Troubling news from a new study, published in the Journals of Gerontology: Social Sciences:  Baby Boomers’ brains aren’t aging well.  Compared to previous generations, Boomers in this ongoing study, of 30,191 Americans over age 50, are experiencing a sharper drop in cognitive function, and are more likely to develop dementia.  And… PAUSE!

Before we start wringing our hands in despair, I want to say right now that I don’t think that shuffling around with an adult diaper is our inevitable fate.  I don’t think that at all, and I don’t think the study’s author, Hui Zheng, Ph.D., from the Department of Sociology, Institute for Population Research, at Ohio State University, believes it.  I think, and I think these results suggest, that this can be changed.

I’m going to come back to this in a minute.  First, let me briefly recap this research project, an analysis of nearly 20 years of results from the Health and Retirement Study.  Among other things, the study’s participants get their cognitive function checked every two years.  Basically, they take a “cognitive battery” of tests:  they do things like remember objects and words they’ve been shown recently, and count backwards from 100 by 7s (If you can’t do this easily, don’t feel bad about yourself; it’s supposed to be a challenge – at least, it is for me!).

In this study, Zheng analyzed the results collected from 1996 to 2014, from people in these groups:  Greatest Generation (born 1890-1923); Early Children of the Depression (born 1924-1930); Late Children of the Depression (born 1931-1941); War Babies (born 1942-1947); early Baby Boomers (born 1948-1953); and mid Baby Boomers (born 1954-1959).  Every generation here born before and during World War II had better cognition scores than the generation before it.

Let’s repeat that:  War Babies did better than Late Children of the Depression, who did better than Early Children of the Depression, who did better than the Greatest Generation on these tests.

The Baby Boomers ended this positive trend.  They not only did not do better than the War Babies; they did worse.  “It is shocking to see this decline in cognitive functioning among Baby Boomers after generations of increases in test scores,” Zheng says.  “But what was most surprising to me is that this decline is seen in all groups: men and women, across all races and ethnicities and across all education, income and wealth levels.”

To make sure the results weren’t being skewed by older members of the Boomer generations, Zheng then looked only at the scores of people in their fifties – and again, Boomers did the worst.  Baby Boomers already started having lower cognition scores than earlier generations at age 50 to 54.  This decline “does not originate from childhood conditions, adult education, or occupation.”

So what’s causing it?  “It can be attributed to lower household wealth, lower likelihood of marriage, higher levels of loneliness, depression and psychiatric problems, and more cardiovascular risk factors – obesity, physical inactivity, hypertension, stroke, diabetes, and heart disease.”

Zheng concludes the study by saying this cognitive decline could become more common in future generations “if no effective interventions and policy responses are in place.”

Now, that’s academic speak; who’s going to make these interventions?  What policy will reverse the course of our brain health?  Let’s sit around with our thumbs and wait for the government and policy-makers to fix it.

Or, let’s see what we can do to make our own brains healthier.  I vote for that option.

As a people, we have never been fatter, had worse diets, or been more depressed and messed-up than we are right now.  We spend too much time on our phones and/or sitting on our butts watching TV.  We don’t exercise enough.  We don’t reach out enough.  We worry too much.  We eat too much processed food.

If you are sitting around watching the news and fueling hatred for one political party or another, you’re not doing your brain a favor.  Step back, turn off the news, and go outside.  You know what they do in Japan?  Take forest baths.  I linked to one story, but there are a bunch of them online, and videos, too.  It’s a “digital detox,” good for your physical and mental health.

If you are overweight, diabetic or borderline diabetic, if you have heart disease or high blood pressure, you are at a higher risk of cognitive impairment.  You have to fight it.  Talk to your doctor, make the effort to eat better, and start some mild exercise.  Every little bit helps.  Go for a walk.  If you can’t go outside, set a timer and walk around your home, or your room.  If you can’t walk, try chair yoga.  No matter your situation, there’s probably something you can do to help your heart, and what’s good for the heart is good for the brain.

I’ve written a lot about dementia on this website.  Just look in the right-hand column for categories, and click on Alzheimer’s (I know, all dementia is not Alzheimer’s; I did that because I thought more people might find my stories on dementia that way).   Here’s one of them, and here’s another, but there are several more.

In addition to diet and exercise, attitude can make a big difference.  Having a positive attitude is good for the brain.  Depression is a risk factor for dementia.  Getting a hearing aid if you need one is good for the brain, because with brain cells, it’s use it or lose it:  if you are just sitting there, not participating in conversation because you can’t hear, if you’re not engaging with other people, your brain figures you don’t need those cells anymore.  Reaching out, getting involved, and volunteering are good for the brain.  Staying connected is important.  Helping other people is important. 

Today I thought of a movie I haven’t seen in way too long, “Apartment for Peggy,” from 1948, starring Jeanne Crain, William Holden, and Edmund Gwenn.  At one point, Edmund Gwenn (Santa Clause in the original “Miracle on 34th Street) says:  “I find it singularly curious that if a doctor tells us that peanut shells are good for us, we eat them.  If a chemist maintains that one gasoline is better than another, we use it.  We’re guided by experts on everything from soap chips to foreign policy and yet on the most important thing of all, how to live, we pay no attention.  Ever since man began to think, great minds have been telling us that the pleasure in living is in helping, that happiness comes from a simple, useful, constructive life.  But yet, we call this kind of advice infantile, impractical and hopelessly idealistic.”

That movie came out just after World War II, and Edmund Gwenn was a member of the Greatest Generation – which means he might score better than today’s Baby Boomers on a cognitive test.  So, give a listen.


