Showing posts with label dementia. Show all posts
Showing posts with label dementia. Show all posts

Monday, 3 May 2021

This Is What To Know About Staying Mentally Sharp, According to a Psychiatrist and a Neurologist

Mental Sharpness 

 

 Emily Laurence 

 

It was once long believed—by the average person and by brain health experts—that each person had a finite number of brain cells, which decreased over time. Lose enough and it can lead to neurological damage or diseases, including dementia. It’s a school of thought that could cause someone to obsess over every soccer ball they’d ever head-butted or night they had one too many alcoholic drinks.

But this line of thinking isn’t exactly true based on what researchers have learned about brain health over the past decade. A wealth of scientific studies are connecting certain food and lifestyle habits with neurogenesis, the process by which new neurons grow in the brain. It’s a topic psychiatrist Drew Ramsey, MD talks about in his new book, Eat to Beat Depression and Anxiety ($22) and means that we can actively protect ourselves from cognitive decline—at least in part. Encouraging, right? The key, of course, is knowing how to do it.

How are brain cells destroyed?

Before we get into brain cell growth, it’s helpful to know what exactly kills them off in the first place. Dr. Ramsey says this comes down to high levels of chronic inflammation. While small doses of short-term inflammation can actually be beneficial, experiencing high-levels of inflammation for extended periods of time can be damaging to the brain (and the body as a whole, TBH).

“Scientific research has been very clear that excess inflammation affects the circuits in the brain,” Dr. Ramsey says. Inflammation not only disrupts brain circuity, it actively kills brain cells, too. He explains that an inflamed brain leads to brain fog, anxiety, depression, low energy, and (over a long period of time) cognitive decline and disease. What causes long-term inflammation? Chronic stress, eating a lot of processed sugar, processed meat, and refined carbs, and not getting enough sleep are some of the major causes.

Something else chronic inflammation does is prohibit neurogenesis, the key process for producing new brain cells, says neurologist Faye Begeti, MD, PhD. (Dr. Begeti says it’s important to note that most of the scientific studies on neurogenesis have been done in mice—very few have been done in humans—so knowledge around the process is still limited.) “The brain is shielded by a blood-brain barrier. This barrier can become leaky, but this would only happen in prolonged, systemic inflammatory states rather than a simple cough or cold,” she says.

Watch the video below to learn more about the connection between diet and inflammation:

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How new brain cells are grown

Okay, so we can blame excess inflammation for killing brain cells. How do we get them back? Actively working to fight off inflammation. This not only prevents neurons from dying, it actively leads to brain cell growth, as well, according to Dr. Ramsey.

When it comes to brain cell growth, though, it’s important to understand the connection between neurogenesis and neuroplasticity—two words that sound similar, but mean different things—says Dr. Begeti. While neurogenesis refers to new brain cell growth, she explains that neuroplasticity is where existing neurons grow and form different connections with each other. “Kind of like interweaving branches from nearby trees,” she says. “Neuroplasticity is vital for shaping our brain into who we are, learning, and recovering from diseases, like a stroke.” Neuroplasticity is how existing and new brain cells are all communicating with each other; that’s why both are important, Dr. Begeti adds.

From what doctors can tell, it seems that neurogenesis only happens in two parts of the brain, the hippocampus being one of them. (The other is the olfactory bulb, linked to smell.) Dr. Ramsey explains that the hippocampus is the part of the brain responsible for emotional health as well as memory function, remembering old memories as well as creating new ones. Because of this, neurogenesis is key for staying mentally sharp and emotionally balanced. And that’s where what you eat and your daily habits can come in.

Food and lifestyle habits that promote neurogenesis

A healthy diet, consistent good sleep, and regular workouts are all beneficial for the hippocampus, studies have shown. “Exercise, socialization, and environmental enrichment—which means having plenty of stimulating activities—increases neurogenesis but these studies have only been done in mice, as it is difficult to study [brain cell growth] in humans,” Dr. Begeti says. This means that while there likely is a strong connection, more human studies need to be done to confirm it.

Though, some nutrients have been linked to benefitting the brain through neurogenesis in humans, according to Dr. Ramsey: omega-3 fatty acids (found in foods like fish, nuts and seeds, and soybeans), phytonutrients (natural compounds found in plants such as vegetables, fruit, whole grains, and legumes), B vitamins (found in meat, dairy, whole grains, dark leafy greens, citrus fruits, avocado, banana, nuts and seeds, and legumes), zinc (found in lean meats, eggs, seafood, lentils, nuts and seeds, and soy), and magnesium (found in whole grains, soy, nuts and seeds, legumes, and dark chocolate). This is one reason why so many doctors are into the Mediterranean diet, which emphasizes all the foods mentioned here.

Besides all the nutrients mentioned above, Dr. Ramsey says there’s a specific brain chemical that plays a role in neuroplasticity and brain cell growth: BDNF, which is a neurotrophin, aka a type of protein that helps brain cells grow and survive. “Some say that BDNF is a lot like ‘Miracle-Gro for the brain’—a fertilizing biomolecule that supports the birth of new brain cells and synapses during development,” he says in his book. He also says that besides helping with brain cell growth, BNDF works to protect the mind from toxins.

Want to boost your BDNF production? Dr. Ramsey says regularly eating foods with omega-3 fatty acids is key. (Yep, the nutrient is doubly good for brain health.) He says flavonoids, a type of antioxidant found in green tea, berries, kale, tomatoes, dark chocolate, and nuts (except for macadamia nuts and Brazil nuts), are also linked to spurring more BDNF production in the brain.

Working all the aforementioned foods into your diet will likely benefit your hippocampus, but Dr. Ramsey says doing what you can to keep excess inflammation away in general is important too, since it’s what kills precious neurons. When it comes to food, cooking with anti-inflammatory spices such as turmeric, rosemary, and ginger can help. So can prioritizing getting enough fiber. In terms of lifestyle, Dr. Ramsey says stress management, good sleep, and regular movement are all key. However, Dr. Begeti says it’s important to acknowledge that there are still many unknowns surrounding cognitive decline. While diet and lifestyle habits are connected, they are just one piece of the puzzle. If someone does get dementia later in life, it’s certainly not their fault.

When it does come to prioritizing these healthy practices, remember that embracing a “mind-over-matter” mindset can help make new habits stick. “Knowing that we can actively grow the size of our brain is really empowering to me personally,” Dr. Ramsey says. “It motivates me to make choices to eat nutrient-rich foods, meditate, and exercise. It’s not always easy to do those things consistently, but when you know how it’s affecting your brain, it’s very motivating.”


Thursday, 9 July 2020

An Effortless Way to Improve Your Memory

Memory

A surprisingly potent technique can boost your short and long-term recall – and it appears to help everyone from students to Alzheimer’s patients.

