud investigation committee, Alan Hudson, a microbiologist then at MCP-Hahnemann School of Medicine in Philadelphia, met Brian Balin.... Soon, Balin began to send Hudson Alzheimer’s brain tissue to test for intracellular bacteria in the Chlamydia genus. Some samples tested positive for C. pneumoniae: specifically, the bacteria resided in microglia and astrocytes in regions of the brain associated with Alzheimer’s neuropathology, such as the hippocampus and other limbic system areas. Hudson had a second technician repeat the tests before he called Balin to unblind the samples. The negatives were from control brains; the positives all had advanced Alzheimer’s disease. "We were floored,” Hudson says.

Thus, as early as the 1990s, three laboratories in different countries, each studying different organisms, had each implicated human pathogens in the etiology of Alzheimer’s disease. But the suggestion that Alzheimer’s might have some microbial infection component was still well outside of the theoretical mainstream. Last year, Itzhaki, Miklossy, Hudson, and Balin, along with 29 other scientists, published a review in the Journal of Alzheimer’s Disease to lay out the evidence implicating a causal role for microbes in the disease.

The microbe theorists freely admit that their proposed microbial triggers are not the only cause of Alzheimer’s disease. In Itzhaki’s case, some 40 percent of cases are not explained by HSV1 infection. Of course, the idea that Alzheimer’s might be linked to infection isn’t limited to any one pathogen; the hypothesis is simply that, following infection, certain pathogens gain access to brain, where immune responses result in the accumulation of amyloid-β, leading to plaque formation.

Surprised...is how I felt after reading this study. According to the study, activity levels and exercise in mid-life are not linked to cognitive fitness and dementia later on in life. Instead, higher levels of physical activity and exercise has a beneficial effect on the brain in the short term (e.g., within 2 years or so). This finding of no long-term benefits, but only short-term benefits to the brain from exercise, is contrary to some other (cross-sectional) studies, but is supported by another recent study ("no evidence of a neuroprotective effect of physical activity").

The beauty of this study is that it followed 646 people for 30 years (from a median age of 46 years in 1978 and 77 years in 2008). The negative is that according to this study, physical exercise in mid-life does not seem to delay or prevent the onset of dementia and Alzheimer's later on in life. Eh... From Medical Xpress:

Physical activity in midlife not linked to cognitive fitness in later years, long-term study shows

A study led by Johns Hopkins Bloomberg School of Public Health researchers that tracked activity levels of 646 adults over 30 years found that, contrary to previous research, exercise in mid-life was not linked to cognitive fitness in later yearsThe finding suggests that physical activity may not help maintain cognitive function, or help avoid or delay the onset of the debilitating conditions like dementia and Alzheimer's

The study, which appears online in the Journal of Alzheimer's Disease, did find that activity levels among study participants in the later years were associated with high cognitive function two years later. This supports earlier research findings that exercise may help to maintain cognitive fitness in the short term.

There is no known treatment or cure for Alzheimer's or dementia, syndromes that involves declining memory, confusion and eventually limited ability to perform daily tasks. To date, there are no preventive measures, such as physical exercise, brain games or a diet regimen, that have been proven to help delay or altogether prevent its onset. The researchers undertook the study because of a growing consensus that physical activity levels helps prevent Alzheimer's, however much of the evidence for this thinking is based on cross-sectional studies that compare responses from one group of participants with another at a given point in time or within a very short duration, typically several years..... That's where longitudinal studies, which look at the same group of participants over a long time, are more helpful.

The researchers used data from the Johns Hopkins Precursors study.... The researchers used responses from 1978 through 2008 from 646 participants (598 men, 48 women) to calculate so-called metabolic equivalents, which quantify physical activity levels. Participants were also asked whether they regularly exercise to a sweat. The team administered cognitive tests in 2008, and, using participants' medical records, scored for dementia through 2011. The researchers identified 28, or 4.5 percent of the cohort, to have Alzheimer's.

No physical activity measure in mid-life was associated with late-life cognitive fitness or onset of dementia. The study confirmed findings of other cross-sectional studies, that higher levels of physical activity and exercise measured close in time to the cognitive testing were associated with better cognitive functioning. The authors also looked at whether patterns of change in physical activity levels over the life span were associated with cognitive health and found no relationships.

The idea that exercise might play a role in preventing or limiting Alzheimer's makes sense, the researchers say, because physical activity, at least in mouse models, has shown less accumulation of B-amyloid plaques, which are thought to play a role in dementia, including Alzheimer's. In addition, physical activity improves blood flow to the brain, which is linked to better cognitive performance. This may explain why studies find that exercise may contribute to cognitive fitness in the short term.