©Janet Farrar Worthington





What does the health of your gums have to do with your brain? Apparently, more than anyone ever knew.  Having periodontal disease raises your risk of getting other serious health problems; one of them is Alzheimer’s disease. New studies may have pinpointed not only the cause of Alzheimer’s; they also may have identified a way to treat or even prevent it. Studying the Wrong Kind of Plaque? Let’s start with some dreary statistics. About 70 percent of those who get dementia have Alzheimer’s disease.  This is a lot of people: according to one study looking at the numbers, Alzheimer’s doubles in frequency every five years after age 65, and the number of people in the U.S. alone with Alzheimer’s is projected to balloon from about 5.5 million to an estimated 14 million people by the year 2050.  Worldwide, the number of people with Alzheimer’s is expected to grow from 35 million to 135 million by 2050. The picture is bleak.  But wait! It gets bleaker!  The study’s authors add that the failure rate of Alzheimer’s drug development is 99 percent, and the failure rate of the development of disease-modifying therapies for Alzheimer’s is 100 percent. Alzheimer’s is truly a nightmare, the devastating, progressive deterioration of memory and cognitive function; of course, you know this already.  I do, too. Everybody I know knows someone who has been affected by Alzheimer’s, and also by the lack of optimism that surrounds it (although there are some things that do seem to help stave off dementia, which we’ve discussed here). Since 1984, scientists have zeroed in on blocking or treating some characteristic changes Alzheimer’s patients have in their brains: plaques, sticky clumps of beta-amyloid proteins, and gnarly tangles of another kind of protein, called tau. Gazillions– $1.9 billion by the National Institutes of Health in 2018 alone, not to mention the big pharma companies, in the U.S. and elsewhere – have been spent on these plaques and tangles – developing animal models (mice) that get them, then making prototype drugs, with the desperate hope that getting rid of this unwanted brain junk will help people think better, and remember more, and get their lives back. Basically, for 35 years, scientists have been trying to make this one idea work, with not much encouragement to keep them going.   In fact, as we have discussed here, there is increasing evidence – besides the utter lack of success in finding a treatment – that plaques and tangles aren’t even the cause of the mental deterioration in Alzheimer’s.  Many people, at autopsy, are found to have the exact same-looking plaques and tangles in their brains, and they showed no sign of impaired memory or thinking. Maybe the plaques and tangles are a response to something else, and not the cause of Alzheimer’s. Maybe we’ve been focusing on the wrong kind of plaque.  Here’s a very interesting study from 2015, led by scientists at NYU College of Dentistry and NYU Langone Medical Center, of “cognitively normal, healthy, community-residing elderly” men and women, average age 61. (I must say, 61 does not seem terribly elderly to me; in fact, it’s getting younger all the time!) In this study, the investigators showed for the first time in humans a link between periodontal disease and the accumulation of plaques in the brain. The scientists said periodontal disease was associated with beta-amyloid buildup in the same areas of the brain “that are prone to beta-amyloid accumulation in patients with Alzheimer’s disease. Our results suggest that periodontal inflammation/infection may increase the risk for brain amyloid deposition.”  More studies are needed, they said, and again, these people were doing fine.  They were cognitively normal.  They had the plaques, but not dementia.  Why – why did they have the plaques, and why didn’t they have dementia? Scientists have speculated that the plaques and tangles are just garbage, like crumpled-up bits of litter floating around in the brain.  But scientists looking at other species have found that humans, in these sticky brain beta-amyloid proteins, share the same genetic sequence of amino acids with many other species.  This particular string of building blocks seems to be something very ancient, something that nature has kept around for a reason.   

Plaques are like Roach Motels for Bacteria

Harvard scientists discovered the reason:  the beta-amyloid plaques are like the brain’s version of Venus fly traps.  They’re anti-microbial Roach Motels: bacteria check in, but they don’t check out.  In effect, the beta-amylolid protein serves as an anti-bacterial goo. When the scientists injected bacteria into the brains of mice that are prone to developing Alzheimer’s-like plaques, in less than 24 hours, the mice had produced plaques that enveloped those bacteria like bubble-wrap.   Other studies have found bacteria in the brains of people who had Alzheimer’s.  Well, here were bacteria, covered up in plaque. Harvard scientist Rudolph Tanzi, Ph.D., said that when they looked in the plaques, “each one had a single bacterium in it.  A single bacterium can induce an entire plaque overnight.”  The study reported that “our findings raise the intriguing possibility that beta-amyloid may play a protective role,” and that infectious or other stimuli may cause these amyloid plaques to be made.  “These data suggest a dual protective/damaging role for beta-amyloid.”  It’s the Pushmi-Pullyu, the two-headed llama from Dr. Doolittle:  the plaques are good!  No, they’re bad!  They’re good and bad! The scientists suspected that maybe the bacteria get in the brain, the brain forms plaques, and somehow the plaques cause inflammation– which, in turn, leads to the tangles of the tau protein to develop; these tangles then cause surrounding neurons to die, and the ongoing domino effect leads to Alzheimer’s disease.  This also seems to answer another question that scientists had about bacteria in the brain of Alzheimer’s patients:  did it get in there because the brains were already damaged – as the result of Alzheimer’s – or did they cause the damage?  It’s really looking like they are causing it. If bacteria are triggering the formation of plaques that somehow are involved in Alzheimer’s disease – although again, some people have them and don’t lose their memory and ability to think – then the big question is this:  How do they get in there?    Gum disease.  We’ve talked about poor gum health and the link to another terrible disease (rheumatoid arthritis), here at VJ.  Gum disease is known to cause problems in the heart, as well – as you probably know, if you’ve got heart disease and you have to be on antibiotics when you have a dental procedure. What happens in the gums does not stay in the gums. The gums are a gateway to the rest of body, including the brain.  The nasty bacterium that scientists now believe is an instigator of Alzheimer’s disease is Porphyromonas gingivalis.  P. gingivalis is the “keystone pathogen” in chronic gum disease.  A new, very promising study, done by scientists at medical centers in the U.S., Europe and Australia, and co-led by Stephen Dominy, M.D., a scientist working for Cortexyme, a San Francisco-based pharmaceutical company, explored P. gingivalis as both the cause and as a target for potential treatment of Alzheimer’s. P. gingivalis uses two toxic proteases, or enzymes, called gingipains – its own bacterial version of meat tenderizer – when it attacks human tissue.   The investigators, using DNA sequencing, confirmed P. gingivalis DNA in Alzheimer’s patients, found these gingipains right there in the plaques, and showed that they were “neurotoxic… exerting detrimental effects on tau, a protein needed for normal neuronal function.  To block this neurotoxicity, we designed and synthesized small-molecule inhibitors targeting gingipains.” So they figured out a way to stop these gingipains, and when they did, they “reduced the bacterial load of an established P. gingivalis brain infection, blocked beta-amyloid production, reduced neuroinflammation, and rescued neurons in the hippocampus,” the part of the brain associated with new memories, emotions, learning, and spatial navigation: the part of the brain that is so cruelly targeted in Alzheimer’s.   “These data suggest that gingipain inhibitors could be valuable for treating P. gingivalis brain colonization and neurodegeneration in Alzheimer’s disease.”

But wait! What about Bad Genes?

 This gingipain breakthrough could be incredible.  It could lead to a vaccine for Alzheimer’s, and also to a drug that could help people struggling with the disease as we speak.  But wait, you may say, what about bad genes?  Maybe Alzheimer’s runs in your family.  Doesn’t that mean it’s inherited?   It may be that what is inherited is the way your body handles the specific inflammation caused by these gingivains; inflammation is part of the immune system’s arsenal.   A major genetic risk factor for Alzheimer’s is a variant of the APOE gene (which makes the Apolipoprotein E immune protein) called APOE4.  In 2018, Swedish researchers who were studying the link between P. gingivalis and heart disease reported that these gingipains cleave the ApoE protein into fragments, and that these fragments — like shards of glass — could hurt nerves.  If you have a normal APOE gene, and this protein is intact, you are less likely to have this nerve damage.  But if you have a mutated APOE gene, you’re more susceptible: P. gingivalis can do more damage in you than it could in someone else. If this truly is the cause of Alzheimer’s, this is very hopeful, because we have a target, we have hope for treatment, for development of a vaccine, and maybe even for a cure someday.  In 2018, Cortexyme reported that its small-molecule gingivain-blocker drug, called COR388, was safe and well tolerated in a Phase 1 clinical trial.  Also, although they weren’t looking specifically for cognitive improvement, they found it:  “COR388 showed positive trends across several cognitive tests in patients suffering from Alzheimer’s disease.”  A phase 2 study of the drug in patients with “mild to moderate” Alzheimer’s is in the works.  More on gum disease and your health in the next post.    Personal note:  I’m no doctor, but my God, if gum disease can be so bad for your health, why wouldn’t you rinse with Listerine, floss your teeth, and see the dentist regularly?  Also cut down on things that lead to gum disease, like sugary foods, smoking, and alcohol consumption — or at least, rinse or brush your teeth right after. I truly hope we will see a vaccine for Alzheimer’s disease very soon.  In the meantime, at least this is something we can do that might really help. © Janet Farrar Worthington

For many of us, dementia is not an inevitable part of growing older. We have talked about this before, but I feel strongly that it’s time to talk about it again. The idea is still a fairly new one to wrap your mind around, no pun intended, and I’m pretty sure that most people are not going around thinking, “What can I do today to prevent dementia?”

