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For years studies have suggested that eating blueberries and other berries is good for our health (here, here, and here). Now another study suggests that eating wild blueberries benefits children's thinking, specifically attention and "executive function" (mental processes which lets people plan, organize, and complete tasks). What was nice in this study was that it was "double-blind"- which meant that biases couldn't influence the results. 

Flavonoids are a diverse group of phytonutrients (plant chemicals) found in almost all fruits and vegetables. They are powerful antioxidants with anti-inflammatory and immune system benefits. And yes, other studies have also found various benefits to mental processes with an increase of flavonoids in the diet - in both children and adults.

What foods contain flavonoids? There are 6 main classes of flavonoids, and each is found in different foods: - Anthocyanidins – found in red, purple,and blue berries, red wine, and red and purple grapes. - Flavonols - found in onions, leeks, broccoli, Brussels sprouts, kale, tea, berries, beans, and apples. - Flavones - found in parsley, celery, and hot peppers. - Isoflavones - found in soybeans, soy products, and legumes. - Flavanones - found in citrus fruit and tomatoes. - Flavanols - found in tea, red wine, grapes, apples, fava beans, and cocoa. From Medical Xpress:

Primary school children could show better attention by consuming flavonoid-rich blueberries, following a study conducted by the University of Reading. In a paper published in Food & Function, a group of 7-10 year olds who consumed a drink containing wild blueberries or a matched placebo and were tested on their speed and accuracy in completing an executive task function on a computer.The double blind trial found that the children who consumed the flavonoid-rich blueberry drink had 9% quicker reaction times on the test without any sacrifice of accuracy. In particular, the effect was more noticeable as the tests got harder.

Previous [Univ. of] Reading research has shown that consuming wild blueberries can improve mood in children and young people, simple memory recall in primary school children, and that other flavonoid rich drinks such as orange juice, can also improve memory and concentration.

Wild blueberries are grown and harvested in North America, and are smaller than regular blueberries, and are higher in flavonoids compared to regular varieties. The double-blind trial used a flavonoid-rich wild blueberry drink, with a matched placebo contained 8.9 g of fructose, 7.99 g of glucose and 4 mg of vitamin C matching the levels of nutrients found in the blueberry drink. [Original study.] 

The following study looked at genes and longevity. Researchers from the University of Edinburgh analysed genetic information from more than 600,000 people along with records of their parents' lifespan.

They found that the following factors were correlated with longevity: not smoking or giving up smoking, a higher educational attainment, openness to new experiences, and good cholesterol levels. On the other hand, the following factors were correlated with reduced longevity ("were negatively correlated"): genetic susceptibility to coronary artery disease (CAD), smoking, lung cancer, diabetes, and higher body fat. For example, 1 year of education adds 11 months to expected lifespan, and gaining weight reduces life-span (lose 2 months for every 2.2 lbs extra weight), while losing extra weight increases it. From Science Daily:

Learning and staying in shape key to longer lifespan, study finds

People who are overweight cut their life expectancy by two months for every extra kilogramme [2.2 lbs.] of weight they carry, research suggests. A major study of the genes that underpin longevity has also found that education leads to a longer life, with almost a year added for each year spent studying beyond schoolOther key findings are that people who give up smoking, study for longer and are open to new experiences might expect to live longer.

Scientists at the University of Edinburgh analysed genetic information from more than 600,000 people alongside records of their parents' lifespan. Because people share half of their genetic information with each of their parents, the team were able to calculate the impact of various genes on life expectancy. Lifestyle choices are influenced to a certain extent by our DNA -- genes, for example, have been linked to increased alcohol consumption and addiction. The researchers were therefore able to work out which have the greatest influence on lifespan.

They found that cigarette smoking and traits associated with lung cancer had the greatest impact on shortening lifespan. For example, smoking a packet of cigarettes per day over a lifetime knocks an average of seven years off life expectancy, they calculated. But smokers who give up can eventually expect to live as long as somebody who has never smoked. Body fat and other factors linked to diabetes also have a negative influence on life expectancy.

