Two recent studies bring good news for those of us who either don’t have a lot of time to exercise, or just don’t like it and don’t want to spend an hour working out: bursts of cardiovascular activity matter. A lot.

For those of us who are getting older (which, unless you’re dead or cryopreserved, or both, is everybody), nothing is better at delaying aging than exercise, say Mayo Clinic investigators, who recently published a very interesting study in the journal, Cell Metabolism.  In other words, there is no magic bullet pill or thing you can eat that will do as much as exercise to keep you living longer and healthier.

Well, we kind of knew that. But the really good news here – especially for those of us who don’t just have scads of time or willpower to spend at the gym – is that it doesn’t have to be for a huge chunk of time every day.

The Mayo researchers didn’t just look at the things we usually think of with exercise – weight loss, better endurance, muscle mass vs. fat, maybe improvements in mood or functioning. Instead, they looked at the effects of exercise in younger and older adults at the molecular level. Particularly, they were interested in the effects on the mitochondria – the battery packs that produce energy in our cells.

The study’s volunteers – 36 men and 36 women in two age groups: young (18-30) and “older” (age 65-80) – were healthy but sedentary. They underwent tests to establish baseline levels for their aerobic fitness, blood sugar, and the gene activity and health of the mitochondria in their muscle cells. Then they were randomly assigned either to a control group (no exercise) or one of three different exercise programs: high-intensity interval biking (pedaling hard for four minutes, resting for three, and repeating three more times); vigorous strength training with weights; and a combined program of light weights and exercise bike-riding (at a moderate pace for 30 minutes, a few times a week).

After 12 weeks, all the participants had repeat lab tests. As you may expect, everybody who exercised had better fitness and blood sugar levels. The people who did weights gained more muscle mass, and the people who did interval training had better endurance.

But the really significant changes were invisible to the naked eye. In the under-30 people who did the interval training – the vigorous bike-riding for four minutes, four times – 274 genes showed increased activity; those who did the more moderate exercise had changes in 170 genes, and the weight-lifters had changes in 74 genes.

Think that’s exciting? Well, it is, but it’s not nearly as exciting as what happened to the seniors who did the interval training: nearly 400 genes showed higher activity, compared with 33 genes in the weight-lifting group and a sad 19 genes in the people who just did the moderate exercise. The oldsters who did the bursts of exercise had healthier mitochondria, too.

What do we take away from this study? That you’re never too old to benefit from exercise, for one thing. And for another, just because you’re older doesn’t mean you are past the point of vigorous exercise – especially if it’s just for a few minutes at a time.

If you aren’t already exercising, you should talk to your doctor to make sure it’s okay. Then, if you’re cleared for takeoff, don’t be like that guy at the gym who’s reading a book or watching the TV on the wall and cycling about one mile a minute, pedaling so slowly that if he were on a regular bike, he would fall over because he’d have no momentum. That barely even counts, and I see people like this at the gym all the time. They have no problem carrying on a full conversation, either; they certainly aren’t short of breath.

Now, how can you apply this to your own life? If you ride a bike or use a treadmill, the timer is your friend. You don’t have to program anything; you can just increase the speed to a comfortable running level, and lower it to a brisk walking level. Do it for one minute. If you can’t do it for a minute, start with 30 seconds of running or pedaling harder, then work your way up. My favorite thing to do on the treadmill is walk at a brisk pace for a minute and a half, then run for a minute, then walk for a minute and a half, then run for a minute, etc., for 20 minutes. When I started, my speeds for walking and running were pretty pokey. Then one day, I was running at my customary pace and I thought, “Hmm. I can go faster,” so I did. I was walking at my customary pace, and I thought, “I can go faster,” so I did. You will be amazed at how much better you get over time.

This is similar to the kind of exercise our ancient ancestors got. I’m not talking about grandpa or even great-grandpa, but way back to the hunter-gatherer days. They didn’t go out jogging for the heck of it, and they certainly didn’t spin or do Zumba – but what they did do was put on bursts of speed when they had to, so they could bring down the animal they were hunting. Thus, I think that at some level, we are hard-wired to do this. Try it. Start small – just a few minutes total, at first – and see how you do.

