Alzheimer’s dementia is not a normal part of the aging process. Still, the most significant risk factor is increasing age, with most of those with Alzheimer’s disease 65 years and older.

For those who get it at a younger age, we refer to it as early-onset Alzheimer’s disease. These younger folks can be in the condition’s early, middle, or late stages.

We may conveniently divide Alzheimer’s disease into two forms:

• Common Alzheimer’s disease. Those with early-onset Alzheimer’s disease have the common form. It progresses similar to AD seen in older adults.
• Genetic (familial) Alzheimer’s disease. This type of AD is uncommon. Symptoms typically emerge while individuals are in their 30s, 40s, or 50s. Family history is the only known risk factor for genetic (familial) Alzheimer’s disease.

Dementia is the product of brain cell damage, with this injury interfering with brain cells’ communicating with one another. Without good inter-nerve cell chatting, behavior and feelings can change.

Dementia: A global public health epidemic

Dementia is a global health issue of increasing importance. There are tremendous negative consequences for numerous socioeconomic measures (and the burden on sufferers).

By 2030, over 82 million people — and over 150 million by 2050 — will have Alzheimer’s dementia. Unfortunately, there are no curative treatments, and we don’t understand why the disease occurs.

For those without the less common genetic form, why does dementia happen? Researchers are examining shared genetics with other diseases to understand better the biological mechanisms underlying Alzheimer’s disease.

A new study adds support for a brain-gut connection.

The gut-dementia connection

Family history is the only known risk factor for Alzheimer’s dementia. We have to do better in identifying causes. Now comes an innovative study connecting the gut microbiome to the brain and dementia risk.

Several studies demonstrate the co-occurrence of dementia (especially Alzheimer’s) with gut disorders such as gastritis, the gut microbiome, and certain medicines (such as proton pump inhibitors) used to treat peptic ulcer disease.

Gut-brain axis

While such studies suggest an association between Alzheimer’s and gastrointestinal tract disorders, it is unclear whether the gut issues are risk factors for dementia or vice-versa. The gut-brain axis exists for other central nervous system problems such as Parkinson’s disease and depression.

Today we examine an Australian study that comprehensively analyzes the link between Alzheimer’s disease and gut disorders. While we will learn that they could not find a causal relationship between dementia and the gastrointestinal tract, they did find shared genes and enrichment of autoimmunity and more.

The gut, the brain, genetics, and dementia

The research investigation incorporated data from historical genome-wide association studies. They looked for patients with Alzheimer’s dementia, gastroesophageal reflux disease (heartburn), peptic ulcer disease, irritable bowel syndrome, inflammation of the stomach and small intestine (gastritis-duodenitis).

The final group analysis represented more than 450,000 individuals. Here are the results:

All the gastrointestinal tract disorders (except irritable bowel syndrome) appeared to correlate with Alzheimer’s dementia.

Among the biological factors examined, abnormal cholesterol appeared to underscore the gut-brain connection. Abnormal cholesterol appeared to be a risk factor for gut disorders and Alzheimer’s dementia.

The study authors suggest that cholesterol-lowering statin drugs (such as atorvastatin or lovastatin) be studied to see if they help protect the gut and, in turn, the brain.

My take — The gut, brain, and dementia

Of course, correlation is not causality: We don’t have evidence that gut disorders cause Alzheimer’s or vice-versa. Still, the researchers point to a Mediterranean-type diet — one rich in natural fats and vegetables — as not a bad idea.

The researchers report no relevant financial relationships. Thank you for joining me in this look at the relationship between the gut and Alzheimer’s dementia.

The post Is Our Gut a Key to Whether We Get Dementia? appeared first on Medika Life.

The Chinese have figured out that they have a giant environmental problem. Folks in Beijing, some days, literally can’t breathe. Over a million Chinese die prematurely every year because of air pollution. — Joe Biden

Alzheimer’s disease isn’t a disease of old age; it begins in infancy, possibly even before birth, because of pollution. Pollution, therefore, initiates the death spiral even before children can walk and talk. 

Babies’ fates are sealed by the pollution created in the air we breathe, the water we drink, and the pollutants in the food we eat as well as the oceans in which we swim. 

Not a fancy of fanatical environmental groups, the facts are coming in daily with ever-increasing disturbing research making a strong case for pollution as the ultimate brain destroyer. 

In the Beginning

Somewhere in the Eastern or Western hemispheres, a baby is born. A gift from God, the people, may say, but the child is already damaged by the greed, carelessness, and behavior that had betrayed this infant’s trust before it even knew trust existed. 