The study also identified two new DNA differences that affect lifespan. The first -- in a gene that affects blood cholesterol levels -- reduces lifespan by around eight months. The second -- in a gene linked to the immune system -- adds around half a year to life expectancy. Data was drawn from 25 separate population studies from Europe, Australia and North America, including the UK Biobank -- a major study into the role of genetics and lifestyle in health and disease.  [Original study.]

A number of recent studies have suggested that as people age, the community of gut microbes (gut microbiota or gut microbiome) becomes less diverse than in younger people. And note that greater gut microbial diversity is generally viewed as healthy and good. However, now a study done in China finds a different result. The study examined the gut microbes of more than 1000 very healthy people, from ages 3 to over 100, and found that the gut microbial communities were very similar among very healthy people in their mid 30s to over 100 years in age.

Whether this is cause or effect is unknown. But the researchers speculate that the similarities in the gut microbiota among people from their 30s to 100+ is a consequence of an active healthy lifestyle and diet. And it suggests that somehow changing an elderly person's gut microbial community (if it's not "normal") to that of a 30-year-old might help promote health. From Science Daily:

'Ridiculously healthy' elderly have the same gut microbiome as healthy 30-year-olds

In one of the largest microbiota studies conducted in humans, researchers at Western University, Lawson Health Research Institute and Tianyi Health Science Institute in Zhenjiang, Jiangsu, China have shown a potential link between healthy aging and a healthy gut.

With the establishment of the China-Canada Institute, the researchers studied the gut bacteria in a cohort of more than 1,000 Chinese individuals in a variety of age-ranges from 3 to over 100 years-old who were self-selected to be extremely healthy with no known health issues and no family history of disease. The results showed a direct correlation between health and the microbes in the intestine. ....The study, published this month in the journal mSphere, showed that the overall microbiota composition of the healthy elderly group was similar to that of people decades younger, and that the gut microbiota differed little between individuals from the ages of 30 to over 100.

"The main conclusion is that if you are ridiculously healthy and 90 years old, your gut microbiota is not that different from a healthy 30 year old in the same population," said Greg Gloor, the principal investigator on the study and also a professor at Western's Schulich School of Medicine & Dentistry and Scientist at Lawson Health Research Institute. Whether this is cause or effect is unknown, but the study authors point out that it is the diversity of the gut microbiota that remained the same through their study group.

"This demonstrates that maintaining diversity of your gut as you age is a biomarker of healthy aging, just like low-cholesterol is a biomarker of a healthy circulatory system," Gloor said. The researchers suggest that resetting an elderly microbiota to that of a 30-year-old might help promote health. "By studying healthy people, we hope to know what we are striving for when people get sick," said Reid. [Original study.]

Centenarian in Bama County, China. Credit: National Geographic.

Interesting study finding - that both high and low levels of magnesium is associated with a higher risk of dementia. Magnesium is an essential mineral needed for more than 300 biochemical reactions in the body. According to a large study done in the Netherlands of people who were followed for about 8 years - there was a U-shaped incidence of dementia based on their levels of magnesium. The lowest incidence was in those with "in the middle" normal levels of magnesium in the blood. All the study participants were mentally healthy when the study started.

The researchers stated that magnesium levels are considered "relatively stable over time", but a limitation of the study is that they only looked at magnesium levels once - at the beginning of the study, so they could have changed over time. Of course further studies are needed. [Other posts on magnesium and health - here, here, and here.]

Magnesium is widely available in foods. Foods that are good sources of magnesium include: spinach and other dark green leafy vegetables, almonds, cashews, peanuts, bananas, soybeans, kidney and black beans (legumes), whole grains, lentils, seeds, yogurt, brown rice, potatoes, and avocados. It is recommended that magnesium is obtained from the diet, and not from supplements (due to health risks from high doses). From Science Daily:

Both high, low levels of magnesium in blood linked to risk of dementia

People with both high and low levels of magnesium in their blood may have a greater risk of developing dementia, according to a study published in the September 20, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology.

The study involved 9,569 people with an average age of 65 who did not have dementia whose blood was tested for magnesium levels. The participants were followed for an average of eight years. During that time, 823 people were diagnosed with dementia. Of those, 662 people had Alzheimer's disease. The participants were divided into five groups based on their magnesium levels. Both those with the highest and the lowest levels of magnesium had an increased risk of dementia, compared to those in the middle group.