This brings us to the next study, published in the Journal of the American Heart Association.

Scientists from the National Cancer Institute and Duke University looked at records of nearly 5,000 people over age 40 from the National Health and Nutrition Examination Survey from 2003-2006, and followed them for more than six years; during that period, there were 700 deaths. Then they looked at the amount of time those people who died had spent in moderate-to-vigorous physical activity (MVPA).

They found that all MVPA counted: even if it was just a few minutes here and there. It all went toward the daily total.

This is huge, because it goes against all the guilt-inducing exercise recommendations we have been treated to for decades. The conventional medical wisdom has been that exercise only counts if it’s sustained – for 20 or 30 minutes, or more. And the worst result of this is that many people have thought, “Well, I don’t have much time today, so I’ll just have to try to get in a good workout tomorrow,” or the next day, or next week.

Au contraire, say the results of this study: All exercise contributes to helping you not die. “For about 30 years, guidelines have suggested that moderate-to-vigorous activity could provide health benefits,” said the study’s senior author, William E. Kraus, M.D., of Duke University School of Medicine,” but only if you sustained the activity for 10 minutes or more. That flies in the face of public health recommendations, like taking the stairs instead of the elevator, and parking farther from your destination. Those don’t take 10 minutes, so why were they recommended?”

Why, indeed? Because every little bit helps. In this study, Kraus and colleagues at the National Cancer Institute found that the length of each period of exercise was not related to the overall benefit of living longer. Five minutes of jogging counts. Five minutes of riding an exercise bike counts.  Or five minutes of swimming a couple laps, or whatever.

The participants in the survey wore an accelerometer (similar to a Fitbit or the activity tracker on a smart phone) for up to a week. Looking at the data, the researchers looked at the people in two groups: those who had bouts of MVPA for about five minutes at a time, and those who exercised for longer than 10 minutes at a time.

People who got about an hour a day of MVPA – not an hour at a time, mind you, but an hour of little bits of exercise here and there, all added up – were half as likely to die. Those who got 100 minutes of exercise a day cut their risk of dying even more, by about 75 percent. Again, it was the total time they spent moving, not how long at a time they exercised, that mattered.

In this study, there was no distinction between intentional exercise and just plain old physical activity, like walking up a flight of stairs, or vacuuming the floor, or running to catch a bus.

“Despite the historical notion that physical activity needs to be performed for a minimum duration to elicit meaningful health benefits,” Kraus and colleagues reported, “we provide novel evidence that sporadic and bouted MVPA are similarly associated with substantially reduced mortality.”

In other words, it’s all good.

In addition to the book, I have written about this story and much more about prostate cancer on the Prostate Cancer Foundation’s website, pcf.org. 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

 

Hey, guys: If you think exercise is just about pumping iron and getting big traps, six-pack abs and “gun show” biceps, your prostate would like to disagree.

To your prostate, how ripped or shredded you are is not nearly as important as your cardiovascular health.

Now, you may be wondering, why should the prostate even care about cardiovascular exercise? Here’s a very good reason: exercise can lower your risk of getting lethal prostate cancer, or of having cancer come back if it’s already been treated.

Epidemiologist June M. Chan, Sc.D., an expert on lifestyle and cancer, heads a research program at the University of California San Francisco that seeks fixable risk factors for prostate cancer progression – things in your lifestyle that you can change to lower your odds of dying of prostate cancer. I recently interviewed her for the Prostate Cancer Foundation’s website.

In previous work, Chan and colleagues were the first to show that vigorous exercise (such as jogging or bicycling) after diagnosis was associated with a reduced risk of prostate cancer death in men with localized disease. “We observed that three or more hours a week of vigorous activity, as opposed to less than one hour a week, was associated with an approximately 60 percent reduction in the risk of dying of prostate cancer.” Chan and colleagues observed similar results among 1,455 men in the Cancer of the Prostate Strategic Urologic Research Endeavor (CaPSURE). These findings suggest that “engaging in relatively vigorous physical activity and/or having higher cardiorespiratory fitness may protect against prostate cancer progression.”

