Alzheimer’s disease is mostly marked by dementia that includes memory problems, cognitive problems, executive dysfunction, and changes in attitude and behavior. Most people with this disease also have signs of a mental disorder. Careful attention and medicine can help with these signs for a short time, but there are no specific ways to stop or cure Alzheimer’s disease.

Dementia mostly affects older people, and the rates of occurrence and prevalence rise with age. This is more common in low- and middle-income countries and places. It is putting a lot of stress on families and societies in terms of money and illness. What does this mean for you if you have someone in your family with AD?

Based on studies of twins, AD is thought to be passed down 70% of the time. Clinically diagnosed AD has found more than 70 genomic loci in people with mostly European heritage. The discovery of these new genomic loci must be taken with a grain of salt.

Let’s look at what genetic inheritance can and cannot do and what may affect it. Even if you had a gene for a specific illness, even a serious mental illness, it might never be what we call “expressed” because there are a variety of things that must coalesce to make that happen.

A cell’s gene expression code is similar to a cookbook. Essential for all bodily functions, each gene is a blueprint for the production of a particular protein. The frequency with which your genes are activated or deactivated, or expressed, depends on a number of conditions.

At birth, you have a blueprint for your genes in the form of your DNA. But environmental factors, including your diet, level of physical activity, and smoking status, can affect gene expression. You name it; it can be impacted by factors including the medications you take.

Also, your gene expression might alter with age or specific medical issues. Although your DNA cannot be changed, there are certain things that can be altered, such as your lifestyle and the environment in which you are born. You can use this to keep yourself healthy and control certain medical issues.

Stress is one of the factors that has been indicated to potentially push these genes to become evident in behaviors, but what else could do it? There are too many variables regarding what might cause it to flare up, and the problem becomes knowing you have a gene for something specific and wondering if you will ever experience it in a behavior of some type.

It is possible that more than a third of cases of dementia could be avoided. Getting kids to go to school and exercise more, keeping up with friends and family, smoking less or quitting altogether, and taking care of hearing loss, depression, diabetes, high blood pressure, and obesity could all help avoid or delay dementia. There is also some early information about other risk factors that might be able to be changed.

What Does This Mean?

It is possible that further research based on these results may help diagnose and cure diseases in the future. Those who are concerned about the possibility of AD, or who have been found to have the genes, should consider the following:

1 Stay Informed: Learn about current research and developments in Alzheimer’s disease, the genetic basis of the disease, and how this can be managed through changes in lifestyle.

2. Talk about genetic risks. If your family has a history of Alzheimer’s disease, you should see your doctor about genetic testing to assess your risk.

3. Stick to the basics when it comes to keeping fit and avoiding illness — a healthy diet, regular exercise, keeping the mind active, and the control of chronic diseases such as diabetes and hypertension.

4. Consider participating in research. It is important that more people from different backgrounds become a part of the study to help advance research and develop more personalized treatments.

5. Keep talking to your doctor. Genetic study is interesting, but the best way to handle health issues is to prevent them from happening in the first place through the help of current treatments. If there is anything that you have concerns about or what to do next, you should report it to your healthcare provider.

How Do Interventions Work?

Lifestyle: Engaging in mental exercises on a regular basis, such as solving puzzles, reading, or picking up new skills, can help build cognitive reserve and potentially postpone the start of symptoms.

Sleep: The brain is able to eliminate toxic proteins and consolidate memories when you maintain a quality sleep routine of seven to eight hours per night.

Stress management: Reduced cortisol levels, which can eventually harm brain cells, are one benefit of stress management practices like mindfulness and meditation.

Smoking and alcohol: Promoting brain health through avoiding smoking and limiting alcohol use helps to maintain adequate blood flow and reduce inflammation. Smoking acts as a stress-reduction technique because nicotine is a natural substance reducing anxiety, but the downside is cancer.

Aerobic exercise promotes neuronal and synaptic growth by increasing blood flow to the brain, which carries oxygen and nutrients. By keeping insulin sensitivity high, resistance exercise protects against cognitive loss caused by diabetes and promotes overall brain health. Physical exercise improves clearance processes, which may lower beta-amyloid plaques, a characteristic of Alzheimer’s disease. Regular moderate exercise, even for just 150 minutes a week, improves cardiovascular health, decreases inflammation, and drastically reduces the risk of Alzheimer’s disease.

Socialization: The brain’s neural connections and plasticity are both supported by the cognitive stimulation that occurs during regular social contact, which is a key component of socialization. Potentially as a result of less stress and a stronger feeling of purpose, those with strong social networks have slower rates of cognitive deterioration. One of the most effective ways to stave off cognitive loss is to participate in group activities that mix socializing with mental or physical demands. Dementia risk factors include social isolation; in fact, research suggests that those who are lonely may have twice the chance of getting Alzheimer’s as those who have strong social connections.

Diet: The anti-inflammatory features of the Mediterranean and MIND diets have been associated with a substantially reduced risk of Alzheimer’s disease. These diets are rich in leafy greens, berries, nuts, fish, and olive oil. Free radicals damage brain cells and contribute to cognitive loss; foods rich in antioxidants can neutralize these radicals.

Overall, despite any genetic inheritance, we may have more power over our cognition than we have been led to believe in the past. Regularly attending to the above points can improve our mental and physical health, as shown by research, and lead to positive outcomes.

The post Alzheimer’s New Gene Discovery May Prove Decisive in Early Diagnosis or Not. What CAN You Do? appeared first on Medika Life.