BBC Future

When trying to memorise new material, it’s easy to assume that the more work you put in, the better you will perform. Yet taking the occasional down time – to do literally nothing – may be exactly what you need. Just dim the lights, sit back, and enjoy 10-15 minutes of quiet contemplation, and you’ll find that your memory of the fac
ts you have just learnt is far better than if you had attempted to use that moment more productively.
Although it’s already well known that we should pace our studies, new research suggests that we should aim for “minimal interference” during these breaks – deliberately avoiding any activity that could tamper with the delicate task of memory formation. So no running errands, checking your emails, or surfing the web on your smartphone. You really need to give your brain the chance for a complete recharge with no distractions.

An excuse to do nothing may seem like a perfect mnemonic technique for the lazy student, but this discovery may also offer some relief for people with amnesia and some forms of dementia, suggesting new ways to release a latent, previously unrecognised, capacity to learn and remember.

 
A simple technique could boost our short and long-term memory. Credit: Getty Images.
The remarkable memory-boosting benefits of undisturbed rest were first documented in 1900 by the German psychologist Georg Elias Muller and his student Alfons Pilzecker. In one of their many experiments on memory consolidation, Muller and Pilzecker first asked their participants to learn a list of meaningless syllables. Following a short study period, half the group were immediately given a second list to learn – while the rest were given a six-minute break before continuing. 

When tested one-and-a-half-hours later, the two groups showed strikingly different patterns of recall. The participants given the break remembered nearly 50 percent of their list, compared to an average of 28 percent for the group who had been given no time to recharge their mental batteries. The finding suggested that our memory for new information is especially fragile just after it has first been encoded, making it more susceptible to interference from new information.

Although a handful of other psychologists occasionally returned to the finding, it was only in the early 2000s that the broader implications of it started to become known, with a pioneering study by Sergio Della Sala at the University of Edinburgh and Nelson Cowan at the University of Missouri. 

 
We could all do with fewer distractions in our lives. Credit: Getty Images.
The team was interested in discovering whether reduced interference might improve the memories of people who had suffered a neurological injury, such as a stroke. Using a similar set-up to Muller and Pilzecker’s original study, they presented their participants with lists of 15 words and tested them 10 minutes later. In some trials, the participants remained busy with some standard cognitive tests; in others, they were asked to lie in a darkened room and avoid falling asleep.

The impact of the small intervention was more profound than anyone might have believed. Although the two most severely amnesic patients showed no benefit, the others tripled the number of words they could remember – from 14 to 49 percent, placing them almost within the range of healthy people with no neurological damage. 

The next results were even more impressive. The participants were asked to listen to some stories and answer questions an hour later. Without the chance to rest, they could recall just 7 percent of the facts in the story; with the rest, this jumped to 79 percent – an astronomical 11-fold increase in the information they retained. 

Della Sala and Cowan’s former student, Michaela Dewer at Heriot-Watt University, has now led several follow-up studies, replicating the finding in many different contexts. In healthy participants, they have found that these short periods of rest can also improve our spatial memories, for instance – helping participants to recall the location of different landmarks in a virtual reality environment. Crucially, this advantage lingers a week after the original learning task, and it seems to benefit young and old people alike. And besides the stroke survivors, they have also found similar benefits for people in the earlier, milder stages of Alzheimer’s disease. 

 
Our memory for new information is especially fragile just after it has been encoded. Credit: Getty Images.
In each case, the researchers simply asked the participants to sit in a dim, quiet room, without their mobile phones or similar distractions. “We don’t give them any specific instructions with regards to what they should or shouldn’t do while resting,” Dewar says. “But questionnaires completed at the end of our experiments suggest that most people simply let their minds wander.” 

Even then, we should be careful not to exert ourselves too hard as we daydream. In one study, for instance, participants were asked to imagine a past or future event during their break, which appeared to reduce their later recall of the newly learnt material. So it may be safest to avoid any concerted mental effort during our down time. 


The exact mechanism is still unknown, though some clues come from a growing understanding of memory formation. It is now well accepted that once memories are initially encoded, they pass through a period of consolidation that cements them in long-term storage. This was once thought to happen primarily during sleep, with heightened communication between the hippocampus – where memories are first formed – and the cortex, a process that may build and strengthen the new neural connections that are necessary for later recall. 

 
The brain might use downtime to cement what it has recently learnt. Credit: Getty Images.
This heightened nocturnal activity may be the reason that we often learn things better just before bed. But in line with Dewar’s work, a 2010 study by Lila Davachi at New York University, found that it was not limited to sleep, and similar neural activity occurs during periods of wakeful rest, too. In the study, participants were first asked to memorise pairs of pictures – matching a face to an object or scene – and then allowed to lie back and let their minds wander for a short period. Sure enough, she found increased communication between the hippocampus and areas of the visual cortex during their rest. Crucially, people who showed a greater increase in connectivity between these areas were the ones who remembered more of the task, she says. 

Perhaps the brain takes any potential down time to cement what it has recently learnt – and reducing extra stimulation at this time may ease that process. It would seem that neurological damage may render the brain especially vulnerable to that interference after learning a new memory, which is why the period of rest proved to be particularly potent for stroke survivors and people with Alzheimer’s disease. 

Other psychologists are excited about the research. “The effect is quite consistent across studies now in a range of experiments and memory tasks,” says Aidan Horner at the University of York. “It’s fascinating.” Horner agrees that it could potentially offer new ways to help individuals with impairments to function. 

 
Scheduling regular periods of rest could help us all hold onto new memories. Credit: Getty Images.
Practically speaking, he points out that it may be difficult to schedule enough periods of rest to increase their overall daily recall. But he thinks it could still be valuable to help a patient learn important new information – such as learning the name and face of a new carer. “Perhaps a short period of wakeful rest after that would increase the chances that they would remember that person, and therefore feel more comfortable with them later on.” Dewar tells me that she is aware of one patient who seems to have benefitted from using a short rest to learn the name of their grandchild, though she emphasises that it is only anecdotal evidence.

Thomas Baguley at Nottingham Trent University in the UK is also cautiously optimistic. He points out that some Alzheimer’s patients are already advised to engage in mindfulness techniques to alleviate stress and improve overall well-being. “Some [of these] interventions may also promote wakeful rest and it is worth exploring whether they work in part because of reducing interference,” he says, though it may be difficult to implement in people with severe dementia, he says. 

Beyond the clinical benefits for these patients, Baguley and Horner both agree that scheduling regular periods of rest, without distraction, could help us all hold onto new material a little more firmly. After all, for many students, the 10-30 percent improvements recorded in these studies could mark the difference between a grade or two. “I can imagine you could embed these 10-15 minute breaks within a revision period,” says Horner, “and that might be a useful way of making small improvements to your ability to remember later on.” 

In the age of information overload, it’s worth remembering that our smartphones aren’t the only thing that needs a regular recharge. Our minds clearly do too.
David Robson is a freelance writer based in London. He is @d_a_robson on Twitter. 


Friday, 22 May 2020

Exercise improves memory, boosts blood flow to brain

Exercise improves memory, boosts blood flow to brain:

Scientists have collected plenty of evidence linking exercise to brain health, with some research suggesting fitness may even improve memory.




