Archive for the “Study Spotlight” Category

Here’s another one of those studies that produced an eye-rolling moment for me.  Actually, it wasn’t the study itself.  The study was fine, which is why I didn’t have a head-bang-on-desk moment.   It was the conclusion – which is the only part of a study many media health reporters read — that produced the eye-rolling.

Here’s part of the abstract:

OBJECTIVE:
The physicochemical properties of soluble oat fiber (β-glucan) affect viscosity-dependent mechanisms that influence satiety. The objective of this study was to compare the satiety impact of oatmeal with the most widely sold ready-to-eat breakfast cereal (RTEC) when either was consumed as a breakfast meal.

METHODS:
Forty-eight healthy individuals ≥18 years of age were enrolled in a randomized crossover trial. Following an overnight fast, subjects consumed either oatmeal or RTEC in random order at least a week apart. The breakfasts were isocaloric and contained 363 kcal (250 kcal cereal, 113 kcal milk). Visual analogue scales measuring appetite and satiety were completed before breakfast and throughout the morning. The content and physicochemical properties of oat β-glucan were determined. Appetite and satiety responses were analyzed by area under the curve (AUC).

So they compared people eating oatmeal to people eating ready-to-eat cereal.  Surprise!  The people who ate oatmeal reported feeling less hungry later in the day.  No kidding.  Ready-to-eat-cereal takes your blood sugar on a wilder roller-coaster ride than oatmeal.

Now here’s the study’s conclusion:

Oatmeal improves appetite control and increases satiety. The effects may be attributed to the viscosity and hydration properties of its β-glucan content.

Oatmeal improves appetite control?  Well, I can already picture the additional sales pitch on boxes of Quaker Oats, right there next to Can Help Reduce Cholesterol! Now they’ll be adding Improves Appetite Control!

Here’s the Science For Smart People question:  Compared to what?

Compared to ready-to-eat-cereal, oatmeal produced greater satiety.  But what if there had been a third group that ate eggs for breakfast?

I haven’t seen a study with a direct oatmeal-to-eggs comparison, but I did find an eggs-to-bagels comparison in my study files.  Here’s part of that abstract:

OBJECTIVE:
To test the hypotheses that among overweight and obese participants, a breakfast consisting of eggs, in comparison to an isocaloric equal-weight bagel-based breakfast, would induce greater satiety, reduce perceived cravings, and reduce subsequent short-term energy intake.

SUBJECTS:
Thirty women with BMI’s of at least 25 kg/M2 between the ages of 25 to 60 y were recruited to participate in a randomized crossover design study in an outpatient clinic setting.

DESIGN:
Following an overnight fast, subjects consumed either an egg or bagel-based breakfast followed by lunch 3.5 h later, in random order two weeks apart. Food intake was weighed at breakfast and lunch and recorded via dietary recall up to 36 h post breakfast. Satiety was assessed using the Fullness Questionnaire and the State-Trait Food Cravings Questionnaire, state version.

The results showed that the women who had eggs for breakfast ate smaller lunches than the bagel-eaters:  574 calories for lunch vs. 738.  They also reported feeling fuller, even though both breakfasts contained the same number of calories.

I’d like to see a head-to-head comparison with four heads:  eggs, bagels, oatmeal and ready-to-eat cereal.  I’d put my money on the eggs for the greatest satiety and appetite control.

But if someone conducted that study and the egg producers slapped a big Helps Reduce Appetite! label on their cartons, I bet somebody at the FDA would get very upset.

NOTE:  The Older Brother will be taking over the blog next week.  I’m giving a speech on Thursday and plan to spend the early part of the week rehearsing and putting the finishing touches on my slides.

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A reader asked me for some information on cancer and sugar, so I pulled up some items from my research database.  As long as I had the articles in front of me, I thought I’d share them.

Nothing listed here proves absolutely that sugars drive cancer or that a ketogenic diet will prevent cancer, but taken together, the articles do paint a picture.  Let’s take a look.

Cancer cells slurp up fructose, US study finds

Pancreatic tumor cells use fructose to divide and proliferate, U.S. researchers said on Monday in a study that challenges the common wisdom that all sugars are the same.

Tumor cells fed both glucose and fructose used the two sugars in two different ways, the team at the University of California Los Angeles found.

They said their finding, published in the journal Cancer Research, may help explain other studies that have linked fructose intake with pancreatic cancer, one of the deadliest cancer types.

“These findings show that cancer cells can readily metabolize fructose to increase proliferation,” Dr. Anthony Heaney of UCLA’s Jonsson Cancer Center and colleagues wrote.

“They have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth.”

I found some suggested meal plans on the USDA’s official My Plate site, which I’ll share in another post.  Whole milk isn’t on the meal plan for breakfast, but orange juice and strawberry-flavored (i.e., sugary) skim milk are.  Remind me again … which of those drinks contains fructose and which doesn’t?