The observational study, which followed a large group of older adults, discovered this:

Individuals with cancer were less likely to develop Alzheimer’s than those without cancer.

The association appeared consistent across several common cancer types, including breast, prostate, and lung cancer.

Study Details

This study utilized a large population-based cohort analysis drawing from the UK Clinical Practice Research Datalink (CPRD), encompassing 3,021,508 individuals aged 60 and older.

Researchers collected data over 30 years (1988–2018).

Study Results

After an average follow-up of 9.3 years, individuals with cancer exhibited a one-quarter (25 percent) lower risk for dementia than the rest of the cohort.

Here are the key findings:

• Overall, cancer was associated with a lower risk of dementia.
• This association was observed regardless of whether cancer developed after database entry or was present at entry.
• When accounting for the competing risk of death, the protective effect of cancer against dementia was even more pronounced.
• Specific cancer types, including breast, prostate, lung, colorectal, and melanoma, were all individually linked to a significantly lower dementia risk (lower risk from one-third to one-fifth).

My Thoughts

The researchers are not sure why cancer may be associated with a lower Alzheimer’s disease risk.

The authors acknowledge some study limitations, including the potential underreporting of dementia.

We need more research to confirm these observational findings.

For now, here are some things we all can do to reduce our Alzheimer’s disease risk potentially:

• Eat a healthy diet.
• Get regular exercise.
• Maintain a healthy weight.
• Don’t smoke.
• Limit alcohol use.
• Get enough sleep.
• Manage stress.
• Stay socially connected.

If you have cancer, it is important to talk to your doctor about ways to reduce your risk of Alzheimer’s disease.

The post Could Cancer Hold the Key to Preventing Alzheimer’s? appeared first on Medika Life.

This peer-reviewed study was directed by lifestyle medicine pioneer Dean Ornish, M.D., founder and president of the nonprofit Preventive Medicine Research Institute and clinical professor of medicine at the University of California, San Francisco, in collaboration with other renowned scientists and neurologists from leading academic medical centers. These include:

• Harvard Medical School / Massachusetts General Hospital (Rudolph E. Tanzi, Ph.D.; Steven E. Arnold, M.D.; Dorene Rentz, Psy.D.)
• Karolinska Institute (Miia Kivipelto, M.D., Ph.D.)
• Preventive Medicine Research Institute (Dean Ornish, M.D.; Catherine Madison, M.D.; Colleen Kemp, R.N.; Anne Ornish, B.A.; Sarah Tranter, R.N.; Nancy DeLamarter, M.S.W.; Noel Wingers, M.S.; Carra Richling, R.D.)
• University of California, San Francisco (Dean Ornish, M.D.; Charles E. McCulloch, Ph.D.; Jue Lin, Ph.D.; Kim Norman, M.D.)
• Renown Health Institute of Neurosciences (Jon Artz, M.D.)
• University of California, San Diego (Douglas Galasko, M.D.; Rob Knight, Ph.D.; Daniel McDonald, Ph.D.; Lucas Patel, B.S.)
• Duke University Medical Center (Rima Kaddurah-Daouk, Ph.D.)
• Buck Institute for Research on Aging (Eric Verdin, M.D.)

“I’m cautiously optimistic and very encouraged by these findings, which may empower many people with new hope and new choices,” said Dr. Ornish. “We do not yet have a cure for Alzheimer’s, but as the scientific community continues to pursue all avenues to identify potential treatments, we are now able to offer an improved quality of life to many people suffering from this terrible disease.”

The research team recruited 51 participants with a diagnosis of mild cognitive impairment or early dementia due to Alzheimer’s disease and randomly assigned them to either an intensive lifestyle intervention group (no drugs added) or a usual-care control (comparison) group. Members of the control group were instructed not to make any lifestyle changes during the 20-week trial.

The intervention group participated in an intensive lifestyle program with four components: (1) a whole-foods, minimally processed plant-based diet low in harmful fats, refined carbohydrates, alcohol and sweeteners — predominantly fruits, vegetables, whole grains and legumes, plus selected supplements — with all meals sent to each patient’s home to maximize adherence; (2) moderate aerobic exercise and strength training for at least 30 minutes per day; (3) stress management, including meditation, stretching, breathing and imagery, for one hour per day; and (4) support groups for patients and their spouses or study partners, for one hour three times per week.

Improvements in patients with early Alzheimer’s disease

To measure pre- and post-trial cognitive function, the researchers utilized four standard tests used in Food and Drug Administration drug trials: the Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog), Clinical Global Impression of Change (CGIC), Clinical Dementia Rating–Sum of Boxes (CDR-SB) and Clinical Dementia Rating Global (CDR-G).

Results after 20 weeks showed overall statistically significant differences between the intervention group and the randomized control group in cognition and function in three of these measures (CGIC, p = 0.001; CDR-SB, p = 0.032; CDR-G, p = 0.037), and differences of borderline significance in the fourth test (ADAS-Cog, p = 0.053). When a mathematical outlier was excluded, all four measures showed significant differences in cognition and function in the experimental group. Three of these measures showed improvement in cognition and function in the intervention group and one test showed significantly less disease progression. In contrast, the randomized control group worsened in all four of these measures.

Not all patients in the intervention group improved; in the CGIC test, 71% improved or were unchanged. In contrast, none of the patients in the control group improved, eight were unchanged and 17 (68%) worsened.

Many patients who experienced improvement reported regaining lost cognition and function. For example, several patients in the intervention group reported that they had been unable to read a book or watch a movie because they kept forgetting what they had just read or viewed and had to keep starting over, but now they were able to do so and retain most of this information. One individual reported that it used to take him weeks to finish reading a book, but after participating in the study he was able to do so in only three or four days and was able to remember most of what he read.