            But they ought to be. We all ought to be.

So here, if you will, is a “Dementia Grab-Bag,” which sounds like a really bad party gift. I have collected some research studies and decided to give them to you all at once. Maybe “Dementia Round-Up” is better, although that just makes me imagine of a lot of sad old cows, or cowboys wearing adult diapers.

What can you do to prevent dementia? In addition to the things we’ve already discussed, here are three easy actions for your consideration. The main thing to think about with all of them is that what is good for the heart is also good for the brain.

Embrace Leafy Greens

Maybe you’re old enough to remember the pickle episode from the Andy Griffith Show, in which Aunt Bee somehow manages to make pickles that taste like kerosene. Andy and Barney try their best to get rid of them, and Aunt Bee makes even more. At length, Andy figures, all they can do is “Learn to love ‘em.”

If you already love salads (not the pale green Iceburg lettuce wedge, but salads with dark green leaves), kale, spinach, collards and other greens, you’re in luck! If not, the best thing you can do is learn to love ‘em, so you can get the brain-helping powers they seem to offer.

In a recent study published in Neurology, scientists found that healthy seniors – there were 960 participants in the study, average age 81 – who ate leafy green vegetables every day had a slower rate of cognitive decline than did those who ate few or no greens.

The seniors (none of whom has dementia) are part of the Memory and Aging Project at Rush University in Chicago, a longitudinal study in which participants undergo yearly tests to assess their memory; they also keep track of what they eat, their exercise, etc. In this study, researchers led by Martha Clare Morris, Sc.D., Director of Nutrition and Nutritional Epidemiology at Rush, divided the participants into five groups, based on the amount of greens they eat. The seniors in the top group ate about 1.3 servings of leafy greens a day (a serving is about half a cup of cooked greens, or a cup of raw greens); those in the bottom group ate hardly any.

After about five years, the rate of decline for those in the top group was “about half the decline rate of those in the lowest,” reports Morris.   And get this: Their mental processes were “the equivalent of being 11 years younger in age.” Higher intakes of leafy greens “were associated with slower cognitive decline.”

Now why is this? Well, the scientists aren’t entirely sure, because even a simple leaf of kale has a bunch of nutrients and bioactive compounds in it, including phylloquinone, lutein, nitrate, folate, alpha-tocopoherol, and kaempferol.   All of these, says Morris, “have different roles and different biological mechanisms to protect the brain.” One thought, she adds, is that if you don’t get enough folate, you can have higher levels of homocysteine (an amino acid), which can lead to inflammation and the buildup of plaque and fat in the arteries – and this, in turn, can lead to a heart attack or stroke. In another recent study, Korean scientists reported that higher blood levels of homocysteine in older adults were associated with cognitive impairment.

And, of course, we can’t overlook the fact that if you’re eating a salad, maybe you’re not also eating fries or chips or macaroni at that particular time.

Note: This study didn’t report that these people never eat red meat, or that they exercised all the time; in fact, they adjusted for a bunch of factors, including education, overall health, exercise, activities, smoking and drinking. All the people in the top group did was eat leafy greens every day. Also, the scientists don’t claim that leafy green vegetables will stop memory decline forever. But there is a definite link: “The association is quite strong,” says Morris.

It’s easy to add greens to your daily diet. You can buy them in a bag salad. Eat collard greens from a can. Drink kale disguised in a strawberry-banana smoothie, if you don’t like the taste.

Embrace Exercise

You need to exercise. Please note that I did not have some condescending headline on here, like, “Get off the couch, you bum.” I don’t presume to know how active you are, and I hate it when people virtue-signal about exercise and diet and just make me feel like a loser because I’m not doing enough.

We’ve all got enough stress – and this is the interesting aspect of the next study I want to tell you about.   Scientists at Brigham Young University (BYU) in Utah found that running sharpens memory and mitigates the damage of chronic stress on the brain.

You don’t like to run? That’s okay. This article is about exercise and the scientists used mice; mice can’t ride a bike, do a rowing machine, or lift weights, so in this study, they ran, maybe with little track suits and sweat bands, I don’t know. The point is, if you don’t like to run, don’t discount this study; you could walk fast, or swim, or ride an exercise bike, or do the rowing machine – anything that gets your cardiovascular system going.

Remember the hippocampus? It’s the part of the brain that’s very important in memory, learning, spatial navigation, and other things. (It’s also deprived of blood flow when you smoke marijuana, which we’ve discussed here.) Well, chronic stress can be hard on the hippocampus; it weakens the synapses (electrical messages fired off by one neuron to another). Specifically, it affects a process called long-term potentiation (LTP), which helps us remember things more clearly.

In other words, prolonged stress hurts the brain and can affect our memory. But exercise acts as an antidote: It is “neuroprotective against the negative effects of stress” on hippocampal LTP, says Jeffrey G. Edwards, Ph.D., on the faculty in the Department of Physiology and Developmental Biology at BYU and the study’s senior author.

For this study, the scientists divided the mice into four groups: sedentary no stress, exercise no stress, exercise with stress, and sedentary with stress. (Don’t worry; they didn’t waterboard the mice or anything like that. They exposed them to some temporary stressful situations, like walking in cold water or on elevated objects).  The mice that had stress but also exercise had “significantly greater LTP” than the sedentary mice did. They also performed much better in a maze – as well as the non-stressed mice did.

Of course, the best way for us to improve our learning and memory “would be to experience no stress and to exercise,” Edwards says. Although we don’t always have a say in how much stress we have in our lives, “we can control how much we exercise,” and it is empowering to know that we can offset the negative effects of stress on our brains simply by giving our cardiovascular system a workout.

How does this relate to dementia? A lifetime of better brain stewardship will put us in a much healthier position to prevent dementia as we get older.

Don’t Drink Too Much

In a new study published in Lancet, French and Canadian scientists showed that too much alcohol is bad for your brain. They weren’t the first to show this, but their research adds to a growing body of evidence showing a clear link between heavy drinking and dementia.

The researchers looked at the French National Hospital Discharge database and examined the association between alcohol use and dementia, particularly early-onset (younger than age 65) dementia. Out of 1,109,343 patients diagnosed with dementia who had been discharged from French hospitals between 2008 and 2013, there were 57,353 cases of early-onset dementia. Most of these cases of dementia, the scientists report, “were either alcohol-related by definition, or had an additional diagnosis of alcohol use disorders.” They did not include patients who already had certain neurological or other diseases that can lead to rare types of dementia; they just wanted to focus on alcohol consumption.