Detailing how this child has been damaged before birth, after birth, and into its childhood and adult years is a torturous route. The journey reveals a total disregard for this planet, its oceans, its air, and every living creature on it. Is that why we want to go to other planets and explore the stars? 

We’ve worked diligently to ruin Earth, and it is going to be an incredibly difficult, dangerous, and expensive repair. Uppermost in this chain of events that must take place to return health to the planet is our behavior and our business models. 

Both go hand-in-hand and contribute to this early beginning demise of an infant’s brain.

Urban planners, too, have played their role in this dire drama of destruction. For example, once the most powerful man in New York State, Robert Moses, believed that highways were the city’s future and that of Long Island. Accordingly, he began to destroy neighborhoods and build highways through the city and out to Long Island. 

In a minor effort at goodwill for children, Moses created something in addition to highways; playgrounds. Where were the playgrounds placed? All of them were along the highways that Moses was building. When air pollution was of no concern to him or most others, the children in those playgrounds inhaled deeply. 

The kids took in the lead and all of the damaging byproducts of automobile emissions. They didn’t have to eat lead paint, they inhaled lead and the residual microgarbage from car tires.

Lead is one of the most invasive substances to burrow its way into the brain, where it stays forever, causing developmental damage. These children would carry this “gift” from Moses with them for the rest of their lives.

Moses’ plans were cut short by an urban activist, Jane Jacobs, who saw how the city plans were damaging. Readers can catch a glimpse of the battle for New York City here and a documentary here.

A Climate Change Pioneer Ignored

One hundred-sixty-four years ago, when no one thought about the environment or the new science of ecology and climate change wasn’t a word in any books, one woman stands out. Eunice Foote published a paper in 1856 on the heat-trapping effects of CO2. Climate change science and the greenhouse effect were born.

Foote’s paper was left to languish (on p. 382) in the back of a prestigious journal, The American Journal of Science and Arts, and basically ignored. A scientist, feminist, and pioneer in climate change science, she would write long before “Silent Spring” by Rachel Carson. A brief animation of the effects of climate change can be viewed here. 

Now that we’ve waited for so many years to notice how the climate is warming, we have to face that infant’s realities and how this all came to be.

The Word Is Plastics

The scene from “The Graduate” comes to mind whenever I hear this word. However, the miracle product, plastics, for consumers and manufacturers has become the bane of our existence. Wrapping everything imaginable in plastic and then discarding it became a way of life. Who thought it wouldn’t break down, and we’d be fine? 

Even clothing contains cloths derived from plastic. Natural fibers have been pushed out of the market, and we are encouraged to keep buying more clothing to keep up with the latest fashions. The garbage keeps piling up as a result.

One of my oceanography professors decades ago told us about plastics and The Sargasso Sea. An area rich in seaweed, the “sea,” serves both as a birthing and protective area for sea life, but it has one other main distinction: the North Atlantic garbage patch. But plastics don’t merely float there.

Plastic debris absorbs toxic chemicals, potentially poisoning anything that eats it. Microbes that eat plastics may not be the solution for which we prayed. This is because “…it’s unclear whether this enzyme or similar enzymes, are safe to use in widespread environmental remediation.” 

But that’s only part of the equation leading us to that baby that greeted the world with its first cry. The real danger, which may be worse than what we can see, is the unseen plastic; microplastic is found in our food and the air we breathe.

The Seen and Unseen Plastic Menace

As the bits of plastic degrade into smaller and smaller bits of microplastic (MP), the danger to that just-born child increases. 

MP are of special concern since their bioaccumulation potential increases with decreasing size. MP may be ingested by various organisms ranging from plankton and fish to birds and even mammals, and accumulate throughout the aquatic food web. In addition, plastics contain a multitude of chemical additives and adsorb organic contaminants from the surrounding media. Since these compounds can transfer to organisms upon ingestion, MP act as vectors for other organic pollutants and are, therefore, a source of wildlife exposure to these chemicals.

By the year 2025, we are estimated to have dumped over 11 billion tons of plastics in our environment where the winds will take the tiny bits and spread them to urban and wilderness areas. We will have done an excellent job of destroying our living space. 

Worse than that, we will have contributed to the painful disabilities of the world’s infants and children with all forms of pollution. What an accomplishment to put into history books.

Some scientists are now referring to a phenomenon called “plastic rain,” which is spiraling the Earth. The normal earth atmospheric movement, the Coriolus Effect, would indicate “that while urban centers may be the initial source, plastics accumulate in the atmosphere over longer time periods, are transported long distances, and are deposited during favorable conditions such as slower air-mass velocities or intersections with mountain ranges.” Contamination by plastic pollution, therefore, can be found anywhere on Earth. How much pollution is on Mt. Everest?