Both the low and high groups were about 30 percent more likely to develop dementia than those in the middle group. Of the 1,771 people in the low magnesium group, 160 people developed dementia, which is a rate of 10.2 per 1,000 person-years. For the high magnesium group, 179 of the 1,748 people developed dementia, for a rate of 11.4 per 1,000 person-years. For the middle group, 102 of the 1,387 people developed dementia, for a rate of 7.8. Kieboom noted that almost all of the participants had magnesium levels in the normal range, with only 108 people with levels below normal and two people with levels above normal[Original study.]

Once again a study finds that pesticide exposure is linked to an adverse health effect - that pesticide exposure in the home during pregnancy and early childhood is linked to an elevated risk of brain tumor in the child. Other studies have also found that pesticides used in the home are associated with a higher risk of childhood cancers.

This is because pesticides do cross the placental barrier, as the study researchers point out: "There is evidence that pesticides cross the fetal-placental barrier since residues of some insecticides have been found in umbilical cord blood, neonatal hair, and meconium following maternal exposure during pregnancy." Also, the International Agency for Research on Cancer (IARC) has classified "more than twenty pesticide chemical compounds as potential human carcinogens".

The following are examples (but there are more) of other studies finding pesticide and childhood cancer links: A meta-analysis published in 2015 in Pediatrics by researchers at Harvard University found that children exposed to indoor insecticides (also herbicides) have a higher risk of certain childhood cancers, specifically leukemia, lymphomas, and brain tumors. A 2013 study published in Cancer Causes and Control found that professional pest control applications in the home within a year of conception and during pregnancy was associated with a higher risk of childhood brain tumors. A review of studies published in 2010 found that pesticide exposure during pregnancy and childhood increased the risk of childhood leukemia.

The good news is that there are alternatives to exposing fetuses and children to toxic pesticides at home - by using alternative ways of dealing with pests, such as least toxic Integrated Pest Management (IPM) or organic methods. That means doing other things (such as sealing or caulking holes, putting out traps and baits, vacuuming), a focus on least toxic methods and on prevention (here and here), rather than routinely applying toxic pesticides. If needed, least toxic pesticides include boric acid and vinegar. Other sources of pesticide exposure for pregnant women and children are foods and exposure in settings outside the home - perhaps even a friend's yard. By the way, pesticide exposure for everyone is linked to a higher risk of health problems, not just pregnant women and children.

From Science Daily: Pesticide use during pregnancy linked to increased risk of childhood brain tumors

Previous epidemiological studies have suggested that exposure to pesticides during pregnancy may have a possible role in the development of childhood brain tumors. In a new International Journal of Cancer analysis, researchers found a link between maternal residential pesticide use -- particularly insecticides -- and the risk of childhood brain tumorsThe analysis included 437 malignant childhood brain tumor cases and 3102 controls from two French studies. Pesticide use was associated with a 1.4-times increased risk of childhood brain tumors.

The investigators noted that many pesticide compounds are classified as probable carcinogens, and there is evidence that some insecticides can pass through the feto-placental barrier. "Although such retrospective studies cannot identify specific chemicals used or quantify the exposure, our findings add another reason to advise mothers to limit their exposure to pesticides around the time of pregnancy," said Nicolas Vidart d'Egurbide Bagazgoïtia, lead author of the study. [Original study.]

The following study was presented at the recent annual meeting of the Infectious Diseases Society of America. A study of women prone to recurrent urinary tract infections (UTIs) found that increasing daily fluid intake by 1.5 liters of water a day (about three 16-ounce glasses) in addition to their usual daily fluid intake - had a reduced incidence of UTIs that year by 48%, as compared to women who drank their usual daily fluid amount (1.2 liters). So the women who drank about 2.8 liters (water and other beverages) a day had 1.6 UTIs that year on average, and the women who drank their usual fluid amount had 3.1 UTIs on average. Which also resulted in fewer courses of antibiotics in the increased water group. A great result.