Compound That Blocks Sugar Pathway Slows Cancer Cell Growth

Scientists at Johns Hopkins have identified a compound that could be used to starve cancers of their sugar-based building blocks. The compound, called a glutaminase inhibitor, has been tested on laboratory-cultured, sugar-hungry brain cancer cells and, the scientists say, may have the potential to be used for many types of primary brain tumors.

The Johns Hopkins scientists, inventors on patent applications related to the discovery, caution that glutaminase inhibitors have not been tested in animals or humans, but their findings may spark new interest in the glutaminase pathway as a target for new therapies.

Glutaminase is an enzyme that controls how glucose-based nutrients are converted into the carbon skeleton of a cell. Additional enzymes that help construct the so-called “bricks” of the carbon skeleton are controlled by a gene called IDH1. In some brain cancer cells, IDH1 is mutated and the resulting enzyme grinds up the bricks into nutrients that feed cancer cells.

Yes, yes, I know what you’re thinking:  if blocking the glucose pathway slows cancer growth, why not just tell people to stop eating foods that spike glucose?  Well, I’m pretty sure the answer lies in the fact that scientists have applied for patents.  You can’t patent dietary advice, but you can patent a drug.

Diabetes Medication May Get New Life as Cancer Treatment

The drug metformin, a mainstay of diabetes care for 15 years, may have a new life as a cancer treatment, researchers said.

In a study in mice, low doses of the drug, combined with a widely used chemotherapy called doxorubicin, shrank breast-cancer tumors and prevented their recurrence more effectively than chemotherapy alone.

The findings add to a growing body of evidence that metformin, marketed as Glucophage by Bristol-Myers Squibb Co. and available in generic versions, could be a potent antitumor medicine.

In the report, being published in the Oct. 1 edition of Cancer Research, a journal of the American Association for Cancer Research, researchers said the combination of metformin and doxorubicin killed both regular cancer cells and cancer stem cells.

In contrast, doxorubicin alone had limited effect on the stem cells.

Mice that grew tumors generated from human breast-cancer cells have remained tumor-free for nearly three months on the combined treatment, while tumors have recurred in those not given the diabetes remedy.

Researchers said the results have potentially broad implications for cancer treatment.

Hmmm, now why would a drug given to type 2 diabetics be effective against cancer?  You have to read pretty far down the article to find out:

How metformin affects cancer isn’t certain, but one possibility is that it deprives tumor cells of sugar.

“Cancer cells are gluttons for glucose,” said George Prendergast, president and chief executive officer of Lankenau Institute for Medical Research, Wynnewood, Pa. “It is likely that metformin is taking advantage of this gluttony of the cancer cell in order to attack it.”

Cancer cells are gluttons for glucose … I’ll be sure to think about when I’m drinking my USDA-approved skim milk with added sugar.

Dietary glycemic load and colorectal cancer risk

The link above is to an observational study based on food questionnaires, so it doesn’t exactly meet the gold standard for research.  Nonetheless, here’s the conclusion:

The positive associations of glycemic index and load with colorectal cancer suggest a detrimental role of refined carbohydrates in the etiology of the disease.

The next time some vegan zealot trots out an observational study showing a weak association between meat and cancer, you can reply with this one and explain that since glycemic load is strongly associated with colorectal cancer, you’re sticking with a low-glycemic diet – meat included.  If the vegan zealot starts quoting the China Study, you can reply with this (sort of) China study of Chinese Americans:

Carbohydrates and colorectal cancer risk among Chinese in North America

Here’s the conclusion:

These data indicate that increased eCarb (non-fiber carb) and total carbohydrate consumption are both associated with increased risk of colorectal cancer in both sexes, and that among women, relative risk appears greatest for the right colon, whereas among men, relative risk appears greatest for the rectum.

So get T. Colin Campbell’s high-carb diet out of my face.

Effects of a ketogenic diet on tumor metabolism

This one isn’t a study; it’s a case report from 1995 of two pediatric cancer patients put on ketogenic diets.  Here are some quotes from the abstact:

OBJECTIVE: Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient’s overall nutritional status.

So all the way back in 1995, at least some doctors suspected that depriving cancers of glucose might help.  Sheesh.  Anyway …

RESULTS:  Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression.

Improvements in mood and skill development?  No, no, no … low-carb diets make you depressed and irritable.  I know that’s true, because I read it on Yahoo Health.

Glucose deprivation activates feedback loop that kills cancer cells

Compared to normal cells, cancer cells have a prodigious appetite for glucose, the result of a shift in cell metabolism known as aerobic glycolysis or the “Warburg effect.” Researchers focusing on this effect as a possible target for cancer therapies have examined how biochemical signals present in cancer cells regulate the altered metabolic state.