A former business executive reported regaining the ability to manage his own finances and investments. “It was so much a part of my life — who I am, and who I was — it was hard saying that part of me was just gone,” he said. “I’m back to reconciling our finances monthly; I keep up to date on our investments. A lot of self-worth comes back.”

A woman said that for five years she had been unable to prepare their family business financial reports, but now she is able to do so accurately. “A deep sense of identity is returning. It’s given me a new lease on life, and yet it’s a familiarity and something I’ve always prided myself on. I’m coming back like I was prior to the disease being diagnosed. I feel like I’m me again — an older but better version of me.”

There was a statistically significant dose-response correlation between the degree of lifestyle changes in both groups and the degree of change in most measures of cognition and function testing. In short, the more these patients changed their lifestyle in the prescribed ways, the greater was the beneficial impact on their cognition and function.

This dose-response correlation adds to the biological plausibility of these findings and may help to explain, in part, why some patients in the intervention group improved and others did not (although other mechanisms may also play a role). Other studies have shown that more moderate lifestyle changes such as adopting the Mediterranean diet may slow the rate of progression (worsening) of Alzheimer’s disease but may not go far enough to improve cognition and function.

In addition to improvements in cognition and function, the intervention group also demonstrated significant improvements in several key blood-based biomarkers. One of the most clinically relevant biomarkers is called the Aβ42/40 ratio, which is a measure of amyloid, thought to be an important mechanism in Alzheimer’s disease. This measure improved in the lifestyle intervention group (with the presumption that this improvement reflected amyloid moving out of the brain and into the blood), but it worsened in the randomized control group, and these differences were statistically significant (p = 0.003).

There was also a statistically significant dose-response correlation between the degree of lifestyle change and the degree of improvement in this amyloid ratio (p = 0.035). This direction of change in amyloid was also a major finding with lecanemab, a drug approved for treating Alzheimer’s disease last year.

Also, the gut microbiome in the intervention group showed a significant decrease in organisms that raise the risk of Alzheimer’s disease and an increase in organisms that are protective against Alzheimer’s disease. These biomarker and gut microbiome results also add to the biological plausibility of the overall findings.

According to renowned Alzheimer’s scientist Miia Kivipelto, M.D., Ph.D., “These findings add to the growing body of evidence that moderate multimodal lifestyle changes may help prevent Alzheimer’s disease or slow its progression, and also suggest that more intensive multimodal lifestyle changes may have additional benefits for improving cognition in patients with early Alzheimer’s disease.”

New hope in tackling a devastating and costly disease

Alzheimer’s disease, the fifth-leading cause of death among Americans aged 65 and older, is not only physically and emotionally devastating; it’s also extremely costly. The disease currently affects more than six million people in the U.S., at an annual cost of more than $345 billion. By 2050, the number affected is expected to reach 13 million, with costs projected to skyrocket to $1.1 trillion annually.

“There’s a desperate need for Alzheimer’s treatments,” said study co-author Rudolph E. Tanzi, Ph.D., an acclaimed professor of neurology at Harvard Medical School and director of the McCance Center for Brain Health at Massachusetts General Hospital, one of the study’s clinical sites. “Biopharma companies have invested billions of dollars in the effort to find medications to treat the disease, but only two Alzheimer’s drugs have been approved in the past 20 years — one of which was recently taken off the market, and the other is minimally effective and extremely expensive and often has serious side effects such as brain swelling or bleeding into the brain. In contrast, the intensive lifestyle changes implemented in this study have been shown here to improve cognition and function, at a fraction of the cost — and the only side effects are positive ones.”

“I am delighted and honored to be a part of this groundbreaking study showing for the first time in a controlled clinical trial what the epidemiology has told us all along: Lifestyle factors are critically important in our efforts to address Alzheimer’s. While efforts to develop drugs to treat this disease will continue, this study provides a blueprint for practical, easily implemented steps that can significantly alter the progression to full Alzheimer’s disease,” said study co-author Eric Verdin, M.D., president and CEO of the Buck Institute for Research on Aging.

This study has implications for preventing Alzheimer’s disease as well. New technologies such as artificial intelligence now make it possible to predict an individual’s likelihood of developing this disease years before it becomes clinically apparent, but many people ask, “Why would I want to know if I’m likely to get Alzheimer’s disease if I can’t do anything about it? It will just make me worry.” Although further research is needed, it is reasonable to believe that the same intensive lifestyle changes that often improve cognition and function in those with mild cognitive impairment or early dementia due to Alzheimer’s may help prevent the disease as well.

“This study finally gives us scientific data to support what many of us in this field have believed instinctively for years, that lifestyle interventions may determine the trajectory of people’s Alzheimer’s journeys,” said Maria Shriver, founder of the Women’s Alzheimer’s Movement (WAM) at Cleveland Clinic, which provided early seed funding for this study. “We opened the WAM Prevention and Research Clinic at Lou Ruvo Center for Brain Health in Las Vegas for women 30 to 60 years of age who are at higher risk than average for developing Alzheimer’s. The protocols we use involve adopting many of the lifestyle interventions employed in this study. So, showing success in improving the health trajectories of those already diagnosed with Alzheimer’s clearly offers hope to those who want to delay or prevent developing the disease altogether. This is a study to give us hope.”

A growing body of lifestyle medicine research

Dr. Ornish has directed peer-reviewed research at the nonprofit Preventive Medicine Research Institute for over four decades. He is often referred to as “the father of lifestyle medicine.”