Bottom line: Drinking a lot more fluids daily (to flush the bacteria in the bladder and urinary tract) may benefit those with recurrent UTIs. [See more posts on UTI research, and the one treatment that many swear by as truly effective (D-mannose)]. From Futurity:

Women who get frequent UTIs may reduce risk by drinking plenty of water

Drinking an additional three pints of water a day may keep the urinary tract infection (UTI) away - at least for women who are prone - suggests a study being presented at IDWeek [Infectious Diseases Society of America Week] 2017. The study found women at risk of UTIs who increased their water intake by about that much water every day were nearly half as likely to get UTIs as women who did not.

Women are more likely to get UTIs than men in part because the urethra is shorter, meaning it is easier for bacteria to travel from the rectum and vagina to the bladder. Drinking more fluids increases the rate of flushing of bacteria from the bladder and also likely reduces the concentration of bacteria that enter the bladder from the vagina. This reduces the opportunities for bacteria to attach to cells that line the urinary tract, which is necessary to cause an infection, Dr. Hooton said.

The study included 140 healthy premenopausal women who had at least three UTIs in the last year and reported low daily fluid intake. Half of the women (70) who served as the control group continued their usual daily fluid intake, while the remainder were told to drink 1.5 liters of water a day (about three 16-ounce glasses) in addition to their usual daily fluid intake. After one year, women in the control group had 3.1 UTIs on average, whereas those in the water group had 1.6 UTIs on average, a 48 percent reduction. As a result, the water group averaged fewer regimens of antibiotics (1.8) than the limited-water group (3.5), a reduction of 47 percent.

Researchers followed the women throughout the year using visits and telephone calls. They documented that over the course of the study, on average women in the water group increased their daily water intake by 1.15 liters (about 2-1/2 pints) for a total daily fluid intake (including water and other beverages) of 2.8 liters, whereas women in the control group did not increase the amount of water they drank and had a total daily fluid intake of 1.2 liters.

OK, this study was done in mice, but it's the kind of study results that everyone hopes (and thinks) is also true for humans. So drink a nice cuppa black tea and think about how you're increasing bacteria in the gut associated with weight loss.

Black tea (as well as green tea) has polyphenols that stimulate the growth of gut bacterium and the formation of short-chain fatty acids. By the way, the mice were given decaffeinated tea extracts, so theoretically both decaf and caffeinated tea should have benefits. The big question though is - will drinking black tea daily actually result in weight loss? From Medical Xpress:

Black tea may help with weight loss, too

UCLA researchers have demonstrated for the first time that black tea may promote weight loss and other health benefits by changing bacteria in the gut. In a study of mice, the scientists showed that black tea alters energy metabolism in the liver by changing gut metabolites. The research is published in the European Journal of Nutrition. The study found that both black and green tea changed the ratio of intestinal bacteria in the animals: The percentage of bacteria associated with obesity decreased, while bacteria associated with lean body mass increased.

Previous studies indicated that chemicals in green tea called polyphenols are absorbed and alter the energy metabolism in the liver. The new findings show that black tea polyphenols, which are too large to be absorbed in the small intestine, stimulate the growth of gut bacterium and the formation of short-chain fatty acids, a type of bacterial metabolites that has been shown to alter the energy metabolism in the liver.

The researchers also collected samples from the mice's large intestines (to measure bacteria content) and liver tissues (to measure fat deposits). In the mice that consumed either type of tea extract, there was less of the type of bacteria associated with obesity and more of the bacteria associated with lean body mass. However, only the mice that consumed black tea extract had an increase in a type of bacteria called Pseudobutyrivibrio, which could help explain the difference between how black tea and green tea change energy metabolism.

The new study also concluded that both green tea and black tea have different effects on liver metabolism. According to Henning, the molecules in green tea are smaller and can more readily be absorbed into the body and reach the liver directly, while black tea molecules are larger and stay in the intestine rather than being absorbed. When black tea molecules stay in the intestinal tract, they enhance the growth of beneficial bacteria and the formation of microbial metabolites involved in the regulation of energy metabolism. [Original study.]