Newswise —
DALLAS – May 20, 2020 – Scientists have collected plenty of evidence linking exercise to brain health, with some research suggesting fitness may even improve memory. But what happens during exercise to trigger these benefits?

New UT Southwestern research that mapped brain changes after one year of aerobic workouts has uncovered a potentially critical process: Exercise boosts blood flow into two key regions of the brain associated with memory. Notably, the study showed this blood flow can help even older people with memory issues improve cognition, a finding that scientists say could guide future Alzheimer’s disease research.

“Perhaps we can one day develop a drug or procedure that safely targets blood flow into these brain regions,” says Binu Thomas, Ph.D., a UT Southwestern senior research scientist in neuroimaging. “But we’re just getting started with exploring the right combination of strategies to help prevent or delay symptoms of Alzheimer’s disease. There’s much more to understand about the brain and aging.”

Blood flow and memory

The study, published in the Journal of Alzheimer’s Disease, documented changes in long-term memory and cerebral blood flow in 30 participants, each of them 60 or older with memory problems. Half of them underwent 12 months of aerobic exercise training; the rest did only stretching.
The exercise group showed a 47 percent improvement in some memory scores after one year compared with minimal change in the stretch participants. Brain imaging of the exercise group, taken while they were at rest at the beginning and end of the study, showed increased blood flow into the anterior cingulate cortex and the hippocampus – neural regions that play important roles in memory function.
Other studies have documented benefits for cognitively normal adults on an exercise program, including previous research from Thomas that showed aging athletes have better blood flow into the cortex than sedentary older adults. But the new research is significant because it plots improvement over a longer period in adults at high risk to develop Alzheimer’s disease.

“We’ve shown that even when your memory starts to fade, you can still do something about it by adding aerobic exercise to your lifestyle,” Thomas says.

Mounting evidence

The search for dementia interventions is becoming increasingly pressing: More than 5 million Americans have Alzheimer’s disease, and the number is expected to triple by 2050.

Recent research has helped scientists gain a greater understanding of the molecular genesis of the disease, including a 2018 discovery from UT Southwestern’s Peter O’Donnell Jr. Brain Institute that is guiding efforts to detect the condition before symptoms arise. Yet extensive research into how to prevent or slow dementia have not yielded proven treatments that would make an early diagnosis actionable for patients.

UT Southwestern scientists are among many teams across the world trying to determine if exercise may be the first such intervention. Evidence is mounting that it could at least play a small role in delaying or reducing the risk of Alzheimer’s disease.

For example, a 2018 study showed that people with lower fitness levels experienced faster deterioration of vital nerve fibers in the brain called white matter. A study published last year showed exercise correlated with slower deterioration of the hippocampus.

Regarding the importance of blood flow, Thomas says it may someday be used in combination with other strategies to preserve brain function in people with mild cognitive impairment.
“Cerebral blood flow is a part of the puzzle, and we need to continue piecing it together,” Thomas says. “But we’ve seen enough data to know that starting a fitness program can have lifelong benefits for our brains as well as our hearts.”

About the study

The Journal of Alzheimer’s Disease study was supported with funds from the National Institute on Aging (NIH grant R01AG033106). It included collaborations with Rong Zhang, Ph.D., at the Institute for Exercise and Environmental Medicine (IEEM), a partnership between UT Southwestern and Texas Health Presbyterian Hospital Dallas; and Hanzhang Lu, Ph.D., at Johns Hopkins Medicine.
About UT Southwestern Medical Center
UT Southwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institution’s faculty has received six Nobel Prizes, and includes 25 members of the National Academy of Sciences, 16 members of the National Academy of Medicine, and 14 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 2,500 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UT Southwestern physicians provide care in about 80 specialties to more than 105,000 hospitalized patients, nearly 370,000 emergency room cases, and oversee approximately 3 million outpatient visits a year.

Wednesday, 31 July 2019

The 'Secret' Healing Properties of Bamboo

The 'Secret' Healing Properties of Bamboo:

 If it Isn't in Your Cup, it Should Be

Views 2696

Originally published on www.thenhf.com
Bamboo: If it Isn't in Your Cup, it Should Be
Considered an invasive species by some, a Panda's favorite treat, "the King of Vegetables" with significant, multi-faceted health and practical-use benefits, bamboo needn't bamboozle or perplex you. Prolifically abundant, it serves us on so many levels. From supporting hair, nails, and building collagen, to rejuvenating skin and joints, to framing houses, creating furniture, and far more, bamboo has proven itself as a sustainable product and supreme provider.

GreenMedInfo.com cites 42 diseases and 29 pharmacological actions where bamboo exerts its powerful influence from cardiovascular to neurodegenerative diseases such as Alzheimer's disease, cognitive decline/dysfunction, dementia, brain damage and ischemia, to inflammation.[1] But bamboo doesn't stop there, from various types of cancers and chemotherapy-induced toxicity to diabetes and its complications, blood sugar, lipid, and immune system regulation, HIV and Cytomegalovirus infections, bamboo is a proven healer. Add more basic actions of bamboo on asthma, atopic dermatitis, anxiety and depression, and it makes me wonder why this isn't in everyone's cup? Toss it in along with whatever else you're steeping for some real health insurance.
Recorded as being consumed by the Chinese during the Ming Dynasty (AD 1368-1644) and found in a note from the Tang Dynasty (AD 618-907), bamboo is literally one of the most useful plants on the Planet. The tallest member of the grass family, bamboo is from the Bambusoideae subfamily. Taxonomically, there are 1,641 bamboo species, 120 genera, and 3 tribes from this subfamily.
Bamboo is characterized by its strong but flexible upright flight to the sky. It can reach astounding heights, growing several feet per day. One chart shows a single cane growing to 25 feet in 25 days! Bamboo spreads vigorously, taking territory vertically as well as horizontally. The weight of a heavy, wet snow merely displays its incredible flexibility as it bends nearly flat only to spring up tall again once the snow melts. These great properties lend themselves well to the creation of health and raw materials from nutraceuticals to flooring, plywood, and even bedding. More uses emerge all the time from this "green" gift. Trendy bamboo has allowed America to surpass China and Japan in having the greatest number of bamboos. My Philippine friend tells me the soil around the bamboo is the best for potting soil.

Why drink plain water when you can potentiate it with an herbal pharmacy in a cup? Bamboo leaves make an herbal decoction that tastes great - like an earthy green tea - and can easily become your daily health-habit ritual either taken alone or mixed with other herbal teas such as jasmine and mint in creative, exotic blends. Use the usual ratio of one teaspoon of dried leaves to a cup of pure water, steeping it for 5-10 minutes. If you have a structured water filter, it will pull the nutrition out without you even having to heat the water. The addition of monk fruit, stevia, raw honey, or lemon enhances the flavor of this delicate tea. However, because some bamboo has been found on DNA testing to be adulterated, pregnant women are advised to avoid it as consumption could induce abortion. Fertile and pregnant women should therefore consult a healthcare provider prior to including bamboo in their diet.