Now, you may be wondering, what’s an alcohol use disorder? It’s problem drinking that become severe. I’m including a link to the National Institute on Alcohol Abuse and Alcoholism, which has some questions to help people determine if they have a problem. They call alcohol use disorder (AUD) a “chronic relapsing brain disease characterized by compulsive alcohol use, loss of control over alcohol intake, and a negative emotional state when not using.” Some questions include: “In the past year, have you had times when you ended up drinking more, or longer than you intended? Spent a lot of time drinking, or being sick or getting over the aftereffects? More than once wanted to cut down or stop drinking, or tried to, but couldn’t?” These and others are here, and they’re good ones.

Also, you may be wondering, what is heavy drinking? The study’s authors used this definition, also used by the World Health Organization and European Medicines Agency: “at least 60 grams of pure alcohol per day for men and at least 40 grams for women.” Definitions for what constitutes a standard drink vary, but in the U.S., a standard drink contains about 14 grams of pure alcohol. This is found in 12 ounces of beer, which is usually about 5 percent alcohol; 5 ounces of wine, typically about 12 percent alcohol; and 1.5 ounces of spirits – your basic shot of whiskey, tequila, etc., — which is about 40 percent alcohol. You can do the math, but if one of those drinks has 14 grams, then knocking back a little over four drinks a day would put you in the heavy drinking category.

Drinking in moderation is one thing; in fact, many reviews show a possible beneficial effect of a glass of wine a day. But drinking more than one or two drinks every day, or even several days a week, is another thing altogether.

We are talking about a big preventable risk factor here. Dementia affects 5 to 7 percent of people age 60 and older worldwide. There are several categories of dementia; Alzheimer’s is the most common, followed by vascular dementia and other types, and some people have mixed types of dementia – problems with the blood flow to the brain, plus some damage from alcohol, disease, or something else.

“Heavy drinking seems detrimentally related to dementia risk, whatever the dementia type,” the researchers say. Too much alcohol affects the brain in several ways. “First, ethanol and its metabolite acetaldehyde have a direct neurotoxic effect, leading to permanent structural and functional brain damage. Second, heavy drinking is associated with thiamine deficiency.” Here’s a link to another paper on thiamine deficiency. Basically, thiamine – vitamin B1 – is an essential nutrient; your body needs it to do many things. It’s especially important for your heart, liver, kidneys, and brain. Thiamine deficiency can harm the body in many ways; mental changes include depression, decrease in short-term memory, confusion, and irritability.

“Third,” the scientists continue, “heavy drinking is a risk factor for other conditions that can also damage the brain, such as epilepsy, head injury, and hepatic encephalopathy in patients with cirrhotic liver disease. Fourth, heavy drinking is indirectly associated with vascular dementia” because it raises vascular risk factors and can cause “high blood pressure, haemorrhagic stroke, atrial fibrillation, and heart failure.” And finally, “heavy drinking is associated with tobacco smoking, depression, and low educational attainment, which are possible risk factors for dementia.” We have talked about cognitive reserve and dementia risk here. “This combined evidence has led to a discussion about establishing a specific diagnosis of alcohol-related dementia.”


© Janet Farrar Worthington

Part Four of Four

It’s challenging enough that you need to be on androgen deprivation therapy (ADT) in the first place.   Now, in addition to prostate cancer, you have to worry about the risk of dementia?

Some studies have shown an increased risk for Alzheimer’s disease, and cognitive impairment and depression are known problems that can go along with ADT. We’ll come back to those in a moment.

There is some reassuring news: a new study, the largest of its kind, published in the Journal of Clinical Oncology, suggests that your risk for Alzheimer’s disease does not go up with ADT.   The study was led by Clement Joseph McDonald, M.D., of the National Institutes of Health. It involves a massive database: the medical records of men with advanced prostate cancer – more than 1.2 million of them, age 67 and older, enrolled in Medicare.

Between 2001 and 2014, 35 percent of these men were treated with ADT (either through drugs such as Lupron or with surgical castration). Of these men, about 9 percent developed Alzheimer’s disease, nearly 19 percent developed dementia, and about a third died without developing either condition.

Now, here’s where it gets a little complicated: the unadjusted rates for dementia in men who were on ADT were slightly higher than for the men not on ADT – nearly 39 percent compared to nearly 33 percent. But when McDonald and colleagues accounted for factors such as other cancer treatment, other health conditions, and age, they found that the risk of Alzheimer’s was not significantly higher in the men on ADT. In fact, it was even slightly lower, but this “possibly was attributable to the high death rate.” In fact, the average time of follow-up was about five and a half years.

If you’re reading this and you think, “Oh, no, they didn’t live very long, and that’s why they didn’t get dementia,” well, you may be right. But treatment for advanced cancer is getting better all the time, and it’s not clear from this study whether these men went on to have second-line treatment, such as abiraterone, enzalutamide, taxotere, or any of the immunotherapy drugs currently being tested in clinical trials across the country.

So take heart: New and better treatments are here, and what happened to these men does not define what’s going to happen to you.

But here’s where the grain of salt comes in: Some of these men did develop dementia. So even if it wasn’t technically Alzheimer’s, the name of the problem doesn’t really matter if you’re the one who’s got it. What do we make of this?

As we’ve discussed before, ADT can cause metabolic syndrome: it can raise your blood pressure, your blood sugar level, your cholesterol and triglycerides, and it’s very easy to gain weight – particularly right in the belly, which raises your risk for diabetes, heart attack, and stroke. You need to burn more calories than you’ve ever had to in your life just to lose a pound. That doesn’t mean it can’t be done – it can. You just have to work harder. But you can do this, and it helps if you don’t eat a lot of carbs.

If you are on ADT, you also need to do your best to help out your cardiovascular system with exercise. It doesn’t have to be anything more strenuous than walking; just keep that blood flowing and the heart pumping, and what’s good for the heart is good for the brain. Which means, you can help prevent cognitive damage by staying active. Many men with ADT also have temporary depression. This also is improved by exercise – but if you need it, medication can help these symptoms, too.


In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington



Part Three of Four

Does ADT cause cognitive impairment? This question seems simple, but really, it’s more like opening a medical can of worms. So let’s ask a different question. Do men on ADT get cognitive impairment? Yes, some do. But many don’t. It is hard to pin down definitive facts here – like, how many men get it? What’s the risk at one year, two years, five years, and ten years?

Nobody knows the exact statistics, and there are several reasons why.

  • There are probably many more men on ADT with cognitive impairment than we know about. But they don’t spend enough time with their doctors, at 5- and 10-minute follow-up visits to renew their Lupron prescription, for their mental status to be evaluated. Cognitive impairment doesn’t always show up in casual conversation.
  • Scientists looking to answer this question aren’t using standardized criteria. For example, does hormonal therapy mean only ADT, or ADT plus another drug, like enzalutamide? Also, are we talking about actual Alzheimer’s disease here, or just an inability to find the right word quickly on a crossword puzzle?

Well, what about men who are actually showing signs of cognitive impairment? That’s not much easier; there are still more questions:

  • Would they have gotten it anyway?
  • Did they start ADT with some risk factors for dementia already on board?
  • If they are showing signs of dementia, is it because when they got on ADT they stopped exercising, gained weight, and experienced depression – and could one of those those factors actually be the tipping point?