Of course, we will have continued our staunch attack on our oceans, too. Almost 16 million tons of microplastics are expected to be currently or soon to be embedded in the ocean floor. The total of it all, including in the Mariana Trench, is “up to 35 times more than the estimated weight of plastic pollution on the ocean’s surface.”

Thanks to all for the discarded plastic coffee cups, the shopping bags, food trays, trinkets, toys, and many other “disposable” plastic objects. And let’s not forget the clothing industry with its ever-changing designs to create a constant need to buy new and discard the old. In 2017, it was estimated to generate $2.5 trillion in business. Many garments are made from plastic-derived fabrics.

Childhood, Pollution, and Alzheimer’s

Research with older adults has found a relationship between Alzheimer’s and air pollution. In one study in China, long-term exposure to air pollution showed poor performance on nonverbal and math tests. Obviously, this does not indicate Alzheimer’s since that disease can only be, at this time, established on autopsy. But it points to a form of cognitive decline and dementia other than Alzheimer’s (SDAT).

A second study in England of adults age 50 to 79 with Alzheimer’s and living in greater London found that 39% of those with the highest annual concentration of air pollution in their areas showed the highest degree of dementia; up to 1.4 times the risk of those living in areas with lower pollution concentration. 

Another study in the United States of 998 women showed a greater decline in the learning of words for those exposed to a high concentration of air pollution in the preceding three years. Neuroimaging also indicated atrophy of the brain in areas typically affected by Alzheimer’s.

A study of 19,000 retired nurses found that those exposed over the years to fine particle pollution experienced faster cognitive decline than those who had not been in these polluted areas.

The internal combustion engine exhaust has been established as one source of pollution, augmenting cognitive decline in numerous studies.

However, children get an early start on pollution-related brain damage, as shown by another study in Mexico City. 

Alzheimer’s disease starts in children’s brainstems and has been found in residents of Mexico City as young as 11 months of age. According to this research, “Alzheimer’s disease starting in the brainstem of young children (is) affecting 99.5% of young urbanites in a serious health crisis.”

On autopsy, typical amyloid-beta was found at age 11 months, and in children and teens, there was a noted loss of neuronal density, loss of synapses, and changes to the hippocampus.

We strongly suggest the first two decades of life are critical for brain damage associated to environmental pollutant exposures, and although there is no doubt considerable individual AD progression differences are likely determined by APOE and factors such as gender, metabolism, nutrition, genetics, occupational history and others.

Pollution Impairment and Dementia

As has been shown by studies of pollution, the air we breathe may have an effect on and possible involvement in diseases such as Parkinson’s and multiple sclerosis. But new research appears to have proven this untrue.

Researchers note a higher incidence of dementia but not Parkinson’s disease or multiple sclerosis related to proximity to major highways. A study in Canada looked at a large cohort of patients who were free of these diseases. 

They did a meta-analysis of a group of 243,611 incident cases of dementia, 31,577 cases of Parkinson’s disease, and 9,247 cases of multiple sclerosis between the years 2001 in 2012. There appeared to be a strong dementia relationship between urban residents who lived in major cities near major traffic roads and who had never moved for a period of years. 

The conclusion of the researchers was that “living close to heavy traffic was associated with a higher incidence of dementia but not with Parkinson’s disease or multiple sclerosis.” 

One pollutant that appears to be evident in many of these studies and it is lead pollution from vehicles. One other problematic pollutant was nitrogen dioxide (NO2), but it is lead that is the greater danger, according to one expert in the field. 

Unlike NO2, lead persists in the human body, with more than 95% of the adult
body burden of lead stored in bones, where it can remain for decades. Stored
lead is mobilised when bone turnover is higher than the normal turnover
rate — ie, in patients with osteoporosis. Consequently, mobilisation of stored
lead coupled with decline of bone mineralisation in elderly Canadian
residents means that their blood lead levels can remain elevated many years
after road-borne lead exposure.Early exposure, therefore, remains with us for a lifetime. 

The evidence regarding children and brain damage, similar to Alzheimer’s related to air pollution, is shocking. If nothing else, it is reasonable to show strong concern for the air we breathe. But pollution may not be confined to lead because plastic rain may also play a role as can the contaminants in the foods we eat. 

The post Is Alzheimer’s Damage Linked to Deadly Pollution of Babies, Not Old Age? appeared first on Medika Life.

“I don’t know who this man is and he keeps getting into bed with me,” the woman said in a noticeably frightened voice. “I keep telling him my husband will be coming home,” she said, “but he won’t leave.”

The man was her husband, and the woman was experiencing Early-onset or Young-onset Alzheimer’s, a neurological disorder that can affect younger persons in their 30s, 40s, or 50s. Seen less frequently in clinical practice, it can be misdiagnosed and is of great concern.