Young shoots of bamboo, harvested the first two weeks after their appearance and under a foot tall, boiled to just crisp-tender, are a staple in Asian countries such as the Philippines, India, Nepal, Japan, Indonesia, Thailand, Korea, and of course, China. Highly versatile, bamboo shoots take on other flavors. Canned or fresh, they are easily available at Asian markets. As a vegetable side dish flavored with seasonings, butter, or ghee, or used in a stir fry with other proteins or vegetables and sauce, or added to soups and salads, bamboo shoots are an invaluable health-addition. In Indonesia and the Philippines, bamboo shoots are made into a type of spring roll called Lumpia. Bamboo-shoot recipes abound on internet sites for both vegan and meat-based versions.

On my own land, a few gallon pots of bamboo planted several years ago have now morphed into a veritable forest both in height and in terrain covered. For this reason, many gardeners contain bamboo plants in a concrete trench or other boundary. Because of its high glass-like silica content, cutting bamboo cane isn't easy but anyone can easily harvest its leaves. While my fresh, organic leaves harvested this morning are dehydrating to use in tea (purchasing it is approximately $6.55 per ounce!), I will tell you more exactly why bamboo leaves and shoots are truly the King of Vegetables.
Last year I was excited about horsetail, which we can wildcraft here, wanting the strong fingernails and beautiful hair that natural silicon imparts. But when I found out that bamboo leaf tea has ten times the silica that horsetail extract has, deciding to jumpstart the process was logical. Horsetail averages 5-8% organic silica. Bamboo leaf contains an amazing 70% organic silica!
Amazingly, this innocuous, ancient plant is a powerhouse of amino acids, fatty acids, vitamins, minerals, chlorophyll, soluble fiber, and carbohydrates. Medicinally, bamboo is cooling and calming. In addition to uses listed above is it also good for digestion, obesity, lung, chest, stomach, heart, and urinary dysfunction. It is detoxifying, quelling inflammation. Bamboo leaves and shoots are important for male fertility, influencing thyroid hormones, balancing blood sugar levels and they are a powerful antioxidant reducing cellular damage. Bamboo is good for bone and dental health and promotes general overall wellness. It is antibacterial and helps in asthma cases too.

Lignins are a complex organic polymer deposited in the cell walls of many plants such as bamboo making them rigid and woody. Lig-8, a lignophenol derivative from bamboo lignin, is a highly potent neuroprotectant protecting against apoptosis (self-induced cell death). One protective mechanism provided by bamboo lignins impacts retinal ganglion cells. With glaucoma diagnosis rising, this 2007 study is of particular interest when it states that, "Apoptotic cell death is associated with neurodegenerative disorders such as Alzheimer, Parkinson, or Huntington disease as well as glaucoma. We believe that the elucidation of the mechanism of antiapoptotic action of lig-8 may help in finding new approaches to the treatment of neurodegenerative disorders." [2]

As we appreciate the multifaceted abilities of bamboo in its many forms, including bamboo vinegar (which is made from bamboo charcoal and used in detox foot pads), you will hopefully find several ways to include bamboo leaves and shoots in your diet to support and balance the body, mind, and spirit. As with any natural substance, add the factor of time, typically a few months, in order to register benefits. Meantime, this ritual will restore health on the cellular level and with a great deal of pleasure in the process. From harvest to cup, processing the bamboo-leaf by dehydration doesn't take long at all. Here's to inexpensive, sustainable health in a cup!

© 2019 Katherine A. Carroll; first published on the National Health Federation website, www.thenhf.com
Want to learn more about bamboo's positive affects on health? Visit the GreenMedInfo database on the subject today.


Thursday, 11 July 2019

Anticholinergic drugs increase your risk for dementia

Risk of Dementia


 We must do everything we can to prevent this condition!  But best to check which drugs make the risk of Dementia more likely!

Story at-a-glance

  • While dementia and Alzheimer’s disease (the most advanced, severe and lethal form of dementia) are primarily diet- and lifestyle-driven, certain medications can also ramp up your risk
  • One of the riskiest classes of drugs in this regard are anticholinergic drugs, prescribed for a wide variety of conditions, including depression, incontinence, insomnia, allergies and epilepsy
  • Recent research assessing effects of 56 anticholinergics found statistically significant associations between dementia and anticholinergic antidepressants, antiparkinson drugs, antipsychotic drugs, bladder antimuscarinics and antiepileptic drugs
  • In the highest exposure group (excess of 1,095 standardized daily doses over the past one to 11 years before diagnosis), the odds ratio for dementia was between 44% and 54%, with an average of 49%; anticholinergic antipsychotics raise risk by 70%
  • A 2009 scientific review found all but two of 27 studies found an association between the anticholinergic activity of medications and either delirium, cognitive impairment or dementia
While dementia and Alzheimer’s disease (the most advanced, severe and lethal form of dementia) are primarily diet- and lifestyle-driven, certain medications can also ramp up your risk.
One of the riskiest classes of drugs in this regard are anticholinergic drugs, prescribed for such widely varying conditions such as depression, incontinence, insomnia, allergies and epilepsy.1 You can find a long list of anticholinergic drugs and the different conditions they’re used for on seniorlist.com.2
Anticholinergic drugs block acetylcholine, a neurotransmitter that performs important functions in your peripheral and central nervous systems, both as an activator and an inhibitor.3
For example, it triggers muscle contractions and pain responses, and is involved in the regulation of your endocrine system and REM sleep cycle. Of all the known neurotransmitters, acetylcholine is the most abundant.4
As reported by CNN,5 a recent observational study6 looking at anticholinergics and dementia risk “suggests that the link is strongest for … antidepressants such as paroxetine or amitriptyline, bladder antimuscarinics such as oxybutynin or tolterodine, antipsychotics such as chlorpromazine or olanzapine and antiepileptic drugs such as oxcarbazepine or carbamazepine.”

Study highlights risks of anticholinergic drugs

The research,7,8 published online in JAMA Internal Medicine, June 24, 2019, assessed data from 58,769 patients over the age of 55 diagnosed with dementia and 225,574 matched controls.
In all, the outcomes for 56 different anticholinergic drugs were assessed by looking at exposure to “standardized daily doses” of the drugs prescribed over the previous one to 11 years before the patient received a diagnosis of dementia.
After controlling for confounding variables that might influence the results, the researchers concluded “there were statistically significant associations of dementia risk with exposure to anticholinergic antidepressants, antiparkinson drugs, antipsychotic drugs, bladder antimuscarinics and antiepileptic drugs.”
Compared to those who did not use anticholinergic drugs, those in the lowest exposure group (taking between just one and 90 standardized doses over the previous one to 11 years), the adjusted odds ratio for dementia was, on average, 6%.
In the highest exposure group (excess of 1,095 standardized daily doses over the past one to 11 years before diagnosis), the odds ratio for dementia was between 44% and 54%, with an average of 49%. Even between the different types of anticholinergics there were significant variations in risk. Among those with the highest exposure:
  • Anticholinergic antidepressants had an average adjusted odds ratio for dementia of 29%
  • Antiepileptic drugs had an average adjusted odds ratio of 39%
  • Antiparkinson drugs 52%
  • Bladder antimuscarinic drugs (prescribed for overactive bladder9) 65%
  • Antipsychotics 70%