The Institute’s studies, published in leading peer-reviewed medical and scientific journals, focus on the power of lifestyle medicine to help prevent and often reverse the progression of many of the most common and costly chronic diseases. These include coronary heart disease, Type 2 diabetes, early-stage prostate cancer, hypertension, hypercholesterolemia, and now, early-stage Alzheimer’s disease.

Dr. Ornish’s most recent bestselling book, “Undo It!,” co-authored with Anne Ornish, puts forth his unifying theory: the reason that the same lifestyle changes may beneficially affect so many different chronic diseases is that these share common biological mechanisms that are directly affected by what people eat, how much they exercise, how they respond to stress, and how much love and support they enjoy. Alzheimer’s is the latest example of why “what’s good for your heart is also good for your brain.”

In 2010, the Centers for Medicare & Medicaid Services (CMS) began providing nationwide Medicare coverage for Dr. Ornish’s program, which has been shown to often reverse the progression of coronary heart disease, as “intensive cardiac rehabilitation.” This nine-week program is offered online, so individuals can join classes from the comfort of their own homes, enabling participation by those who cannot afford to take time off work, who live far from a hospital or who cannot afford childcare, thereby reducing health disparities and inequities. “I’m very grateful to CMS for providing Medicare coverage. Having seen what a powerful difference this program of lifestyle changes can make, I appreciate very much that it is now available to all eligible Medicare beneficiaries with heart disease who can benefit from it,” Dr. Ornish said.

About the Preventive Medicine Research Institute 

The Preventive Medicine Research Institute (PMRI), a 501(c)(3) nonprofit organization, was founded in 1984 by Dean Ornish, M.D., to conduct pioneering research evaluating the power of lifestyle medicine and to make healthy lifestyle changes more widely available to those who can benefit from them. PMRI’s research uses the latest in high-tech medical and scientific technologies to assess the benefits of these low-tech and low-cost lifestyle changes. For more information about PMRI’s four decades of peer-reviewed lifestyle medicine research, please visit https://pmri.org.

The post Lifestyle Changes Significantly Improve Cognition and Function in Early Alzheimer’s Disease for the First Time in a Randomized Controlled Trial appeared first on Medika Life.

Even as researchers are making some progress in their various hypotheses regarding Alzheimer’s, we are still contending with a very troubling one: it might be an infectious viral disease. But there might only be sporadic instances of this form of SDAT (Senile Dementia of the Alzheimer’s Type). If that’s the case, there may need to be multiple treatment modalities for Alzheimer’s and not one drug. Two broad categories of SDAT have been designated: familial and sporadic, with the latter being poorly understood.

Now, more focus is being placed on factors that were previously thought to be unrelated to AD, such as diet, lifestyle choices, and gut microbiome. Studies have shown that these factors all affect the progression of AD, which raises the possibility that these factors could be key to combating the disease.

Recently, there has been speculation that the gut microbiota-brain axis, a bidirectional communication link between the GI tract and the central nervous system (CNS), may have a role in the etiology and pathogenesis of AD. There may be a link between this axis and the disruption of certain metabolisms or clearances by microbes, the increased permeability of the blood-brain barrier, changes in the neuroinflammatory response, and the blocking of vital hippocampal neurogenesis needed for memory maintenance. These changes in this axis may help explain how AD develops.

Think about how certain foods can alter the gut microbiota, which may lead to changes more in line with the onset of Alzheimer’s. The analysis of the fermented food research has shown promising effects on amyloid-β metabolism, inflammation, and cognitive impairment in animals and humans. The pathogenesis of Alzheimer’s disease emphasizes the role of the gut-brain axis, and studies examining the use of fermented foods are showing promising new research routes. But there’s even more research outside the plumbing of foods and lifestyles.

Globally, the prevalence of mild cognitive impairment, which ranges from 7 % to 25 % in adults aged 60 to 84, continues to increase with advancing age.

Depression, an emotional change seen in Alzheimer’s patients, deserves more attention than it has received in the past. I can remember asking researchers why they weren’t going further in studying depression in these patients. The answer? The patients had depression because of the changes it brought to their lives. Little thought was given to depression as a signaling area of potential research. How might depression, in the biological sense, be involved in this disease? Now that area is opening up to study.

Multiple pathophysiological mechanisms have been proposed to explain the bidirectional relationship between depression and AD. Evidence suggests that midlife depression may be an AD risk factor, while a chronic course of depression in late life may be a sign or symptom of dementia.

There are possible explanations for the possible reciprocal relationship between MCI and depressive symptoms. One is the scarring theory, which holds that depressive episodes make people more vulnerable to cognitive deficits that frequently persist long after affective symptoms have decreased. But, even here, there is a more nuanced approach to both depression and AD and it lies in one hormone, known as the “happiness hormone,” serotonin.

In one study, it was discovered that MCI patients had up to 25% lower serotonin transporter levels in brain regions specifically linked to executive function, emotion, and memory than healthy controls. In addition, the MCI patients had higher levels of plaque material.

Foods that contain preservatives may also play a role in the regulation of serotonin, appetite suppression, and cognition. Sodium benzoate and sodium metabisulfite have the potential to increase serotonin production, which would activate calorie restriction, prolong life expectancy, and improve cognitive performance. Unfortunately, highly processed foods that may contain these two preservatives can bring on other health issues.