One current theory is that this type of Alzheimer’s may be familial, but a similar form is found in those with Down Syndrome. Estimates suggest that 50 percent or more of people with Down syndrome will develop dementia due to Alzheimer’s disease as they age.

Younger Alzheimer’s patients may face stigmas and stereotypes about the disease. Due to their young age, people with young-onset Alzheimer’s may find that others do not believe they have the disease or question the diagnosis. It’s also not uncommon to be told your symptoms may be related to stress, menopause, or depression.

People with young-onset Alzheimer’s may lose relationships or jobs as a consequence of this misunderstanding instead of being identified as medically ill or disabled.

The woman, in this case, was in her mid-50s, attractive, well-groomed, and was from a socially prominent family with considerable financial resources. Beginning a year or two before her clinical assessment at an Alzheimer’s clinic, she had persuaded her husband that thieves were coming into their home. She began to have insomnia because of her fear and became socially isolated.

Triple security systems were installed, but she still insisted they were in danger and should keep a gun in their bedroom. Then, she began to suspect that her husband wasn’t her husband at all.

It was time for more certain clinical measures. The diagnosis was Early-onset Alzheimer’s, but since no records were available, a familial connection couldn’t be made.

Although it is Early-Onset Alzheimer’s Disease (EOAD), there are several differences in symptoms that increase the likelihood of misdiagnosis.

Individuals with early-onset Alzheimer’s demonstrate more often atypical presentations than those with late-onset Alzheimer’s disease. Many of those with early-onset don’t have significant memory loss initially — the classic hallmark symptom of Alzheimer’s.

Their disease progression does not begin with symptoms of forgetfulness. Some of these individuals present with visual symptoms — inability to see the full picture giving them in essence a “tunnel vision”, impaired depth perception or inability to recognize faces — or impaired speech/difficulty coming up with words in conversation.

But, according to some studies, early-onset Alzheimer’s disease also progresses much faster than late-onset.

Why Early-onset Alzheimer’s?

Most types of early-onset Alzheimer’s disease are the same, but there are a few small distinctions:

Common Alzheimer’s disease. The majority of people with early-onset Alzheimer’s disease have the common form of Alzheimer’s disease. The disease will progress in roughly the same way as it does in older people with Alzheimer’s disease.

Genetic Alzheimer’s disease. This form is extremely rare. A few hundred people have genes that directly contribute to Alzheimer’s disease. These people begin showing symptoms of the disease in their 30s, 40s, or 50s.

Although much is still to be discovered about both types of Alzheimer’s, one study of nuns in the Midwest has provided some interesting insights. The researchers noted that mood and education might play significant roles in any dementia.

One interesting aspect of the lives of the nuns was that they maintained a lifestyle of continuous learning. One nun made it her chore to learn a new language every year, if possible.

“A pattern of emotional expression that accentuates positive
affect undoubtedly has behavioral correlates that could enhance or
disrupt the positive effects on physiology and health.”

One nun in the study had physiological evidence at her death that defied the theories about how Alzheimer’s develops in any patient.

Sister Mary, the gold standard for the Nun Study, was a remarkable woman who had high cognitive test scores before her death at 101 years of age. What is more remarkable is that she maintained this high status despite having abundant neurofibrillary tangles and senile plaques, the classic lesions of Alzheimer’s disease.

Education, too, may play a significant role in the development of Alzheimer’s (AD). As noted in recent work in neurology, “protective environmental factors, like increased education, may promote brain resistance against β-amyloid pathology in both sporadic and autosomal dominant AD.” The accumulation of amyloid is believed to promote the development of memory impairment. Is learning one of the keys to prevention?

Is Prevention Possible?

The theories about the development of AD have centered around genetics, the tau protein, beta-amyloid plaques, and tangles, and now diet is being considered.

Not all studies have shown a link between eating well and a boost in cognition. Overall, the evidence suggests, but does not prove, that following a Mediterranean or similar diet might help reduce the risk for Alzheimer’s dementia or slow cognitive decline.

The dietary theory is based on the fact that certain foods like fish may provide anti-inflammatory and antioxidant properties that protect the brain. These foods, then, could inhibit the development of beta-amyloid deposits and promote the maintenance of normal brain functioning.

The jury is still out on both Early-Onset Alzheimer’s and the form in older patients, but a number of both environmental and genetic factors are in play.

Resources:

1. Early-Onset Alzheimer’s Disease: A Resource List
2. Living with Alzheimer’s: For Younger-Onset Alzheimer’s
3. Education may be protective for people with gene for familial early-onset Alzheimer’s

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