Now, exactly why is this? That’s what Chan and colleagues are hoping to figure out. “We have a number of studies here at UCSF examining lifestyle and prostate cancer,” she says. “One trial is for men on Active Surveillance, and our main goal is to look at changes in prostate tissue.” Investigators are comparing prostate biopsy samples taken at diagnosis and again after a 16-week period in which men are randomly assigned either to continue their usual activities or to take part in a personalized exercise program that is designed to increase their cardiopulmonary fitness. The researchers also are measuring chemical processes involving circulation and metabolism, looking for specific differences in the two groups.

In this study, Chan is not as interested in studying the men who are already exercising a lot. “We anticipated that the biggest benefits would be observed in individuals who are relatively sedentary and who adopt moderate exercise. If men are already highly fit, they’re probably already exercising several hours a week, and we thought it would be harder to ask them to do more or spend more time, so that we could observe a relative change in fitness,” she says. “Our main goal is to increase the fitness levels gradually through a walking program in men who are at low to intermediate levels of fitness at the beginning of the study.”

The idea here is that even moderate exercise can help lower the risk of lethal prostate cancer. We’re talking about the kind of exercise that almost everyone can do. It is “purposely scaled to be relative to someone’s baseline fitness, and we are choosing men who are low- to moderate-fit,” Chan notes. Men in this study start out just by walking, and then walking faster, and then escalating – literally – to walking uphill.

The men aren’t going flat-out, like someone in a high-intensity workout. They’re just doing a little more than they could, and after they get used to that, they do a little bit more – slowly building up their fitness.

Chan speculates that the tissue samples in the exercise group will show changes in indicators of angiogenesis (cancer’s ability to build a scaffolding of blood vessels and other infrastructure so it can grow and move beyond the prostate); in inflammatory processes; in insulin and insulin-like growth factor signaling; in androgen receptor signaling pathways; and in oxidative stress mechanisms. “Biochemically, exercise could help deter metastasis of the tumor by changing the environment for the cancer” – in effect, spraying fire retardant on the tumor. Not necessarily extinguishing the flame altogether, but making it burn slower, and helping the body set up fire breaks to keep the cancer confined to its current location.

Making Prostate Cancer Fat and Happy

“Prostate cancer may be the most common cancer where exercise, used like a drug, can confer an increase in survival,” says medical oncologist Jonathan Simons, M.D., CEO of the Prostate Cancer Foundation. “There is no form of treatment that has this effect, and certainly not one as beneficial to the entire body as exercise.”

It may be, Simons adds, that what exercise does – just as it improves blood flow in the arteries – is give cancer a better blood supply that keeps it happy where it is, “so the tumor has no motivation to leave.” So basically, exercise makes cancer feel like it’s at a nice hotel, with free cable TV, continental breakfast, and a pool. It’s content to stay there indefinitely, ordering room service. “When tumors are stressed” – when they’re in a bad neighborhood, in effect – “they have genes that are programmed to help them survive by getting them to crawl away to someplace that better serves their needs.”

One of those genes, Simons found in research at Johns Hopkins, not only pipes in more blood to supply the tumor; it gets rid of waste products – the cancer cells’ sewage, in effect. “When tumors try to turn on blood vessel growth to get more nutrients, they also build their own plumbing for both intake and waste disposal. Angiogenesis is not just about getting oxygen and food – glucose and protein – to the cancer. It’s getting rid of byproducts, too. That kicks off a genetic program so the cancers can relocate” – start to spread.

But giving the cancer a better blood flow might subvert the cancer’s need to boost its own blood supply. It just may be that exercise makes cancer, rather than head for the door, sit back in the recliner and reach for the remote. A contrary notion, isn’t it – that in order to turn your prostate cancer into a couch potato, your best chance is not to be one yourself?