Are “happiness” and Alzheimer’s related in some way, as are the foods that aid the gut-microbiota-brain axis in regulating mood and, potentially, Alzheimer’s? The jury is out on this one, but important evidence is being accumulated that may bring new hypotheses and treatments early on in the disease or, potentially, halt it in its tracks. Maybe the lowly pickle will pave the way to a new understanding of fermented foods’ involvement.

The post Is Happiness Related to Alzheimer’s and a Specific Hormone? appeared first on Medika Life.

We will visit Mars in person in the coming decades, a months-long trip one-way. As I look forward to playing Bethesda Game Studio’s Starfield after recently finishing all nine books of Iain M. Banks’s Culture series, I think about the plans that incorporate even further destinations. Being a physician-scientist, it is hard not to think of the challenges that come from long-distance travel! While some health concerns of space travel are already reasonably well known, such as muscle deconditioning or the bombardment from cosmic radiation, several conditions have not yet been considered hazards in space travel. This is mainly because the technologies that would make them a reasonable point of alarm for an astronaut have not been invented yet!

Eventually, there will be a way for everything that a human needs to be synthesized onboard a spaceship. Means of accomplishing this are already being investigated, such as through harnessing microorganisms, like bacteria, towards producing everything a human could need, like oxygen, food, and raw materials. As for putting a human in “stasis” for a long journey, artificial hibernation has been academically engaged as a concept, making applications more feasible for the future (although it will take time to evaluate such a procedure due to ethical and safety concerns).

So, let us say that we can keep some humans alive indefinitely in a space shuttle. What else do we need to think of? As a physician and Alzheimer’s disease researcher, I think you can guess one such thing.

Alzheimer’s disease is the most common form of dementia, typically affecting around 10% of individuals older than 65. One’s risk of Alzheimer’s increases as one gets older, with one in three over age 85 having the disease. Alzheimer’s is believed to be caused by the progressive death of neurons, the cells in your brain that contribute to memory and your ability to function.

If I were to jump on a NASA mission right now, travel time to the nearest star system, Alpha Centauri, is a greater concern (130,000 years!). In 2017, NASA proposed a new technology for space travel called solar sails, which could speed this up (44 years). Despite this design remaining a concept and its construction proposed for over 40 years from now (and likely not going to host an astronaut), what would happen if I boarded this vehicle in my seventies and placed in stasis until I arrived?

With every year of traveling, you could count on the risk of developing Alzheimer’s persisting. Unless hibernation technologies find a way to prevent neuronal cell death or the natural deposition of debris in the brain as we age, it is possible that I could wake up having Alzheimer’s! Imagine that, after traveling further than anyone ever had before? While there are “modifiable” risks for Alzheimer’s that could arguably be addressed to reduce the risk of disease, like reducing the risk of blood vessel disease through a healthy diet and exercise, one can only do so much.

One day, we will have to face the music of how we will keep our astronauts healthy on long trips. As with other health conditions, which I will touch on in future articles (be sure to give this article a clap and subscribe), medical research will have to address possible problems arising across body systems rather than a singular goal of having our own intergalactic visitor survive a long trip because there is a lot more to life than simply living, as many of us could agree.

There is reason to be optimistic! In the Alzheimer’s and Aging research fields that I am part of, energy (including mine) and money are going towards finding out how we can help people live longer and better. While science takes longer to yield results than we would like (even AI took decades to develop before it was ready for consumers as ChatGPT), progress is always happening, and getting human life out among the stars is something that people care about.

Let me know your thoughts on prioritizing traveling among the stars! Do you think we should try going as far as possible or focus more on taking it slow?

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Yes, it’s a rhetorical question because plastics aren’t supposed to be in your blood, much less your brain. But research is revealing disturbing facts about the extent of plastic pollution and its far-reaching consequences.

According to research, microplastics can cross the placenta and enter breast milk, where infants can then consume them. The use of plastic feeding bottles and teething toys raises the risk. What about smoothie shakers made of plastic? Do they also provide another dose of microplastics with the drink?

Ecologists have discovered that microplastics frequently get into foods like salt, honey, and sugar, and some research indicates that people consume more than 100,000 microplastic particles annually. It was no surprise when one scientist estimated that there are 24.4 trillion microplastics in the world’s upper oceans.

Microplastics can be absorbed through the skin through personal care items like exfoliating skincare gels, in addition to being inhaled or consumed. These minute particles contaminate human bodies and are found almost everywhere in the natural environment.

Plastics play such an ingrained role in our lives that eliminating them is almost unthinkable or nonexistent in our current world. What would we do without plastic? Converting from supermarket bags to bringing our own to carry groceries is worthy of a comic’s routine in a club. It’s less than an itch on the belly of a flea in terms of the billions of pieces of microplastic pollution circulating our planet, much less the incalculable tons floating in our oceans and polluting our shorelines.

These microparticles are in our food, the water we drink, the air we breathe, and even in places we have no idea they might exist, like hospital tubing, medical supplies, etc. Plastics have overtaken our world, and not in a good way at all. If they clog our waterways, what do you think they do to us internally in our circulatory system and our brain?

Our brains require a constant, surging flow of blood-filled nutrients and oxygen to work effectively. If those nutrients also help carry microplastics to our brain that somehow worm their way through the blood-brain barrier and into that delicate tissue, what might be the result? Researchers are asking that question, too.

Can we protect ourselves from the invasion of microplastics into our bodies? It seems we can’t. The most common microplastic particles in our environment originate from car tire dust, artificial grass, and washing of clothes made of artificial fibers. Humans are exposed to microplastics mainly through nutrition and air, and although this exposure is known to happen on a daily basis, the health effects of microplastics remain largely unknown.