Middle-aged individuals urged to minimize exposure

The strongest associations were seen in those diagnosed with dementia before the age of 80. The adjusted odds ratio for those in the highest exposure group who were diagnosed with dementia after the age of 80 was 35%, while the odds for those diagnosed before the age of 80 was a whopping 81%.10
No significant gender differences were found. Overall, vascular dementia was more common than Alzheimer’s disease, with odds for vascular dementia in the highest exposure group being 68% compared to 37% for Alzheimer’s.11 As noted by the authors:
“Exposure to several types of strong anticholinergic drugs is associated with an increased risk of dementia. These findings highlight the importance of reducing exposure to anticholinergic drugs in middle-aged and older people.”
“No significant increases in risk” for dementia were found for anticholinergic antihistamines, muscle relaxants, antispasmodics (prescribed for gastrointestinal problems), antiarrhythmics and antimuscarinic bronchodilators.12



Avoiding anticholinergics may improve cognition, says JAMA study

While the authors of the featured JAMA study point out it cannot prove causality, it’s not the first study to find this link. There are quite a few of them in the medical literature, which you can find by searching PubMed.gov, the free online library of medicine run by the U.S. National Institutes of Health.13
Among them you’ll find the 2009 paper,14 “The Cognitive Impact of Anticholinergics: A Clinical Review,” which analyzed the results of 27 studies in which “anticholinergic activity was systematically measured and correlated with standard measurements of cognitive performance.”
According to the authors, “All but two studies found an association between the anticholinergic activity of medications and either delirium, cognitive impairment or dementia,” which led to the conclusion that:
“Medications with anticholinergic activity negatively affect the cognitive performance of older adults. Recognizing the anticholinergic activity of certain medications may represent a potential tool to improve cognition.”

Some anticholinergics clearly worse than others

A case-control study15 published in 2018 in the BMJ — which like the featured JAMA study looked at the effects of various classes of anticholinergics — also found that antidepressant, urological and antiparkinson drugs posed the greatest risk. As noted by the authors:16
“It is well known that anticholinergics affect cognition, and guidelines suggest they are to be avoided among frail older people. Use of anticholinergic drugs among people with dementia is recognized as inappropriate by both the Beers and the Screening Tool of Older Persons' potentially inappropriate Prescriptions (STOPP) criteria.
Over the past decade, prolonged exposure to anticholinergic drugs has been linked to long term cognitive decline or dementia incidence among community living cohorts and nursing home residents.”
Here, the researchers included 40,770 patients newly diagnosed with dementia, and compared their outcomes with their use of anticholinergic drugs four to 20 years before their diagnosis.
Each patient was compared to as many as seven matched controls who did not have dementia. The median age at diagnosis was 83 and the median drug exposure period was 7.1 years.17 The study had three stated objectives:18
  1. Assessing the effect of chronic anticholinergic drug use on dementia incidence
  2. Exploring whether observed effects are restricted to any particular drug class. Drugs were divided into three groups based on the “anticholinergic cognitive burden (ACB) scale,”19 where a score of 3 means the drug has “definite anticholinergic activity” and is known to significantly raise the risk of cognitive impairment
  3. Testing how the risk might vary based on the amount of exposure to any given drug class and the timing of use
The primary analysis found “a positive and significant association” between anticholinergics and dementia, regardless of their ACB score. Those with an ACB score of 1 and 2 had an odds ratio of 10% and drugs with an ACB score of 3 had an odds ratio of 11%.
The primary difference between the ACB classes were the dose-response effect. Drugs with an ACB score of 2 or 3 had a clear dose-dependent response, whereas drugs with a score of 1 did not.20 As for objective 2, the researchers found:
“When analyzed by class, there was a significant association between dementia incidence and any prescription of antidepressant, antiparkinson, or urological drugs with an ACB score of 3, but no association with antispasmodic, antipsychotic, antihistamine, or other drugs with an ACB score of 3.
Prescriptions for drugs with an ACB score of 2 were relatively rare, and so results are imprecise in this group, but there is some evidence for an association between dementia incidence and prescription of antiparkinson drugs.
We found positive associations for antidepressant drugs with an ACB score of 1 with an increased risk of dementia, but not with any other drugs with an ACB score of 1.”
Lastly, the timing of the drug exposure was assessed, looking at three different sets of time intervals: four to 10 years, 10 to 15 years, and 15 to 20 years of use before dementia diagnosis. For drugs with an ACB score of 3, the risk was “consistent” across all three exposure periods, although the strongest association was seen for ACB 3-class drugs used for 15 to 20 years before diagnosis. For this group, the odds ratio for dementia was between 10% and 24%, with an average of 17%.
Antidepressants and urological drugs with an ACB score of 3 “remained consistently significantly associated with dementia incidence,” with antidepressants having an average odds ratio of 19% and urological drugs 27%.21 For drugs with ACB scores of 1 and 2, the risks became more apparent closer to the date of diagnosis. As noted by the authors:
“[F]or antidepressants with an ACB score of 1, the association with dementia increased for prescriptions given in periods closer to a diagnosis of dementia. Similarly, the negative association between gastrointestinal drugs and dementia was not seen for exposures 15-20 years before the index date.”

Behavioral changes can be an early sign of dementia

As you can see, even within a single class of drugs, in this case, drugs broadly classified as anticholinergics, you find all sorts of factors that can increase or decrease their risks to any given individual.
Overall, however, anticholinergics as a group are risky, and the risk of dementia increases the longer you’re on them. Even if the drug in question has a low ACB score, if you’re on it for decades, the risk of dementia creeps up. It would be wise for everyone to be on the lookout for early signs of dementia, but especially so if you’re on an anticholinergic drug.
Now, dementia is not a disease in itself; it’s a term used to describe a number of different brain illnesses that may affect your memory, thinking, behavior and ability to perform everyday activities. Many people associate dementia with memory loss — and this is a red flag — however, not all memory problems are due to dementia or Alzheimer’s.
As noted by the Alzheimer’s Association,22 some causes of dementia-like symptoms (including memory loss), such as those related to thyroid problems and vitamin deficiencies, are reversible with proper treatment.
Before memory and thinking problems become obvious, people with dementia will often display changes in mood and behavior. A person may, for instance, stop doing something they’ve always loved to do, be it cooking a certain dish for your birthday or watching the evening news.
Apathy is another common sign, although some people may display more blatant changes like suddenly becoming sexually promiscuous or developing the habit of snatching food from other people’s plates.23,24
At the 2016 Alzheimer’s Association International Conference, a group of Alzheimer’s experts presented a 34-question checklist25 of signs of mild behavioral impairment (MBI), which they believe might help identify patients at high risk for Alzheimer’s.
Those with sudden mood or behavioral changes that persist tend to develop dementia at a faster rate.26,27 The MBI checklist was published in the Journal of Alzheimer’s Disease in 2017.28 You can find a copy of the questionnaire here.