This doesn’t mean, of course, that men who exercise are immune to prostate cancer. “There are very fit athletes who have had forms of prostate cancer that are so aggressive, so genetically mutated, that have proved fatal,” notes Simons. However, those men are at one end of the spectrum of prostate cancer. There are many thousands of men at the other end or in the middle, for whom exercise may make a real difference. “What if you have a Gleason 8 cancer, you had surgery, your PSA was undetectable, and now it’s starting to creep up. And what if you could exercise and delay its colonizing in your bones by eight or nine years, because you so shifted the chemistry in your body that the cancer cells just sat there? That’s a very abstract concept, one that’s still not widely appreciated. But if we could get even three times as many men right now exercising, we could change the overall survival of the disease.” And if scientists like Chan can figure out precisely why this is happening, it may lead to development of new treatments that could make exercise even more effective in deterring the return or spread of prostate cancer.

Is it ever too late to start to exercise? No!

In other trials, including one funded by Movember, Chan and colleagues from around the globe are studying the benefit of aerobic exercise and also strength training in men with castrate-resistant prostate cancer, to see if these interventions can help men at a later stage of cancer live longer. “There are data in men with advanced disease also suggesting that exercise may impart not only quality of life but also clinical benefits” she says.

Body Size and Prostate Cancer

Prostate cancer loves fat. Fat increases inflammation in the body, lowers insulin resistance, and just generally makes a more inviting environment for prostate cancer.

But exercise burns fat. And this, in turn, lowers your body mass index (BMI).   “Increasing evidence suggests that being overweight, either before or at the time of diagnosis with prostate cancer, is strongly associated with the risk of cancer progression and of dying from prostate cancer,” says Chan. “For example, among 2,546 men diagnosed with localized prostate cancer in the Physicians’ Health Study, a one-unit increase in BMI before cancer diagnosis was associated with about a 10-percent increase in a man’s risk of dying of prostate cancer.”

BMI calculators are available on the internet, but briefly, if you are at a healthy weight, your BMI is between 19 and 24.9 kg/m2.  In the Physicians’ Health Study, having a BMI of 30 kg/ m2 or greater “was associated with a nearly twofold increased risk of prostate cancer death,” notes Chan. Further, “a meta-analysis of six studies in prostate cancer patients reported that a 5 kg/m2 increase in BMI raised the risk of dying of prostate cancer by 20 percent, and of biochemical recurrence (having the PSA start to rise again after treatment) by 21 percent.”

 More of this story and much more about prostate cancer are on the Prostate Cancer Foundation’s website, pcf.org. The stories I’ve written are under the categories, “Understanding Prostate Cancer,” and “For Patients.” The PCF is funding the research that is going to cure this disease, and they have a new movement called MANy Versus Cancer that aims to crowd-fund the cure, and also empower men to find out their risks and determine the best treatment. 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 for the disease. Many doctors don’t do this, so it’s up to you to ask for it.

 ©Janet Farrar Worthington

 

In 1993, I actually wrote that sugar and carbs were fine. Want to be healthy? Eat more pasta and healthy grains, I wrote. Fats were the big evil. I was so wrong – but this was what the studies showed. This is what many doctors believed. Fat was our enemy. Fat was the reason we were becoming – not nearly so much as we are now, I might add – a nation of lard butts.

For decades, this was reflected in packaged “healthy” foods. Eat as many cookies as you want: yes, they’re chock full of carbs and junk calories, but no worries! They’re LOW FAT. This was the new food gospel, and we saw it proclaimed on our grocery store shelves – low-fat chips, ice cream, cakes. Guilt-free! Breakfast cereal – great! It’s got NO FAT! We saw the birth of olestra, which not only had no fat – it was indigestible! Side effects included gas, cramps, bloating, diarrhea, and, most appalling of all, “anal leakage.” Lays potato chips, Ruffles, and Doritos at the time that were “FAT FREE” and contained olestra had the word “WOW” in huge letters right there on the bag. I guess they meant the taste, but maybe they were referring to what happened when you ate it, as in: “Wow! I just pooped my brains out!”

In 1967, Nancy Sinatra had a hit song called “Sugartown.” She sang, “I got some troubles, but they won’t last. I’m gonna lay right down here in the grass, and pretty soon all my troubles will pass” (most likely, she did not mean “pass” in the olestra way) “ ‘Cause I’m in shoo-shoo-shoo, shoo-shoo-shoo, Sugar Town.” There were about five more “shoos” in that line, but you get the drift.