I recently interviewed medical oncologist Jonathan Simons, M.D., CEO of the Prostate Cancer Foundation (PCF), and medical oncologist Alicia Morgans, M.D., of Northwestern University, about ADT for the PCF’s website.  “We have reached a crossroads, and in some ways, it’s actually a sign of progress,” notes Simons. Long, long ago, heart disease wasn’t a big health problem – because people died of other things, like accidents and infections, and diseases that we now get routinely vaccinated for. Diabetes wasn’t a huge risk for many people; sugar wasn’t widely available, there was no such thing as soda, obesity was rare, and people were more physically active. Prostate cancer wasn’t that big a deal, either, because most men didn’t live long enough to get it.  “Not too long ago, men with metastatic cancer died within months or a few years of their diagnosis. Today, men with metastatic prostate cancer are living long enough to develop other problems, and doctors – who previously had just been focused on keeping these patients alive – are trying to figure out how best to keep them alive and well.”

What we have here is an issue of survivorship – living with metastatic prostate cancer, and dealing with the side effects and challenges of treatment.   Medical oncologist Alicia Morgans, M.D., M.P.H., of Northwestern University, is a pioneer in studying survivorship. Cognitive issues have not been much studied in prostate cancer, and scientists are playing catch-up. “It’s not fair for us just to look at the benefits of treatment anymore,” she says, “now that we are starting to understanding the risks better.”

One easy place to start is to make sure that all men who are put on ADT really need it.   Next, men on ADT need better follow-up to monitor their cognitive function.   Morgans believes cognitive impairment in men on ADT is “underreported, underappreciated, and underdiagnosed.” In a PCF-funded study, Morgans’ patients are taking brief neuropsychological tests; the tests look for changes in verbal memory, visual memory, attention, and executive function. She hopes to develop reliable tests that can be done online – tests that could be given to many more patients in clinical trials, so that investigators can get an idea of the scope of the problem.

Family and friends can help: Someone who is having cognitive impairment may not be aware of changes, or may not be able to articulate them well. But his family and friends can help bring worrisome symptoms to the doctor’s attention.

Layers of medication: One of Morgans’ patients, a 76-year-old man, had been doing fine on Lupron for years. But when his PSA started to rise, Morgans added abiraterone, and then enzalutamide. For this man, enzalutamide might have been the tipping point, “one thing on top of another thing, on top of another thing. He was experiencing confusion and forgetfulness,” she says. The man, a minister, was not able to write or deliver sermons anymore. “We decided, despite the fall in his PSA, to stop the enzalutamide.” Four weeks later, his cognitive function had improved, and “he continues to give sermons today.”

For this man, the key to cognitive issues seemed to be enzalutamide. For another man, it could be something different. It could be a different kind of domino effect – the higher risk of diabetes and cardiovascular disease, for instance; maybe these other health problems, in turn, affect the vitality of the brain. “There may be subclinical strokes or cerebrovascular disease that we don’t know about,” Morgans says.

Loss of estrogen? Morgans suspects that a change in cognitive function might also have something to do with a man’s estrogen levels. Women aren’t the only ones who make estrogen; men make it, too, at lower levels. But ADT causes men to have “very low levels of estrogens, lower than postmenopausal women have.”  In studies of women with breast cancer, she points out, “low estrogen levels on their own can be associated with cognitive decline. It’s not ‘chemo brain,’ it’s something different.”

Men with prostate cancer don’t need to have low estrogen levels in order for their cancer to be treated; it just happens as a byproduct. Normally, men need some level of testosterone in order to make estrogens. “Estrogen doesn’t have to fall for us to treat prostate cancer, but it does fall with the method we use – we know testosterone drops to a place it’s never been since puberty.” Would giving some type of estrogen along with the ADT be helpful? No one knows.

Depression is a risk factor for dementia; big changes in sleep habits can also be a risk factor. It may be that addressing each of these separately – with an antidepressant, with exercise, and with melatonin to help with sleeping – could help keep the brain working better.

What about changes in the way ADT is given? Intermittent therapy may be an option. This could mean giving ADT, stopping it for a few months, and then starting back up again. “When men go off ADT, their testosterone comes back, they feel better, think better, their executive function is better – their ability to do a crossword puzzle, or find a synonym, or find the word they’re searching for – and they feel more like themselves again.” Another approach, as investigator Samuel Denmeade is testing at Johns Hopkins, is “bipolar” hormonal therapy: alternating ADT with its polar opposite – high-dose testosterone.

Could “brain exercise” help? Maybe. Crossword puzzles and mind-challenging games may indeed act as mental push-ups and sit-ups, says Simons.

The ultimate goal for treatment, scientists and doctors agree, is to find a way around ADT altogether, or to change it somehow so that the prostate cancer is affected, but the brain is not. Until then, it’s up to doctors to use ADT wisely, only when it is medically appropriate. “Using hormonal therapy has to be more than just a reflex, like giving people penicillin for a head cold,” Simons states. “The PCF, in fact, is actively funding research for other ways to treat metastatic cancer that don’t involve hormones at all.”

It’s also up to you, too, to make sure you start ADT only if and when you need it. If you are at intermediate- to high-risk of recurrence, or if you have a rising PSA but no evidence of metastatic disease and your doctor wants to put you on ADT, get a second opinion. You may also be eligible for a clinical trial of a different kind of therapy that does not affect your hormones, including treatment for oligometastasis — SBRT radiation to a few spots of cancer in your bones, or surgery to remove cancer that is just in one lymph node.

If you do have metastatic disease, right now ADT is the standard of care, and it could put your cancer into remission for many years. There is a lot you can do to help mitigate the side effects – which, in turn, may help protect your brain.


In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.”  As Patrick Walsh and I have said for years in our books, Knowledge is power: Saving your life may start with you going to the doctor, and knowing the right questions to ask. I hope all men will put prostate cancer on their radar. Get a baseline PSA blood test in your early 40s, and if you are of African descent, or if cancer and/or prostate cancer runs in your family, you need to be screened regularly for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington


marijuana fieldBefore we start this discussion, please hear these words:  this is not about your right to smoke marijuana.  I don’t care if you spend every waking moment high as a kite, as long as you don’t operate heavy machinery or endanger anyone else.  I do not care.  That’s not my business.

However, I’m worried about your brain, because scientists are worried about it.  I also worry that some states have gotten so caught up in the political correctness of marijuana that they have fast-tracked legalizing it without fully understanding the science of what it does, and the biggest thing it does is reduce the circulation to every cell in your body, including the brain.  New studies have linked using marijuana to a higher risk of dementia, depression, and even schizophrenia.

The part of the brain that marijuana particularly seems to affect is the hippocampus, which is the same region of the brain that’s damaged in Alzheimer’s disease.  Wait a minute, hippo-what?  Let’s backtrack a minute, and:

Get to Know Your Hippocampus!

Actually, there are two of these in the brain, so technically it’s “hippocampi.”  There’s one on the right side, and one on the left, roughly over each ear, about an inch and a half inside your head.   

When you make a new memory, it happens in your hippocampus.  When you file that memory away in your brain and assign emotions to it, that happens in your hippocampus.  When you smell fresh oranges and think of that box of fruit your grandfather used to send your family at Christmas:  that happens in the hippocampus.  When you see an ad for “White Linen” perfume and think of the crush you had on your high school math teacher, who used to bathe in the stuff:  that happens… you guessed it.