Is it age-related forgetfulness or something more serious?

Aside from that, the Alzheimer's Association has also compiled a list29 of early signs and symptoms of Alzheimer’s, along with suggestions for how to determine whether you’re dealing with typical age-related changes or something more serious:
Signs of Alzheimer's/dementia Typical age-related changes
Poor judgment and decision-making Making a bad decision once in a while
Inability to manage a budget Missing a monthly payment
Losing track of the date or the season Forgetting which day it is and remembering it later
Difficulty having a conversation Sometimes forgetting which word to use
Misplacing things and being unable to retrace steps to find them Losing things from time to time
As mentioned at the outset, Alzheimer’s is primarily diet- and lifestyle driven. In fact, it shares many risk factors with heart disease, including insulin resistance and diabetes. For a list of dietary strategies and general lifestyle guidelines that can help prevent Alzheimer’s, see “Link Between Sugar and Alzheimer's Strengthens.”
To learn more about Alzheimer’s and the tests that can help diagnose it early, see my interview with Dr. Dale Bredesen, author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline.”

Friday, 29 March 2019

B Vitamins Slow Alzheimer's and Grey Matter Loss

Memory Loss



Views 9403
B Vitamins Slow Alzheimer's and Grey Matter Loss
Researchers from the University of Oxford have determined that B vitamin supplementation can slow and possibly reverse the progression of Alzheimer's symptoms along with cognitive impairment.
The researchers – from Oxford's Nuffield Department of Clinical Neurosciences - conducted a clinical trial with 156 elderly patients who had mild cognitive impairment and a high risk of dementia and Alzheimer's disease. The researchers randomized the patients and for two years, gave one group a daily supplement with 800 micrograms of folic acid, 20 milligrams of vitamin B6, and 500 micrograms of vitamin B12. They gave a placebo supplement to the control group.
Before the trial and during the testing period, the researchers utilized magnetic resonance imaging (MRI) to measure the patients' atrophy levels of grey matter in their brains. Atrophying grey matter is a sign of the progression of Alzheimer's disease and other forms of dementia. Atrophy in the grey matter is shown as the amount of grey matter shrinks in the imaging tests.
While grey matter regions did shrink among both groups, the researchers found that those given the B vitamin supplements had about seven times less grey matter shrinkage than did the placebo group.
The researchers also found that those whose grey matter shrunk fastest had higher levels of homocysteine, and those with higher homocysteine levels received the greatest benefit from the B vitamin supplements. They summarized the effects thus:
"B vitamins lower homocysteine, which directly leads to a decrease in grey matter atrophy, thereby slowing cognitive decline."
The researchers also conducted neuropsychological testing on the patients to correlate their grey matter losses with neuropsychological function. Their testing concluded that the B vitamins not only helped reduce grey matter losses, but also reduced the drop in neuropsychological scores among the supplement group.
In their conclusion the researchers stated:
"Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the Alzheimer disease process and that are associated with cognitive decline."
Researchers from the University of Oxford have determined that B vitamin supplementation can slow and possibly reverse the progression of Alzheimer's symptoms along with cognitive impairment.
The researchers – from Oxford's Nuffield Department of Clinical Neurosciences - conducted a clinical trial with 156 elderly patients who had mild cognitive impairment and a high risk of dementia and Alzheimer's disease. The researchers randomized the patients and for two years, gave one group a daily supplement with 800 micrograms of folic acid, 20 milligrams of vitamin B6, and 500 micrograms of vitamin B12. They gave a placebo supplement to the control group.
Before the trial and during the testing period, the researchers utilized magnetic resonance imaging (MRI) to measure the patients' atrophy levels of grey matter in their brains. Atrophying grey matter is a sign of the progression of Alzheimer's disease and other forms of dementia. Atrophy in the grey matter is shown as the amount of grey matter shrinks in the imaging tests.
While grey matter regions did shrink among both groups, the researchers found that those given the B vitamin supplements had about seven times less grey matter shrinkage than did the placebo group.
The researchers also found that those whose grey matter shrunk fastest had higher levels of homocysteine, and those with higher homocysteine levels received the greatest benefit from the B vitamin supplements. They summarized the effects thus:
"B vitamins lower homocysteine, which directly leads to a decrease in grey matter atrophy, thereby slowing cognitive decline."
The researchers also conducted neuropsychological testing on the patients to correlate their grey matter losses with neuropsychological function. Their testing concluded that the B vitamins not only helped reduce grey matter losses, but also reduced the drop in neuropsychological scores among the supplement group.
In their conclusion the researchers stated:
Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the Alzheimer disease process and that are associated with cognitive decline."

Other Studies Confirm the Link Between B Vitamins, Homocysteine and Alzheimer's

However, other studies have linked B vitamins and high homocysteine levels with cognitive decline, Alzheimer's disease and dementia.
For example, in a study from Korea's Ewha Womans University, 321 elderly people were studied and tested for cognitive function, together with their levels of vitamin B12, folate and homocysteine.
After using multiple regression analysis, low folate levels were associated with low scores on naming tests, and low levels of vitamin B12 in the blood were related to low scores on word list memory. High homocysteine levels were also associated with low scores on word memory and construction recall testing.
The researchers stated in their conclusion:
"These results suggest that plasma folate, vitamin B12, homocysteine and tissue factor pathway inhibitor are associated with cognitive function in cognitively impaired (Alzheimer's disease and Mild cognitive impairment) elderly and that the association was stronger in patients with Alzheimer's disease."

What is Homocysteine and why are High Levels so Bad?


Increased homocysteine levels have also been linked with cardiovascular disease – more specifically the progression of atherosclerosis or the hardening of the arteries. Thus, high homocysteine levels have been found among those who have suffered from strokes and heart attacks.
Elevated homocysteine levels are anything higher than 10-15 μmol/L depending upon the age and health of the patient. The Oxford researchers classified their high homocysteine patients as those with levels of 11 μmol.
Homocysteine and its two partners methionine and cysteine, is involved in the metabolic detoxification process called methylation. This transfers methyl groups from one molecule to another. When a methyl group is transferred to a oxidative toxin it speeds its discharge from the body. Higher levels of homocysteine are typically accompanied by higher levels of oxidative radicals and toxins in the liver and blood stream.
If not neutralized, these toxins cause oxidative damage to blood vessels and cells - including brain and nerve cells.
Various nutrients – including B vitamins as well as many other phytonutrients – are considered methyl donors: They donate methyl groups, which assists the body's detoxification and healing efforts. Healthy methylation also helps protect cellular DNA from mutation.
It should also be noted that folate - nature's form - may be a better form of the B9 vitamin than folic acid. Excessive folic acid supplementation has been linked with increased cancer risk. A 2009 study showed folic acid fortification increased colon cancer risk.
Food sources of folate include parsley, turnip and mustard greens, collard greens, romaine lettuce, spinach, asparagus, broccoli, cauliflower and beets. Lentils and brewer's yeast are also good sources. In supplements, the 5-methyltetrahydrofolate (5-MTHF) nutrient offers an option to synthesized folic acid.