What about our brains? There is another study that addresses this danger. We now demonstrate that nanoplastics can be deposited in the brain via nasal inhalation, triggering neuron toxicity and altering…behavior.

The researchers also suggested that the presence of microplastics could contribute to neurological impairments in fetuses and children. Studies have shown that the presence of nanoplastic particles in the brain reduced vital brain enzymes that were found to malfunction in the brains of patients with Parkinson’s and Alzheimer’s.

The long-term effects of microplastic exposure on human health require further study. In the interim, plastics production is at ever-increasing levels, meaning the risk for all of us and future generations is reaching extremely dangerous levels. It is not a medication, a vaccine, or a lifestyle issue, but an environmental one, and this one is external and internal.

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The drug industry, patient advocates, and congressional Republicans have all attacked federal officials’ decision to decline routine Medicare coverage for a controversial Alzheimer’s drug. They’ve gone as far as to accuse them of tacit racism, ageism, and discrimination against the disabled — and hinted at a lawsuit — over the decision to pay only for patients taking the drug in a clinical trial.

The drug, Aduhelm, with a listed price tag of $28,500 a year, has had few takers in the medical world. Brain doctors are leery of administering the intravenous drug because it appears dangerous and largely ineffective. Many of the nation’s most prestigious hospitals — such as the Cleveland Clinic, Johns Hopkins Hospital, and Massachusetts General in Boston — have declined to offer it to patients.

While groups representing the pharmaceutical industry and patients press to undo Medicare’s decision, industry critics applaud the Centers for Medicare & Medicaid Services for throwing obstacles in the way of a drug they think the FDA should never have approved in the first place.

For the industry, the campaign has a broader existential target: to prevent CMS from using its payment decisions to keep FDA-approved drugs off the market. In recent years, FDA programs to speed approval of new drugs have led to a rash of entries with often minimal scientifically sound evidence to prove they work, critics say.

The FDA’s own expert panel recommended against approving Aduhelm for that reason. Last June, the agency approved it anyway.

CMS then announced Medicare would pay only when the drug was used in further clinical trials to assess its true benefit. That Jan. 11 announcement has drawn more than 9,000 comments to the agency’s website — a tsunami compared with most approval decisions. The remarks are roughly divided among pros and cons, and many appear to be organized by groups on the pro side of the debate (such as the Alzheimer’s Association) or those opposed (such as the nonprofit More Perfect Union). The agency could change or even reverse its decision, though experts believe the latter is unlikely.

“If the FDA were doing its job, CMS wouldn’t have had to step in. But good for the CMS, they are helping to protect the public from drugs whose harms outweigh benefits,” said Dr. Adriane Fugh-Berman, a Georgetown University professor of pharmacology who directs PharmedOut, a group that publicizes what it sees as poor industry practices.

Aduhelm is the first FDA approval for a class of laboratory-made antibodies designed to clear away so-called amyloid plaques, which gradually accumulate in the brains of people with Alzheimer’s disease.

In clinical trials, Aduhelm did well dissolving the plaques, but its impact on the functioning of patients in earlier stages of Alzheimer’s was so meager that an expert panel voted 10-0 (an 11th panelist was uncertain) in November 2020 to advise FDA to reject it. The science is unclear about whether the presence of such plaques — a so-called surrogate marker — correlates with the mental functioning of patients.

As such, the FDA gave “provisional approval” to Biogen, the maker of Aduhelm, allowing it nine years to provide evidence that the drug slows the progression of Alzheimer’s. In that period, Biogen would make far more money than if the application had been rejected. Even under the CMS decision, it would reap Medicare payments from whatever is used in clinical trials, which would need to include thousands of participants to assess the drug’s performance.

Drug companies and pharma investors have responded to CMS’ ruling with special alarm because they have spent decades improving their relationships with the FDA, only to have CMS seemingly pull the rug out by exerting its own power over an expensive drug.

“The drug companies are worried that this could be a precedent for other drugs. And it should be,” Fugh-Berman said. “This isn’t just about money; it’s about protecting the public.”

This “accelerated approval” employed for Aduhelm got its start in 1992 and is aimed at moving promising new classes of drugs to the public faster. Companies whose drugs go through the process — more than 250 drugs or vaccines have been approved so far — are supposed to quickly gather evidence that the products likely improve health once they’re on the market. But such follow-up studies often lag or are never performed. For example, the makers of the Duchenne muscular dystrophy drug eteplirsen, approved in 2016, didn’t start recruiting patients into a post-marketing trial until 2020 and don’t expect results until 2026.

Biogen originally said it would get confirmatory results for Aduhelm within seven years of approval. In response to the Medicare decision, it promised to trim that to four years. The company also hinted that it might sue the agency, calling its decision “arbitrary and capricious.”

In the meantime, patients eager to get access to the drug are furious about the coverage decision. Jim Taylor, a New Yorker whose wife, Geri, says she improved on Aduhelm during a clinical trial, said Medicare had made an “unconscionable decision” that puts Alzheimer’s patients “on a dark roller coaster.”

Many patients’ groups are organized or at least funded and fueled by drugmakers, providing sympathetic stories that buttress a manufacturer’s commercial interests. Advocacy groups also receive large donations from the makers of certain drugs. A 2020 report by UsAgainstAlzheimer’s shows at least $900,000 in donations from monoclonal antibody producers. The Alzheimer’s Association’s top corporate donors — Biogen, Lilly, Eisai, and Genentech — all have monoclonal antibody candidates and have provided the group $1.6 million in fiscal year 2021.