A newly published study suggests that exercising an hour or more per week could lower the incidence of depression. The study followed 33,000 adults in Norway  for 11 years, and found that an hour or more of weekly exercise was associated with 12% fewer cases of developing depression. But note that it didn't prevent anxiety. Interestingly, the researchers found that "regular leisure-time exercise of any intensity" had these positive effects - it doesn't have to be aerobic or incredibly strenuous exercise. Exercise is associated with a number of biological changes that could have an impact on mental health. From Science Daily:

One hour of exercise a week can prevent depression

A landmark study led by the Black Dog Institute has revealed that regular exercise of any intensity can prevent future depression -- and just one hour can help. Published in the American Journal of Psychiatry, the results show even small amounts of exercise can protect against depression, with mental health benefits seen regardless of age or gender.

In the largest and most extensive study of its kind, the analysis involved 33,908 Norwegian adults who had their levels of exercise and symptoms of depression and anxiety monitored over 11 years. The international research team found that 12 percent of cases of depression could have been prevented if participants undertook just one hour of physical activity each week.

A healthy cohort of participants was asked at baseline to report the frequency of exercise they participated in and at what intensity: without becoming breathless or sweating, becoming breathless and sweating, or exhausting themselves. At follow-up stage, they completed a self-report questionnaire (the Hospital Anxiety and Depression Scale) to indicate any emerging anxiety or depression.

Results showed that people who reported doing no exercise at all at baseline had a 44% increased chance of developing depression compared to those who were exercising one to two hours a week. However, these benefits did not carry through to protecting against anxiety, with no association identified between level and intensity of exercise and the chances of developing the disorder. [Original article.]

Is frequent sauna bathing beneficial? That's what one study suggests. When the study started all 1621 men (aged 42 to 60) had normal blood pressure and none had been diagnosed with hypertension, and the follow-up was about 22 years later. The study took place in Finland, where sauna bathing is an important part of the culture - for all men, from all walks of life. The study found that frequent sauna bathing lowered the risk of developing hypertension - 46% when comparing men who sauna bathed once a week vs those who sauna bathed 4 to 7 times a week.

How could sauna bathing have these effects? There are several possibilities, but one is that sauna bathing produces "acute vasodilation" of the blood vessels, which leads to a significant drop in blood pressure. The temperature in the sauna is usually from 80 °C to 100 °C (176 to 212 degrees Fahrenheit), and the average sauna session (in this study) lasted an average of 14.4 minutes. From Science Daily:

Frequent sauna bathing keeps blood pressure in check

Frequent sauna bathing reduces the risk of elevated blood pressure, according to an extensive follow-up population-based study carried out at the University of Eastern Finland. The risk of developing elevated blood pressure was nearly 50% lower among men who had a sauna 4-7 times a week compared to men who had a sauna only once a weekThe same researchers have previously shown that frequent sauna bathing reduces the risk of sudden cardiac death, and cardiovascular and all-cause mortality. Elevated blood pressure is documented to be one of the most important risk factors of cardiovascular diseases.

The Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD) involved 1,621 middle-aged men living in the eastern part of Finland. Study participants without elevated blood pressure of over 140/90 mmHg or with diagnosed hypertension at the study baseline were included in this long-term follow-up study. Based on their sauna bathing habits, men were divided into three sauna frequency groups: those taking a sauna once a week, 2-3 times a week, or 4-7 times a week. During an average follow-up of 22 years, 15.5% of the men developed clinically defined hypertension. The risk of hypertension was 24% decreased among men with a sauna frequency of 2-3 times a week, and 46% lowered among men who had a sauna 4-7 times a week.

Sauna bathing may decrease systemic blood pressure through different biological mechanisms. During sauna bathing, the body temperature may rise up to 2 °C degrees, causing vessels vasodilation. Regular sauna bathing improves endothelial function, i.e. the function of the inside layer of blood vessels, which has beneficial effects on systemic blood pressure. Sweating, in turn, removes fluid from the body, which is a contributing factor to decreased blood pressure levels. Additionally, sauna bathing may also lower systemic blood pressure due to overall relaxation of the body and mind.

[NOTE: Above photo is of interior of a modern Finnish sauna. Credit: Wikipedia]

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.