Learn how to naturally speed up the detoxification process.

REFERENCES:
Douaud G, Refsum H, de Jager CA, Jacoby R, Nichols TE, Smith SM, Smith AD. Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment. Proc Natl Acad Sci U S A. 2013 Jun 4;110(23):9523-8.
Morris MS. The role of B vitamins in preventing and treating cognitive impairment and decline. Adv Nutr. 2012 Nov 1;3(6):801-12.
Kim G, Kim H, Kim KN, Son JI, Kim SY, Tamura T, Chang N. Relationship of cognitive function with B vitamin status, homocysteine, and tissue factor pathway inhibitor in cognitively impaired elderly: a cross-sectional survey. J Alzheimers Dis. 2013;33(3):853-62.
Hirsch S, Sanchez H, Albala C, de la Maza MP, Barrera G, Leiva L, Bunout D. Colon cancer in Chile before and after the start of the flour fortification program with folic acid. Eur J Gastroenterol Hepatol. 2009 Apr;21(4):436-9.
Pietrzik K, Bailey L, Shane B. Folic acid and L-5-methyltetrahydrofolate: comparison of clinical pharmacokinetics and pharmacodynamics. Clin Pharmacokinet. 2010 Aug;49(8):535-48.
Originally published: 2013-08-08
Article updated: 2019-05-25
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.

Saturday, 17 November 2018

Stress, A Dangerous Killer

Stress is detrimental to your health



Story at-a-glance

  • Research has linked chronic stress with brain shrinkage, working memory impairment and an increased risk for early onset of Alzheimer’s disease
  • Having elevated blood levels of the stress hormone cortisol can impair your thinking skills and memory over time. A previous study suggests elevated cortisol affects your memory by causing a gradual loss of synapses in your prefrontal cortex
  • Research suggests you can slow down the rate of cognitive decline by 75 percent by restoring your hearing with hearing aids, and by 50 percent by restoring vision through cataract surgery
  • Among the most valuable dementia prevention strategies is a cyclical ketogenic diet, as it optimizes mitochondrial function and supports healthy brain function
  • Other important lifestyle factors that influence your dementia risk include sleep, physical fitness and exposure to electromagnetic fields
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  • Studies have found strong links between acute and/or chronic stress and a wide variety of health issues, including your brain function and risk for dementia. For example, animal research1 published in 2014 reported that elevated levels of stress hormones can speed up short-term memory loss in older adults by inducing structural changes in the brain.
    The findings indicate that how your body responds to stress may be a factor that influences how your brain ages over time. Previous research has also linked chronic stress with working memory impairment2 and an increased risk for early onset of Alzheimer's disease.3
    Fortunately, there's compelling research showing your brain has great plasticity and capacity for regeneration, which you control through your diet and lifestyle.
    Based on the findings linking dementia with chronic stress, having effective tools to address stress can be an important part of Alzheimer's prevention, not to mention achieving and maintaining optimal health in general.

    Stress Impairs Cognition and Memory, Recent Research Shows

    Most recently, researchers warn that having elevated blood levels of the stress hormone cortisol can impair your thinking skills and memory over time.4,5,6,7 The researchers used the government-sponsored Framingham Heart Study database to identify more than 2,200 people who did not have any signs of dementia, and followed them for eight years. As reported by The New York Times:8
    "Researchers gave tests for memory, abstract reasoning, visual perception and attention to 2,231 people, average age 49 and free of dementia. They recorded blood levels of cortisol and did MRI examinations to assess brain volume.
    The study,9 in Neurology, controlled for age, sex, education, body mass index, blood pressure and many other variables, and found that compared with people with average levels of cortisol, those with the highest levels had lower scores on the cognitive tests.
    In women, but not in men, higher cortisol was also associated with reduced brain volume. There was no association of the lowest cortisol levels with either cognitive test scores or brain size."
    A significant limitation of the study is the fact that blood levels of cortisol were only checked once, at the end of the study, and may therefore not be representative of people's long-term exposure to this stress chemical.
    Still, a number of other studies have reported similar findings, so the link between stress and cognitive decline certainly appears to be real. Lead author Dr. Justin Echouffo-Tcheugui, assistant professor of medicine at Johns Hopkins School of Medicine, commented on the findings:10
    "Our research detected memory loss and brain shrinkage in middle-aged people before symptoms started to show in ordinary, daily activities.
    So, it's important for people to find ways to reduce stress, such as getting enough sleep, engaging in moderate exercise, incorporating relaxation techniques into their daily lives, or asking their doctor about their cortisol levels and taking a cortisol-reducing medication if needed. It's important for physicians to counsel all people with higher cortisol levels."

    Stress Hormones Have a Corrosive Effect in Your Brain

    When you're stressed, your cortisol rises and, together with adrenaline, triggers your body's fight-or-flight response. Cortisol also increases the glucose level in your bloodstream and temporarily enhances your brain's use of that glucose, while simultaneously suppressing bodily functions deemed irrelevant during an emergency, such as digestion.
    While this cascade of biochemical effects is beneficial when you're in immediate physical danger, cortisol has a corrosive effect that, over time, actually wears down the synapses responsible for memory storage and processing. This was demonstrated in the 2014 animal study11 mentioned earlier.
    According to that study,12 elevated levels of cortisol affect your memory by causing a gradual loss of synapses in your prefrontal cortex, the brain region associated with short-term memory. As noted by the authors:
    "Short-term increases in cortisol are critical for survival. They promote coping and help us respond to life's challenges by making us more alert and able to think on our feet.
    But abnormally high or prolonged spikes in cortisol — like what happens when we are dealing with long-term stress — can lead to negative consequences that numerous bodies of research have shown to include digestion problems, anxiety, weight gain and high blood pressure."
    While the authors of the Neurology study state that it is "premature to consider intervention" based on their findings,13 they suggest that lowering your cortisol may be a beneficial first step. The 2014 study authors also suggested you may be able to protect your future memory function by normalizing your cortisol levels.
    Such intervention would be particularly beneficial for those who are at high risk for elevated cortisol, such as those who are depressed or are dealing with long-term stress following a traumatic event.

    Stress May Trigger Clinical Onset of Alzheimer's

    Other scientific findings have linked stress and severe dementia. Argentinian research14 presented at the World Congress of Neurology in 2013 suggests stress may actually act as a trigger for the onset of Alzheimer's disease, as nearly 3 in 4 Alzheimer's patients (72 percent) had experienced severe emotional stress during the two years preceding their diagnosis.
    In the control group, only 26 percent, or 1 in 4, had undergone major stress or grief. Most of the stresses encountered by the Alzheimer's group involved:
  • Bereavement — death of a spouse, partner, or child
  • Violent experiences, such as assault or robbery
  • Car accidents
  • Financial problems, including "pension shock"
  • Diagnosis of a family member's severe illness
According to lead author Dr. Edgardo Reich:15
"Stress, according to our findings, is probably a trigger for initial symptoms of dementia. Though I rule out stress as monocausal in dementia, research is solidifying the evidence that stress can trigger a degenerative process in the brain and precipitate dysfunction in the neuroendocrine and immune system. It is an observational finding and does not imply direct causality. Further studies are needed to examine these mechanisms in detail."