These donations are a tiny part of the group’s funding, its policy director, Robert Egge, told KHN, and any alignment of its position with industry is “coincidental, because of what we and our constituents believe is right.”

The Taylors appeared at an online news event with activists from UsAgainstAlzheimer’s and the National Minority Quality Forum, a group focused on health inequities, who argued that the decision discriminated against Black and Hispanic patients, who are more likely to suffer from Alzheimer’s and less likely to join clinical trials. In fact, CMS demanded that evidence for Aduhelm be collected more extensively from minority patients. Biogen’s two major trials of the drug included only 19 Black patients out of a total of 3,285.

Groups representing people with Down syndrome wrote more than 1,000 letters to CMS because its decision requires that confirmatory trials exclude people who have additional neurological conditions. Rep. Cathy McMorris Rodgers, a top drug industry cash recipient and the leading Republican on the House Energy and Commerce Committee with significant sway over pharma issues, said at a hearing last week that it was “extremely concerning and unacceptable” that Down syndrome patients would be ineligible.

But neither Biogen nor any other drug company has recruited Down syndrome patients for a major trial of a monoclonal antibody treatment. AC Immune, a Swiss company, conducted a safety study last year on 16 people with Down syndrome.

It’s not surprising that groups representing those suffering from Alzheimer’s placed high hopes on the monoclonal antibody drugs, which have seemed like a ray in the darkness for the estimated 2 million Americans with early Alzheimer’s symptoms.

When asked why his group is so gung-ho about a product in which the medical profession shows such little confidence, Egge said the drug seems to have some benefits and that its risks — especially to patients who lack other means to slow a miserable, deadly disease — may be exaggerated. He acknowledged that 40% of patients in the biggest Aduhelm trial experienced brain swelling or bleeding, but Biogen’s research showed these resolved with no apparent harm in most cases.

That said, the sluggish purchases of the drug — which earned a modest $1 million in the last quarter of 2021 — signal the market is responding to its deficiencies.

In response to the lackluster response, Biogen halved its initial $56,000 price to $28,500. If CMS had granted full approval, that would have been followed by “marketing, marketing, marketing,” said Dr. Joseph Ross, a public health professor at Yale University. Hospitals that wanted to attract patient business for a lucrative infusion — patients receiving the drug also require brain scans and other tests and monitoring — could advertise their willingness to give Aduhelm.

CMS’ decision came under a policy called coverage with evidence development. Though the program began in 2005, Aduhelm is by far the most important product CMS has declined to reimburse without further study.

The agency’s decision “is a little inelegant” because it puts the brakes on an FDA approval, said former CMS chief medical officer Dr. Sean Tunis, now a consultant and senior fellow at Tufts Medical Center, but “it seems completely justifiable since the evidence of benefit is pretty weak and the evidence of harm is pretty strong.”

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First, a brief look at dementia. We will then pivot to the new study results before ending with some potential risk-reducing maneuvers.

Dementia is not a single entity; instead, dementia is a grab bag descriptor for a range of conditions marked by cognitive impairment. Think problems with memory, thinking, or decision-making. Late in its course, dementia can reduce one’s awareness of the world. The most common form of dementia is Alzheimer’s disease.

Let’s be clear — while dementia is primarily (but not exclusively) a disease of older folks, it is not a part of normal aging. Unfortunately, Alzheimer’s disease gets progressively worse over time. Alas, there is no cure. The focus tends to be on symptom management.

Here are some of the risk factors for dementia, according to the United States Centers for Disease Control:

• Age. The probability of developing dementia increases with age. Most cases of dementia are among individuals ages 65 years and older.
• Inherited genetics. Individuals with parents or siblings with dementia are more likely to develop the condition.
• Race and ethnicity. Older African-Americans are twice as likely to develop dementia than their white counterparts. Hispanic individuals overall have a 1.5-fold increased risk.
• Poor heart health. One more reason to watch our blood pressure and cholesterol. Don’t even think about using tobacco.
• Traumatic brain injury (TBI). Head injury can increase the risk of dementia, especially if the trauma is severe or repeated.

Light exercise and dementia

Let’s move on to our research investigation. Researchers looked at whether light-intensity physical activity is associated with a lower risk of developing dementia.

The investigators gathered data from over 62,000 subjects at least 65 years old, with a median age of 73.2 years. None had dementia, and all had medical records in the Korean National Health Insurance Service database.

The study authors tracked physical activity at the study start, with participants completing a questionnaire. The scientists then examined the frequency, intensity, and duration of physical activity to calculate how much energy expenditure was due to physical activity.

After a median 42 months follow-up, the research findings are: Six percent of the subjects developed dementia. Looking by quartiles of activity (ranging from inactive to insufficiently active to active to highly active):

The insufficiently active individuals had a 10 percent lower risk of getting dementia compared with the inactive group members. The active participants had a one-fifth drop in risk, and the highly active group had a more than one-quarter (28 percent) lower risk.

When adjusted for sex, age, and other medical conditions, the findings held.

Takeaway messages

Light-intensity physical activity (as opposed to being sedentary) is associated with a lower probability of developing dementia. While the study is well-done and is in line with the results of other studies, the results are not evidence of a causal relationship between light-intensity exercise and a lower risk of dementia. The reverse may be true — those developing exercise may exercise less.

I am encouraged by this type of study. Some believe that lifestyle may prevent approximately one-third of dementia cases. That’s the view of Professor Tara Spires-Jones of the University of Edinburgh (United Kingdom).