Sugartown was the place to be. We believed it because of review articles like one that appeared in the New England Journal of Medicine (NEJM) the same year as “Sugartown” – 1967. It discounted evidence that linked sucrose consumption to coronary heart disease. Doctors believed it. They told their patients. Their patients believed them.

It turns out that this particular study was secretly funded by the Sugar Research Foundation (SRF). Now we know, thanks to a bombshell article recently published by University of California-San Francisco scientists in the journal, PLoS Biology, that the SRF (now defunct) was completely evil. It manipulated the science.

It not only “discounted evidence linking sucrose consumption to blood lipid levels and hence coronary heart disease,” report the study’s authors, Cristin Kearns, Dorie Apollonio, and Stanton Glantz. It also “withheld information from the public” linking sugar to changes in the microbiome that can lead to bladder cancer.

But it’s not just the SRF, which later became the International Sugar Research Foundation (ISRF); it’s a bunch of sugar industry trade associations. And it wasn’t just back in the 1960s. All of these groups have “consistently denied that sucrose has any metabolic effects related to chronic disease beyond its caloric effects,” Kearns, Apollonio and Glantz state. In other words, the main side effect these groups are willing to acknowledge is that sugar makes you gain weight.

Let’s take a moment here for me to say that I love sugar. I do. I love cookies, and chocolate cake, and coconut custard pie, and Mexican Coke with real cane sugar instead of corn syrup.  But I really limit it.  I don’t like food Nazis, who tend to be snarky and condescending and who alienate people who really could benefit from what they’re trying to say by making snide statements like, “What’s next, a deep fried stick of butter?” (I actually read that this week in a nutrition magazine that means well, but its tone is so snotty that it’s off-putting.)

That’s not what I’m trying to do at all. What I’m writing about here is the disturbing idea that sugar has been linked to serious illnesses and that the sugar industry has suppressed this information. If we had known six decades ago, maybe a lot more people would be alive now, and maybe our country wouldn’t be struggling so hard with obesity, heart disease, and diabetes.

In case you’re wondering, Kearns, D.D.S., M.B.A., is an assistant professor at the University of California San Francisco (UCSF) School of Dentistry. Stanton Glantz, Ph.D., is Distinguished Professor of Tobacco Control in the Department of Medicine at UCSF. He’s seen this same kind of twisting and distorting of medical evidence a lot; the tobacco industry did it for years. Dorie Apollonio, Ph.D., is an associate professor in the Department of Clinical Pharmacy at UCSF. Together, these UCSF researchers make a formidable team.

Now, back to the 60 years of manipulating the science and hiding the harmful effects of too much sugar. As recently as 2016, the Sugar Association issued a press release blasting findings from a study published in Cancer Research. In that study, done in mice, scientists found that dietary sugar induces increased tumor growth and metastasis when compared to a non-sugar starch diet. But instead of saying, “Hey, you know, maybe you might want to consider not eating so much sugar – all things in moderation,” the Sugar Association doubled down, stating that “no credible link between ingested sugars and cancer has been established.” Nothing to see here, move along, move along. Look over there – doughnuts with sprinkles!

In this PLoS paper, the UCSF scientists lay out a trail of damning evidence. In that first project in the 1960s, one group of rats was given a diet of 75 percent fat but no sugar. A second group of rats ate a diet of less fat, just 15 percent, but 60 percent sucrose, and their little bodies metabolized all that sugar as a carbohydrate. The sugar-eating rats developed thiamine deficiency, which then led to heart failure. But in the rats that ate more complex carbohydrates and no sugar, the gut bacteria, or microbiome, changed and actually started synthesizing thiamine.

This study intrigued SRF scientists, who thought that maybe, if the microbiome could be adjusted, the gut could tolerate sugar better. This idea led to Project 259, in which scientists led by W.F.R. Pover at the University of Birmingham in the UK studied the effect of sugar in the gut between 1967 and 1971. Pover’s team showed, in rats and guinea pigs, that eating more sugar led to higher levels of triglycerides; in turn, this led to higher levels of beta-glucoronidase in urine a finding that’s linked to bladder cancer and in an internal document, scientists described this research as “one of the first demonstrations of a biological difference” between rats that eat a lot of sugar and rats that don’t.