Now, within the hippocampus, there are different compartments.  One handles spatial memories; in fact, when scientists studied London cab drivers, who have to commit the intricate labyrinth of 500-year-old city streets largely to memory, they found a connection to growth in the rear part of the hippocampus. 

marijuana bagsThe hippocampus is where, when you sleep, you process all the stuff you saw and felt during the day, and then you ship it off to your brain’s equivalent of the warehouse where they put the Ark of the Covenant after Indiana Jones found it – long-term memory.  The hippocampus is the triage area.  It’s short-term memory we’re talking about here, people. 

So, what happens when the hippocampus is damaged?  Well, autopsy studies of people with amnesia have shown damage to the hippocampus.  Damage here is linked to problems remembering names and events.  Dates, too. 

Is there any redundancy – a failsafe against damage, since we have two hippocampi?  Well, not exactly, because they’re specialized.  Damage to the left hippocampus can affect your ability to come up with the right words, and damage to the right can affect your ability to process visual information.

Cell degeneration in the hippocampus is connected to the onset of Alzheimer’s.   

Hold that thought.

Risk of Alzheimer’s

Marijuana causes abnormally low blood flow to virtually every part of your brain.  In a study published in the Jan. 12, 2017, issue of the Journal of Alzheimer’s Disease, scientists at Amen Clinics in California looked at the brains of more than 26,000 patients at American neuropsychiatric clinics between 1995 and 2005.  Of these, nearly 1,000 were pot smokers. 

All of the marijuana users had abnormal blood levels in the brain, particularly in the same regions of the brain affected by Alzheimer’s, namely the hippocampus.  They used SPECT imaging to show the brains of marijuana users compared to controls (people who did not smoke pot), and the difference was striking.   Every single pot smoker had “significantly lower blood flow” in the right hippocampus compared to the controls.  Even the investigators were surprised.  Lantie Elisabeth Jorandby, a psychiatrist and one of the study’s co-authors, said when the paper came out, “What struck me was not only the global reduction in blood flow in the marijuana users’ brains but that the hippocampus was the most affected region, due to its role in memory and Alzheimer’s disease.  Our research has proven that marijuana users have lower cerebral blood flow than non-users.”  The study’s authors concluded, “The most predictive region distinguishing marijuana users from healthy controls, the hippocampus, is a key target of Alzheimer’s disease pathology.  This study raises the possibility of deleterious (harmful) brain effects of marijuana use.”

In a blog post ( the study’s authors talk about their findings.  There are also images of two brains (one from a marijuana user, and one from the control group) and it’s kind of like looking at a fresh piece of fruit vs. one that’s been in a dehydrator and put into some trail mix.  “Our research demonstrates that marijuana can have significant negative effects on brain function,” the investigators wrote.  “The media has given the general impression that marijuana is a safe recreational drug, this research directly challenges that notion.  Several studies of perfusion imaging in marijuana users have shown similar results compared to ours. A small … PET study in a sample of 12 marijuana users used a randomized clinical trial design to examine brain perfusion before and after marijuana use. The study results found frontal, temporal and occipital lobe hypo-perfusion (lower than normal blood flow) – all findings concordant with our study.”

In previous posts here at Vital Jake, we have talked about the importance of cerebrovascular health in preventing dementia.  Good blood flow to the brain is really important.  Trust me, you want good circulation up there, and there are ways to do this, which we’ve talked about in previous posts.   If you exercise and eat right and do all the things that have been proven to help reduce your risk of dementia – and then smoke pot, you might be wasting all that effort.

Risk of Schizophrenia

In a landmark report released by the National Academies of Sciences, Engineering, and Medicine, scientists said what we don’t know about marijuana “poses a public health risk.”  And yet, 28 states and Washington, D.C., have legalized marijuana for medical use, and eight states and D.C. have legalized it for recreational use. 

marijuana budThe report also said there is strong evidence to link using marijuana to the likelihood of developing schizophrenia and other causes of psychosis, with the highest risk among the most frequent users.   

The Royal College of Psychiatrists issued a statement that says, “There is growing evidence that people with serious mental illness, including depression and psychosis, are more likely to use cannabis or have used it for long periods of time in the past.  Regular use of the drug has appeared to double the risk of developing a psychotic episode or long-term schizophrenia.”

Now, you may wonder, does marijuana actually cause these problems, or are people who are prone to depression and/or schizophrenia trying to self-medicate, to find some relief of their symptoms?  That’s a reasonable question.

It appears that marijuana is more likely to be the cause than the cure.   Australian scientists followed 1,600 adolescents, aged 14 to 15, for seven years.  They found that “while children who use cannabis regularly have a significantly higher risk of depression, the opposite was not the case – children who already suffered from depression were not more likely than anyone else to use cannabis. However, adolescents who used cannabis daily were five times more likely to develop depression and anxiety in later life.”

Other studies show that the risk of schizophrenia or bipolar disorder appears to be dose-related, especially in adolescents.  Australian scientists found that adolescents who smoked pot were more likely to develop a psychotic illness, and to develop it about 2.7 years sooner, than those who did not.  These kids may also have a genetic predisposition to a psychiatric illness; so it may be that the ones who developed problems had a lower threshold for damage.  Would they have developed it without the marijuana use, however?  Nobody knows.

Risk of Depression

In another imaging study of 48 people, published in the Proceedings of the National Academy of Sciences, scientists showed that smoking marijuana increases the risk of depression, anxiety, restlessness, and other “negative” emotions.

They showed it in an interesting way, by looking at how the brains of study participants – pot smokers and controls – reacted to dopamine, the “feel-good” neurotransmitter (brain chemical) that affects your emotions, your movements, your ability to sense pleasure and pain, to learn, to pay attention, and to think.  Dopamine affects your mood, your sleep, and your memory, too.   

Dopamine is also part of your brain’s reward system.  Eat a sugary snack: get a hit of dopamine.  Do cocaine:  get a hit of dopamine. 

The ADHD drug Ritalin, a stimulant, raises the levels of dopamine in the brain, too, and this is what the researchers used in the study.

The pot smokers met the criteria for marijuana “abuse or dependence.”  That is, they smoked a lot of pot.  In personality tests and brain scans, the pot smokers had “significantly blunted” responses to dopamine compared with controls.  They were more lethargic, apathetic, anxious, and depressed.  Psychiatrist Nora Volkow said the scientists believe dopamine has a “downstream effect” in another area of the brain called the striatum, where your motivation comes from.

The study’s authors expressed their concern that “moves to legalize marijuana highlight the urgency to investigate effects of chronic marijuana in the human brain.” 

They used the word “urgency” because they are worried that people may be doing themselves significant harm.   

Here are some things to think about:

Another study from Imperial College London found that long-term pot use destroys dopamine.  Dopamine levels decline as we age, already; they also decline in Parkinson’s disease. 

People who already have a history of depression might not be ideally suited for marijuana.

People with a higher risk of stroke (high blood pressure, high cholesterol, prior heart disease, a history of TIA, or cerebrovascular disease) should not use marijuana because it will almost certainly diminish circulation even further and this could make them more likely to get dementia.

©Janet Farrar Worthington

I’ve had a lot of requests to print a talk I recently gave. Here it is. — Janet

Recently, I took part in a large, two-day dementia seminar in Prescott, Arizona, presented by Prescott United Methodist Church for the community.  There was a full house both days; hundreds of people came, which shows that the need is great for all kinds of information about dementia. 