I will continue to walk (and more). Even though this new study adds to a growing body of evidence pointing to lifestyle influencing dementia risk, I know activities such as walking can help lower the risk of heart attack, stroke, cancer, and more.

Thank you for joining me today.

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Alzheimer’s is a terrible disease or disorder, whichever way you wish to categorize it. The current thinking is that unless someone finds a cure, treatment, or some way to address the cognitive decline associated with this neurologic disorder adequately, we will be swamped, drowning in effect in Alzheimer’s patients who require 24-hours-a-day care. It is known as the Silver Tsunami.

There is no question about it. As we improve our ability to live longer, thanks to advances in medical technology, we also decrease our ability to pay trillions of dollars for care worldwide. Too many questions are still involved in this complicated area, but one thing we know is that whoever finds the goose that lays the golden egg will be assured to be a billionaire.

Racing to find ways to address Alzheimer’s or other forms of cognitive decline has proven to be an area of intense interest. We have no idea or a limited idea regarding what causes Alzheimer’s, what neurobiological elements are involved in it, and when Alzheimer’s might first present itself.

Testing, whether paper and pencil and active questioning, serologic testing, or even dermatologic testing, have led us to too many blind alleys. The thinking had been that we nailed down the culprit, and it was a material called tau produced in cells in the brain and even in the skin.

Is tau truly diagnostic of Alzheimer’s, or is it something that is produced naturally in everyone’s body and varying levels of it may not be diagnostic of a cognitive declining disorder? When not involved in brain tissue entanglements, tau is natural and serves a good, supportive purpose in brain cells.

Today, I came across two interesting studies. One was that tea and coffee might, somehow, be involved in forestalling cognitive decline. My antenna immediately went up since it seemed that this was yet another attempt by someone to promote their product, namely coffee or tea.

We know that tea has specific properties that may help maintain our health. If you want an example, you might look at countries like India, where people drink tea exclusively and have numbers of citizens living over the age of 100.

I had seen an article about a woman who was 104 who had just learned to read. If anything, that is an outstanding accomplishment, but the fact that she was over 100 and learning to read was astonishing. Was it due to her drinking tea all of her life?

Findings from some research studies may prove interesting but not diagnostic. Another study that came to my attention was of persons with alopecia Arriaga (AA), a hair loss problem. The investigators found that persons with AA “were more likely to develop any dementia such as Alzheimer’s or unspecified dementia than the control group.” While this may seem shocking or exciting, please keep in mind that it may only point to the immune system having an active role in our developing certain types of dementia and depression.

Therefore, anyone with a disordered immune system may develop varying types of dementia. Dementia is wide-ranging and often difficult to nail down, even in clinical practice.

Many dementia misdiagnoses have been written in stone in charts, and then the patients have been treated accordingly. I suppose you think this is unacceptable or unethical. In that case, I agree with you, but I would also suggest that we need more robust testing, and we also need persons who are aware of their own biases when they test. Too often, older patients suffer from being the recipients of this ageist bias.

And it’s not restricted to dementia. A physician once told me he was asked to consult on a patient in a hospital. When he met the man, he asked one question: Has your hat size increased? After reviewing the man’s chart, the physician thought he might have gout, and an increase in head size would be potentially diagnostic. He was correct, and the man then received the proper treatment. Previously, they diagnosed him with hearing and cognitive deficits. Was it because he was elderly?

Allow me to provide a small bit of insight regarding testing. Psychiatrists are not trained the way psychologists are in psychological testing, yet they are expected to use cognitive testing in their practice, primarily in hospital settings.

The internet provides many tests from pharmaceutical firms to test for various psychiatric/psychological disorders. The tests may, in my estimation, not be as adequately validated as we might wish. Validation of test administration is also problematic. And they are not used by test-production companies that make them available for licensed mental healthcare personnel and detail the qualifications needed. Anyone can download them, even those tests that indicate they are not for clinical use.

I sat and watched a psychiatrist attempt to administer a cognition test for Alzheimer’s, and he did the one thing all of us are trained not to do. He led the patient in her responses. “You don’t know the city we’re in, do you?” was his first question. He was supposed to ask her (the list of questions was right in front of him) what city they were in, not offer that she didn’t know the name of the town.

Providing that kind of opening indicates to the patient that they are not likely to know the answer to the following questions that will be asked. It was a significant mistake, but the patient was obviously impaired and wouldn’t have gotten a good score regardless of how the task was administered. That is not the point, however. If someone is going to do psychological testing of any type, they should be adequately trained. The guidelines are online.

Intelligence testing is another area of contention, and I have seen too many psychologists administer them improperly. I recall a professor telling a student, “This is the Wechsler Adult Intelligence Scale, not the Wechsler Adult Intelligence Scale with Smile.” Smiling is not permitted in the rigid protocol.

A significant example of this related to a licensed clinical psychologist who was picked up on a highway on the West Coast of the US. She had abandoned her car and was in distress. The officers took her for an evaluation to the nearest hospital. It happened to provide care for persons with mental deficiencies. They administered an IQ test at the facility, and she scored less than 50, placing her in an impaired group.

The woman had a doctorate and, after a month, someone thought to look into her background and discovered facts that immediately indicated she needed to be transferred. Once at another facility, she was diagnosed with bipolar disorder, treated, and returned to her home on the East Coast. It is a stunning example of testing under the wrong conditions and with a person who is not in a condition to be tested for intelligence.

Remember that no one is perfect regardless of where they went to school or work. We all make mistakes, but in medicine or healthcare, the errors can be life-threatening or result in isolation and a major restriction of liberties. Power must be used with this knowledge.

Always question authority.

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