Project 259 didn’t just link sugar consumption to cancer, but to hypertriglyceridemia, an elevated level of triclycerides (a type of fat) that raises the risk of heart disease, say the UCSF scientists, and these findings stayed hidden for decades until the UCSF scientists uncovered them. Also suppressed was evidence linking higher doses of sugar to other “renal disorders, urinary tract infections, and renal transplant rejection.” Eat sugar – reject your donor kidney!

Even worse, the sugar industry did what every good magician knows how to do: misdirect. In previous research, published in the Journal of the American Medical Association (JAMA), Glantz and Kearns, with colleague Laura Schmidt, examined SRF internal documents and historical reports and found that the SRF secretly funded studies, including one published in 1965 in the NEJM, “promoting fat as the dietary culprit in coronary heart disease.”

Imagine there’s a gunshot, and the killer quickly places the murder weapon in somebody else’s hands and starts shouting, “He did it! It’s that guy!” and then slinks away. That’s what the sugar industry did.

For six decades, we have blamed fat – and as a society, we now look more and more like the tubby earthlings on the big spaceship in the Pixar movie, “Wall-e.” We’re huge, and we’re unhealthy.

Sugartown is not so sweet.

©Janet Farrar Worthington

 

If an illness can have a stereotype, gout has one: its poster boy is a portly, wealthy gentleman who drinks too much red wine and eats too much rich food. In literature, gout is an Epicurean affliction, the runoff of opulence and “disease of kings.”

In fact, gout attacks the poor as well as the rich; it’s more like a creepy shadow that follows other diseases, piggybacks off of their risk factors, and kicks sick people when they’re down. It is also becoming more common. Read more

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 (http://www.amenclinics.com/blog/amen-research-marijuana-affects-blood-flow-brain/) 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

Does the Paleo diet, basically, eating lean meats, nuts, fresh fruits and vegetables – foods our Stone Age, hunter-gatherer ancestors could have eaten – really make you feel better?

If it does, then why?  And how, exactly? 

What happens to the microbiome – the countless bacteria that live inside the gut – when you stop eating dairy, processed sugars and carbs?

paleo diet foodsThis is what doctors at the Amos Center for Food, Body & Mind at Johns Hopkins Bayview Medical Center want to know.  Some of their patients who have irritable bowel syndrome (characterized by constipation, diarrhea, and nausea, it also can include anxiety or depression) have reported that they have been doing better after changing to a Paleo diet. 

To help find out why, Kimberly Harer, M.D., gastroenterology fellow at the Center, designed a short-term study.  I recently interviewed Harer and her colleague, epidemiologist Noel Mueller, Ph.D., for Breakthrough, a publication of the Center for Innovative Medicine at Johns Hopkins. 

For two weeks, she says, 40 patients with IBS will be randomly assigned to eat either a Paleo diet or a standard, healthful diet.  Harer and Mueller will be looking at many things in these study participants, including “how the diet affects their GI symptoms, their quality of life, their vitality,” says Harer.  In people who have been experiencing anxiety or depression, the investigators will look for changes in these symptoms, as well.  They will study blood samples and patient responses to questionnaires about their health, and then, looking at the bacteria in stool specimens, the scientists will analyze the gut “microbiome” before and after. 

Let’s just take a moment to reflect on the concept – still fairly new in research – of a microbiome: It’s a small ecosystem made up of bacteria; this is more complex than it sounds.  Just as the earth has its own ecosystems – tundra, tropical rainforests, grasslands – your body has them, too.  Except instead of plants, these microbiomes are populated by bacteria: dozens of them, picky little cliques that only thrive in one particular spot. For example, the bacteria on the inside of your elbow are different from the bacteria on your face – and even on your face, the bacteria on the bridge of your nose are different from the bacteria between your nose and mouth; and those bacteria are different from bacteria on your chin. 