But with all the doctors, nurses, social workers, financial people, and other experts talking about caring for people with dementia, and caring for the caregivers, and the desperate needs for daycare, home care, and for respite care so that exhausted, stretched-to-their-limit caregivers can have a break, there was only one person who talked about preventing dementia.  I was it.  What’s wrong with this picture?

Why was I the only one?  Why aren’t very many doctors talking about this?  Why do so many patients and their families hear that there is nothing they can do?  I wasn’t there to paint an artificially rosy picture.  I know what it’s like to try to care for someone with dementia; I know what it costs, financially, physically, mentally, spiritually.  It’s happened to two people I love, and it’s heartbreaking. 

But I also know from my work as a science writer that dementia is not always inevitable, and new research has shown that even when someone has Alzheimer’s, changes in diet, sleep, and exercise may make symptoms better. 

Many people have asked for copies of my talk, so here it is.  Longtime readers of this blog will find some of this material familiar, but I’ve collected it all into one place.  I’m sharing it with you now because I want you to know that there really is hope.

* * *

I’m going to start talking about the brain via an organ I know a little bit better: the prostate.  Bear with me.

Scientists have long known that, at autopsy, many men are found to have prostate cancer that never spread, never caused a problem, and never needed to be treated. They died with it, not of it. Sometimes, diseases only show up at autopsy. Men live a good long life and never show any signs of disease, and yet, when they die, there it is under the microscope.  But the disease never got out of hand. Men died with it, not of it

I did not know, until I interviewed Dr. Richard O’Brien, that the same thing happens with Alzheimer’s. O’Brien, who was Chairman of Neurology at Johns Hopkins Bayview Medical Center, now Chairman of Neurology at Duke, told me that some people, at autopsy, have Alzheimer’s pathology. They have the telltale brain plaques and protein tangles seen in Alzheimer’s disease – but they never develop any cognitive impairment. Other people have the exact same pathology, and they die of heartbreaking dementia. Why is this?

O’Brien sees opposing forces at work in the brains of people as they age.

In Alzheimer’s, the tipping point – the game-changer, the key factor that weights the scales toward dementia – seems to be ischemic diseaseStroke, or mini-stroke. “With a given amount of Alzheimer’s disease pathology in the brain,” O’Brien told me, “there are two forces at work. One is driving you to become demented, and the other is protecting you from being demented. The biggest force that we’ve found thus far is cerebrovascular disease.”

This does not mean that everyone who has had a stroke or who has cerebrovascular disease is going to get Alzheimer’s. That’s not what he’s saying at all.

What it does suggest is that if someone has significant atherosclerosis, or has had a stroke, even if it’s asymptomatic – AND also has the plaques and tangles, that is a very powerful predictor that he or she will develop dementia.

The body has a limited capacity for insults. Stroke is an insult. Plaques are an insult. Think of a boxer who can take a lot of punches, but he can only withstand so much. The brain has a tipping point, too. O’Brien believes that “either one of these alone isn’t enough, but the two existing together in the same brain are enough to tip you over.”

Here’s some very good news:

Doctors are getting better at spotting and treating the risk factors that lead to stroke. Two recent studies found that the incidence of dementia has declined over the last 30 years. “The primary reason for that is the treatment of coexisting cardiovascular risk factors,” O’Brien says.

None of these treatments prevents the Alzheimer’s pathology from building up – but they “prevent it from becoming manifest. So you die with your plaques and tangles, but you’re still cognitively intact.”

So, what can you do to protect your brain?

One thing is Exercise. In a report published in the Annals of Internal Medicine, scientists followed about 20,000 people who took part in treadmill testing in the 1960s as part of a cardiovascular study. Today, these people are in their eighties, nineties, or are deceased. “The scientists found that the people who had been in the fittest 30 percent of that group had a dementia rate that was half that of the other people in the cohort… One of the side effects of regular exercise is a significant reduction in your risk of dementia.”

Another huge factor is cognitive reserve, and this is from education. It turns out that people who go to college tend to have more cognitive reserve than people who don’t.  If you didn’t go to college, don’t worry.  If you read and learn a lot, you are building up a cognitive reserve, too. Learning a language or playing a musical instrument, doing research for your work, or singing in a choir – basically, anything that challenges your brain, as opposed to sitting on the couch and staring passively at the TV – these have beneficial effects on your ability to think, on the brain’s ability to make neural connections.

Not being obese plays a similar role, too. Fat, especially belly fat, changes your levels of hormones. It also increases your risk of dying of cancer. Scientists are still figuring it out, but chances are good that obesity is not of great benefit to the brain.

“People with certain types of personality traits are less likely to get demented,” says O’Brien.  Wait, personality traits?

pexels-photo-156731People who are positive and upbeat seem to have some protection from dementia. Why? Well, it may be that people who are positive are more likely to educate themselves and exercise.  The good news is that positivity and resilience can be learned. You can actually become more positive by working on gratitude, being around more positive people, and being more connected to your family and community. 

Positive people may also be more likely to do crossword puzzles or sign onto Luminosity, although O’Brien doesn’t think doing a puzzle here or there is enough by itself; in other words, you probably can’t Luminosity yourself out of dementia.  Now, one study published in the New England Journal of Medicine showed that people who did crossword puzzles had a lower rate of dementia than did people who spent a lot of time watching TV. But O’Brien thinks the brains of people who choose to do crossword puzzles are different from those of people who like to watch TV. “If you forced the people who are watching TV all the time to do crossword puzzles, would they have a lower incidence of dementia? I doubt it.”

Cognitive reserve is a very robust thing, according to O’Brien. “If you look at the neurons of people with high levels of cognitive reserve, they’re pretty resistant to the toxic effects of Alzheimer’s disease pathology. They actually have bigger neurons in the key areas of the brain. Their neurons are more healthy, even if there’s a lot of Alzheimer’s disease pathology.”

And then there’s diet.

O’Brien suspects that the Mediterranean diet might have a significant effect on dementia, because it also has significant effects on cardiovascular health. “The data’s pretty clear that if you can prevent cerebrovascular disease, your chances of becoming demented are much lower.”

In 2014, scientists at UCLA published a priority research paper in the journal, Aging, that showed for the first time, memory loss being reversed.  It wasn’t because of a drug or procedure, but a comprehensive and personal approach that showed how Alzheimer’s is a complex disease, affected by diet, exercise, and even sleep.  All of these things contribute to the brain’s plasticity, said Dale Bredesen, the study’s principal investigator.  Ten people with memory loss, some with brain scan-confirmed patterns of Alzheimer’s, participated in a small study called MEND, for Metabolic Enhancement for NeuroDegeneration.

The participants made dramatic lifestyle changes.  They avoided simple carbs, gluten, and processed foods.  They ate more fish, did yoga, and meditated.  If they didn’t sleep well, they took melatonin.  They took vitamin B-12, vitamin D-3, and fish oil.  Within 6 months, 9 patients had a noticeable improvement in memory.  One patient, who was in the late stages of Alzheimer’s, did not show improvement, so there may be a point at which it’s too late.  But these findings suggest that at least early on, changing your metabolism can improve your cognitive function. 