Vision and Hearing Problems Also Linked to Dementia

Aside from managing daily stresses, protecting your vision and hearing are other important factors that can influence your dementia risk. In fact, recent research16 suggests you can actually slow down cognitive decline by restoring your hearing and/or vision, and by a significant degree.
Lead author Dr. Asri Maharani, a researcher at the University of Manchester in the division of neuroscience and experimental psychology, told NPR,17 "We found the rate of cognitive decline was slowed by 75 percent following the adoption of hearing aids. It is a surprising result."
While the researchers were surprised by the findings, it does make sense. As noted by Dina Rollins, an audiologist who was not involved in the study, "Stimulating your ears stimulates the nerves that stimulate your brain," so by restoring hearing, you're "giving your brain what it needs to make sense of what you're hearing."
Another possible reason for this link has to do with the fact that hearing loss leads to social isolation, which has also been shown to speed cognitive decline and raise your risk of dementia. A related study18 by the same research group shows cognitive decline is also slowed by restoring vision. Here, Maharani's team found that cataract surgery slowed the rate of cognitive decline by 50 percent.

Ketogenic Diet Protects Against Dementia

As mentioned, there's good news in all of this, and it's that your brain has a natural capacity for regeneration and rejuvenation. Among the most valuable dementia prevention strategies is a cyclical ketogenic diet described in my book, "Fat for Fuel" and many other articles. If you're new to this topic, see "Burn Fat for Fuel" or "A Beginner's Guide to the Ketogenic Diet" for an introduction.
In short, a ketogenic diet, being high in healthy fats and low in net carbohydrates, allows your body to start burning fat as its primary fuel and results in the creation of ketones. And, compared to glucose, ketones:
  • Burn more efficiently
  • Are a superior fuel for your brain
  • Generate fewer reactive oxygen species and less free radical damage
  • Influence DNA expression to increase detoxification and antioxidant production
  • Inhibit inflammation
Recent research19,20,21,22,23 shows a ketogenic diet improves neurovascular integrity and function and clearance of amyloid-beta (a main component of the plaque that accumulates in the brains of those with Alzheimer’s disease) — in part by improving the gut microbiome — and neurovascular function plays a major role in cognitive capability.
More specifically, poor neurovascular function is strongly associated with loss of language, memory and attention, while reduced cerebral blood flow raises your risk for depression, anxiety and dementia. Impaired blood-brain barrier function has also been linked to brain inflammation, dysfunction of synapses, impaired clearance of amyloid-beta plaques, psychiatric disorders and dementia.24
According to the authors, "Our findings suggest that ketogenic diet intervention started in the early stage may enhance brain vascular function, increase beneficial gut microbiota, improve metabolic profile, and reduce risk for Alzheimer's disease."

High-Sugar Diet Is a Recipe for Dementia

It's important to realize the adverse impact sugar has on your brain. A high-sugar diet triggers insulin resistance, and there's a very strong link between insulin resistance and Alzheimer's.25 For example, a longitudinal study26 published in the journal Diabetologia in January 2018, found that the higher an individual's blood sugar, the faster their rate of cognitive decline.
Even mild elevation of blood sugar and mild insulin resistance are associated with an elevated risk for dementia.27,28 Research29 published in 2013 showed that sugar and other carbohydrates disrupt your brain function primarily by shrinking your hippocampus, a brain region involved with the formation, organization and storage of memories.
The authors suggest that “strategies aimed at lowering glucose levels even in the normal range may beneficially influence cognition in the older population.” A similar study30 published in 2014 found that Type 2 diabetics lose more gray matter with age than expected, and this brain atrophy also helps explain why diabetics have a higher risk for dementia, and have earlier onset of dementia than nondiabetics.
As noted by Dr. Sam Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York City, these findings “suggest that chronic high levels of insulin and sugar may be directly toxic to brain cells” and that “this would definitely be a potential cause of dementia."31
Perhaps one of the most striking studies32 on carbohydrates and brain health revealed high-carb diets increase your risk of dementia by 89 percent, while high-fat diets lower it by 44 percent.

Sleep, Exercise and EMF Avoidance Are Other Key Dementia Prevention Strategies

Aside from stress and diet, three other lifestyle areas that play important roles in the development of dementia are sleep, physical fitness and exposure to electromagnetic fields (EMFs), the influence of which are summarized below.
• Sleep — Wakefulness is associated with mitochondrial stress. Without sufficient sleep, neuron degeneration sets in, which can lead to dementia.33,34,35 In fact, sleep deprivation is a risk factor for severe dementia, and animal research36 reveals inconsistent, intermittent sleep results in considerable and irreversible brain damage.
Research published in the journal Neurobiology of Aging37 suggests people with chronic sleep problems also develop Alzheimer's disease sooner than those who sleep well.
Your blood-brain barrier becomes more permeable with age, allowing more toxins to enter.38 This, in conjunction with reduced efficiency of the glymphatic system due to lack of sleep, allows for more rapid damage to occur in your brain and this deterioration is thought to play a significant role in the development of Alzheimer's.
• Exercise — Recent research39 found women with the highest cardiovascular fitness had an 88 percent lower risk of dementia than those with moderate fitness. Even maintaining average fitness is worthwhile, as women with the lowest fitness had a 41 percent greater risk of dementia than those of average fitness.
• Electromagnetic field (EMF) exposure — Microwaves emitted from cellphones, Wi-Fi routers, computers and tablets (when not in airplane mode) harm your brain by increasing intracellular calcium through the voltage gated calcium channels (VGCCs) in your cells.
The tissues with the highest density of VGCCs are your brain, the pacemaker in your heart and male testes. Once VGCCs are stimulated, they trigger the release of neurotransmitters, neuroendocrine hormones and highly damaging reactive oxygen species, significantly raising your risk of anxiety, depression and neurodegenerative diseases like Alzheimer's.40
Basic prevention strategies include turning your Wi-Fi off at night, not carrying your cellphone on your body and not keeping portable phones, cellphones and other electric devices in your bedroom. To learn more, see my interview with professor Martin Pall. A more extensive list of prevention strategies to minimize your EMF exposure can be found in "Electromagnetic Radiation Specialist Reveals the Hidden Dangers of Electric Fields."
While I believe these are among the most important prevention strategies, there are of course many other factors that can come into play. To learn more about the prevention and reversal of cognitive decline, see my interview with Dr. Dale Bredesen, director of neurodegenerative disease research at the University of California, Los Angeles School of Medicine, whose unique ReCODE (Reversal of Cognitive Decline) program offers hope for many.