But the gut takes it to another level; it is the microbial mother lode.  In numbers alone, it’s intimidating.  “There are trillions of microbiota (tiny habitats) in the gut,” says Mueller.  And get this:  All of those bacteria in all those micro-habitats have their own genes and their own genomes, which scientists now know how to sequence.  “There are 100 to one more microbial genes than in your own human genome.”

 paleo diet pancakeThis is why scientists at the Amos Center are convinced that the microbiome has an important influence on our health.  It’s not just numbers, it’s sheer mass:  All those bacteria that live inside our gut, if you somehow got them all together in one lump, would weigh and take up about as much space as your brain – three or four pounds.  Trying to get a handle on that would be overwhelming without sophisticated computers and software, sequencing technology, and bioinformatics tools that allow scientists to recognize patterns and identify gene signatures.

Because the study of the gut’s microbiome is still so new, nobody is sure what it’s supposed to look like, and how the gut flora relates to symptoms.  “Maybe we won’t ever be able to define what is the normal gut microbiome,” says Mueller.  “Normal might be different for everybody.”

Even in identical twins, Mueller continues, the bacteria in the gut can be very different.  It is not unheard of for one twin to have a normal weight, and one to be obese. 

Already, at many hospitals gut doctors are waging war with bacteria, successfully treating patients who suffer debilitating diarrhea from recurrent Clostridium difficile (C.diff) colitis with fecal microbiota transplants.  Basically, uninfected fecal material from a relative with healthy gut bacteria is inserted into the patient’s colon, the good bacteria overwhelm the bad bacteria and the C.diff. is conquered. 

In mice, Mueller notes, scientists have found that if they take the microbiota from the fecal sample of an obese individual and inject it into a germ-free mouse, that germ-free mouse will start to become overweight, too.  “The phenotype of obesity can be replicated just through the sharing of bacteria,” he says.  There is a lot of evidence to suggest that gut bacteria play a huge role in diseases of the metabolism – which also suggests that if these bacteria can be changed, there is great potential to improve someone’s health.

In this study, says Harer, “we will look at the microbiome at three different time points.  First, the baseline, before the diet changes; then, after the Paleo or study diet.”  And then one more time: after participants go back to eating whatever they used to eat for four weeks.  Blood samples will be taken after that four-week period, as well, and patients will fill out questionnaires to report any change in their symptoms.

  “If there are differences in the blood and the stool samples, it will be interesting to see if those correlate with changes in their symptoms,” says Harer.  “And we are very interested to see whether reverting back to their old diet causes the former symptoms to come back, or whether there are lasting changes.” 

Certain families of bacteria thrive on a diet full of macaroni and cheese, soda, and ham sandwiches.  Entirely different bacteria could show up if that diet changes to lean meat, nuts, berries, and veggies.  Which raises another question: If someone gets better with the Paleo diet, “what part is the beneficial part?  Is it the lower carbs?  Is it the increase in plants, or in protein content?  Is it cutting out gluten?”  Or is it some new, beneficial bacteria that have taken precedence in the gut?

paleo diet meatIt’s important to remember that “the microbiome is just part of the study,” Harer continues.  “The question is, does this diet improve symptoms in IBS patients?  Unfortunately, there is a huge unmet need in these patients, because there are few effective treatments.”   

Many people who have IBS are not treated very thoughtfully; they get laxatives for constipation, medicine for diarrhea, and often the symptoms don’t go away because the underlying cause is still there.  The Amos Center takes a team approach with gastroenterologists, allergists and immunologists, psychiatrists, nutritionists, and scientists.  Sometimes, Harer says, people who come to the Center are “frustrated, at the end of their rope sometimes when they come to see us.  We use everyone’s input to treat them holistically, and also to try new things.”

One of these new things is a diet so simple that – as the commercials put it – “a caveman could do it.”  If the Paleo diet does indeed help make people with IBS feel better, understanding why it works at gut level is something we’re only beginning to have the scientific knowledge and tools to decipher.

©Janet Farrar Worthington

What weird quirk of human nature makes us more excited about a cure than prevention?  Imagine the headlines:  “Cure for Dementia!”  Wouldn’t you want to be one of the lucky ones to have bought stock in that company?