Six of the people in the study who’d had to quit working were able to return to their jobs.  Some patients were followed up to two and a half years, and the memory improvements remained.  Larger studies are under way.

Let’s come back to exercise.

300_200_walk_gravelA study led by scientists from the University of Maryland School of Public Health, published in the Journal of Alzheimer‘s Disease, found that just 12 weeks of moderate exercise – basically, walking fast enough on a treadmill to get your heart rate up, but not so much that you couldn’t carry on a conversation with someone else while you did it – made a difference in how people’s brains functioned.

It made their brains work better; their neurons were more efficient. People could remember things more easily, and their brains didn’t have to work as hard to do it.

Scientist, J. Carson Smith, of the University of Maryland’s Neuroimaging Center, and said, “No study has shown that a drug can do what we showed is possible with exercise.”

The people in the study weren’t spring chickens, either. They ranged in age from 60 to 88. They weren’t athletes – far from it; they were considered “physically inactive older adults.” Some had already shown mild cognitive impairment. The people in both groups – those with the mild impairment and those with healthy brain function – improved their cardiovascular fitness by about 10 percent in the three months of the program.

They also improved their memory. MRI brain scans taken before and after the study showed “a significant improvement in 11 brain regions.” Even more exciting, the places in the brain that got better are the same ones that are affected in Alzheimer’s – the precuneus region, the temporal lobe, and the parahippocampal gyrus. Their word recall – remembering as many as possible out of a list of 15 words – improved.

What does this mean for you? It means that, whatever age you are, you can make your brain work better even with a small amount of effort. You don’t have to be in marathon-running shape. You don’t have to go grunt and sweat and dead-lift huge weights. Just walk for two and a half hours a week – 30 minutes a day, five days a week. If you don’t have 30 minutes, do it twice for 15 minutes. Any effort is going to pay off.

Other Things:

Prevent frailty. Frailty is your enemy.  But O’Brien says:  “I don’t think that falling apart when you get old is something that has to happen.”

Recently, Johns Hopkins geriatrician Jeremy Walston looked at what healthy older people have in common — at what they eat and don’t eat, and how they live – and came up with some practical tips. 

Nutrition:  Make Every Bite Count

If you do it right, just about everything you eat can help your body.  This doesn’t mean you have to eat just nuts and berries or be a food martyr who never eats comfort food.  What does it mean?

Eat Fresh Fruits and Veggies

grilled veggiesI know, duh.  Who doesn’t know that fresh fruits and vegetables are good for you?  But what’s in them matters, too. Walston says potassium is important, and “Fresh fruits and vegetables are rich in potassium.” 

When you get your blood pressure tested, it’s a fraction, one number over another.  That top number is systolic blood pressure, and potassium can lower it by several points.  It also helps regulate the heart rhythm.  If you are eating foods rich in potassium, this also means you’re not loading up on saturated fat, and this will help lower your cholesterol.

Get More Protein

As we get older, we need more protein.  “Protein helps muscles function better, and it is also important to help maintain muscle mass.” You don’t have to spend big bucks; you can get salmon in a can, or yogurt, or eggs, or an energy bar. Epic Bars are good sources of meat protein when you’re on the go.

Get Plenty of Vitamin D

Vitamin D helps keep your bones strong.  It also helps keep your muscles, heart, brain and immune system healthy, and can help prevent cancer.  Having low levels of Vitamin D is bad: A study published in the Archives of Internal Medicine found that people with the lowest levels of Vitamin D had more then twice the risk of dying from heart disease as people with higher levels.  You can get it from sunlight, 20 minutes a day twice a week or so, or in a supplement.  The National Institutes of Health recommends 600 international units of Vitamin D a day if you’re under 70, and 800 IU a day if you’re over 70.

Get your shots

Lower your risk of getting the flu, or pneumonia, or shingles by getting a shot. Anything you can do to prevent being laid up is a good thing. 

Keep Moving

My husband, Mark Worthington, is a gastroenterologist, and he tells me that many of the older people he sees fall into two categories.  He always asks them what they do, and some will say, “We volunteer, we hike, we love to go out to dinner with our friends.”  Others basically do nothing.  All day.  Not good.  These people tend not to do as well.

Jeremy Walston says, “Stay active as long as possible.  Don’t sit for long periods of time, especially in the late afternoon or evening.  Studies show that those are low-activity times for many people, so it’s good to try to boost your activity during those times.”  Go for a walk after dinner.  Walking is good; in fact, you should walk a lot, or do some aerobic activity – there’s plenty to choose from. 

“It’s also important to do exercises that help you stay flexible, that help your balance and gait, and that help strengthen your muscles.  Don’t forget your shoulders,” which are important for maintaining core body strength and higher levels of function.  And if you have an “orthopedic issue,” like knee or hip trouble, address it, so you can keep moving as long as possible.”


Don’t Fall

Falling is bad.  The body literally takes a hit when you fall.  Many older people, who otherwise have been doing pretty well, take a turn for the worse after a fall.  Just being laid up for a few days can be difficult for the elderly because they tend to lose strength quickly.  The best way not to fall is to prevent it, says Walston.  “Things that can make you fall include: not watching your medication; vision problems; weakness in the lower extremities; and balance and gait problems.” 

One huge risk factor is easy to fix:  “low lighting and a cluttered living area.”  Make sure your rooms are well lit – that you not only have enough lights, but that the bulbs are high-powered enough so you can see where you’re going.  And go after the clutter.  It doesn’t take much – maybe a stack of books or magazines that slips over, a puzzle left by a grandchild on the floor, or pet toys – to make a walkway treacherous.  Sometimes, you’re so used to looking at clutter that you don’t see it.  This is why Walston recommends bringing in a friend or relative who is not used to your home, who can see potential trouble spots you haven’t noticed.

A personal note: When my aunt, who had dementia caused by a stroke, had to go to the nursing home, we asked what we could bring for her room.  They said:  Only one thing, because clutter makes demented people more agitated.  I figure, if demented people are the canary in the coal mine, and clutter stresses them out a lot, it most likely stresses us out, too, on a low level.  So not only can you trip on it, clutter agitates.

You can lower the odds of falling by working on your balance.  Tai Chi is a great way to do this, and so is yoga. 

What else?

“Cognitive risk factors include diabetes, elevated lipids, and high blood pressure,” says Walston.  Medications can keep all of these problems in check, which will help your blood vessels, which will help your brain.

Poor hearing:  If you don’t feel connected, you may tend to withdraw from the conversation, smiling politely, not engaging, because you don’t know what people are saying.  This is bad.  “Get a hearing aid if you need one.”  It won’t just help your hearing; it will help your brain.  There’s a feedback loop: When you stay connected, you are giving of yourself, talking and listening, and that stimulates your brain. When you don’t hear, you just sit there and don’t participate, you’re not getting that stimulation, and if you don’t use your brain as much as possible, you may lose function.

Depression:  If you are depressed, you are going to be withdrawn, you may not eat or sleep very well, and you may not get enough exercise.  Treating it is good “cognitive protection,” says Walston. 

Finally, Stay connected.  Talking to people — volunteering, driving, interacting with others in church, clubs, or other groups, being around family or friends – protects your brain.

©Janet Farrar Worthington