I have a friend who’s a dental hygienist, and you couldn’t pay me to do her job: Nobody wants to go to the dentist, nobody wants to hear about all the things they’re not doing to protect their teeth and not get gum disease. 

Nobody wants to be preached at.  We all know we need to floss our teeth*, and brush twice a day.  It’s pretty simple.  But how many people don’t floss, except maybe right before they go to the dentist?  How many of us have lied through our teeth, so to speak, and vehemently denied doing this? 

Dude, all they have to do is start poking around in there, and when they see plaque and your gums bleed at the drop of a hat, they know.  How many of us say, “I hate going to the dentist,” and then pay big money to have fillings and root canals, or worse, to get bad teeth pulled and get dentures.

Well, it’s the same thing happening here, except instead of losing your teeth, you could lose your memory, and your ability to think right. 

This story appeared in the news last week.  It didn’t make nearly as big of a splash as I thought it should:  “Exercising in Mid-Life Prevents Dementia.” 

Prevents dementia!  If you’ve ever watched a loved one struggle with dementia or Alzheimer’s, you know that this is hell on all sides. 

But this! This is really wonderful news:  Some basic lifestyle choices can delay or even prevent this from happening. 

Can you imagine if some drug company had developed a magic pill, something you take in your 40s and 50s, that prevents dementia?  People would be saying, “Sign me up!”

exerciseThis is better than a pill.  Also, it’s free!  The good news from this story is that – like many things we’ve talked about in this blog – every little thing you do makes a difference.  You don’t even need to lift weights or buy a gym membership.  You get points for walking the dog.  Just keep moving!  Any activity is good! 

An Australian researcher, Cassandra Szoeke, Ph.D., and colleagues just published these findings in the American Journal of Geriatric Psychiatry.   They followed nearly 400 women, aged 45 to 55, for more than 20 years, and gave them periodic memory tests; the women learned 10 unrelated words, and then tried to remember them 30 minutes later.

The investigators looked at everything – diet, education, marital status, employment, children, smoking, mood, physical activity, Body Mass Index, blood pressure, cholesterol, hormone levels, etc.   Although younger age and better education (this goes with the “cognitive reservoir” that seems to protect against Alzheimer’s that we talked about in this post) were linked to a better baseline test, the one factor that proved most powerful in determining who didn’t get dementia was regular physical activity

Note: In these posts, I talked about weight loss and smoking, and exercise as a way of not dying of cancer.  This isn’t even about big-effort activity.  You don’t have to jog, or pump iron, or do some extreme sport to keep your brain working. 

According to Szoeke: “Regular exercise of any type, from walking the dog to mountain climbing, emerged as the Number One protective factor against memory loss.”  Also, she continues:  “The effect of exercise is cumulative.  How much and how often you do over the course of your life adds up.”

walkingEvery little bit helps.  What if you didn’t start at age 40?  That’s okay!  Even if you start at 50, “you can make up for lost time.”  I’m going to add my two cents here and say that at any age, doing something is better than nothing, and if you can do your brain a tiny favor every time you move around, then do it.  Don’t cop out and say, “Well, I’m too old to start now, I’m toast.”  No, you’re not.  Conversely, “I’m way younger than 40, I’ve got plenty of time,” is just a terrible attitude.  You’ve got an even better chance of making a difference in your lifetime health!  

After exercise, the other things that proved to be strong protectors against memory loss were having normal blood pressure and having a high level of “good” cholesterol. 

One neat thing about this study, funded by the National Health and Medical Research Council and the Alzheimer’s Association, is that a lot of studies of memory loss start over age 60.  This is because the risk of dementia doubles every five years over age 65. 

The other:  There’s no prescription here for what you do, how hard you work out or how fast you run or walk.  The researchers found that it didn’t matter what people did, just that they did something.  The key is just daily exercise.  Seven days a week. 

“Start now,” says Szoeke, because if you wait, you will disadvantage your health.” 

*Note:  It turns out that dentists have been recommending flossing for a century without having done scientific studies to prove that it works.  Oops.  However, flossing does make your gums stronger and healthier, and removes food that otherwise might remain stuck between your teeth indefinitely, so it is a good thing to do.

©Janet Farrar Worthington