Now, in a unique study, a UCLA research team led by Thomas Graeber, a professor of molecular and medical pharmacology, has investigated the reverse aspect: how the metabolism of glucose affects the biochemical signals present in cancer cells.

In research published June 26 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation — that is, depriving cancer cells of glucose —activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species, the cell-damaging molecules and ions targeted by antioxidants like vitamin C.

Hey, I don’t care if it’s an amplification loop that does the job or if the cancer cells just die off from a lack of fuel.  The point is, once again we see that depriving cancer cells of sugars can kill them.

Keep starving those cancer cells, folks.

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I explained in yesterday’s post that I wasn’t going to do a full analysis of the latest “meat kills!” study because it’s full of the same old garbage I’ve covered in previous posts about other “meat kills!” studies.

If you’d still like to see a full analysis, Zoe Harcombe gave the study a well-deserved pounding. You can read her analysis here.

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A reader sent me a link to a blog post claiming that paleo types who advise against eating grains are scaring people for no reason.  (No, I’m not going to link to it.)  Grains are good for us, you see, because the Mayo Clinic, the USDA and numerous other experts say so.  That’s the main evidence offered:  a mindless appeal to authority.

The writer acknowledges that the number of people diagnosed with celiac disease has gone up, as have claims of gluten intolerance, but suggests the increases are a matter of increased awareness.  In other words, we’ve been scared into the thinking wheat is bad for us, so we’re reporting more problems with wheat.

The reported increase in celiac isn’t due to better diagnosis, however.  As Dr. William Davis explained in Wheat Belly, the rate of celiac disease really and truly has gone up – it’s quadrupled, in fact.  We know that because researchers found blood samples taken from soldiers 50 years ago and compared them to blood samples taken from soldiers today.  Sure enough, today’s soldiers were four times more likely to have celiac antibodies in their blood.

As for the argument that gluten intolerance is all in our heads, perhaps a double-blind study would answer that.  You know, feed some subjects foods containing gluten, feed other subjects similar foods without gluten, with neither group knowing which foods they’re eating.  If only someone had conducted such a study …

… oh, wait.  It’s been done, as reported in a New York Times article about gluten sensitivity:

Crucial in the evolving understanding of gluten were the findings, published in 2011, in The American Journal of Gastroenterology, of an experiment in Australia. In the double-blind study, people who suffered from irritable bowel syndrome, did not have celiac and were on a gluten-free diet were given bread and muffins to eat for up to six weeks. Some of them were given gluten-free baked goods; the others got muffins and bread with gluten. Thirty-four patients completed the study. Those who ate gluten reported they felt significantly worse.

So gluten intolerance isn’t all in people’s heads.  It’s in their guts too.  At least that was the case in this study.

Ahh, but if you eliminate grains, you’ll miss out on all the health benefits who grains provide, the blogger assured us.  Oodles of studies have shown that whole grains are good for us.

I’ve written about those studies many times.  Every time I tracked down a study purporting to prove the benefits of whole grains, the comparison was between people consuming whole grains and people consuming white flour.  All we can determine from those studies is that whole grains aren’t as bad for us as white flour.  To prove whole grains have real benefits, we’d have to compare people who eat whole grains to people who eat no grains.

Ask the USDA, a doctor, a dietitian, or almost anyone who writes health articles for the mainstream press, and they’ll go on and on about hearthealthywholegrains.  Well, here’s one study that actually measured changes in heart-disease risk factors after feeding subjects whole grains:

A total of 316 participants (aged 18-65 years; BMI>25 kg/m2) consuming < 30 g WG/d were randomly assigned to three groups: control (no dietary change), intervention 1 (60 g WG/d for 16 weeks) and intervention 2 (60 g WG/d for 8 weeks followed by 120 g WG/d for 8 weeks). Markers of CVD risk, measured at 0 (baseline), 8 and 16 weeks, were: BMI, percentage body fat, waist circumference; fasting plasma lipid profile, glucose and insulin; and indicators of inflammatory, coagulation, and endothelial function. Differences between study groups were compared using a random intercepts model with time and WG intake as factors.

120 grams of whole grains … that’s a lot of hearthealthywholegrain goodness.  Now let’s look at the results:

Although reported WG intake was significantly increased among intervention groups, and demonstrated good participant compliance, there were no significant differences in any markers of CVD risk between groups. A period of 4 months may be insufficient to change the lifelong disease trajectory associated with CVD. The lack of impact of increasing WG consumption on CVD risk markers implies that public health messages may need to be clarified to consider the source of WG and/or other diet and lifestyle factors linked to the benefits of whole-grain consumption seen in observational studies.

Yes, I’d say the public-health messages regarding whole grains need to be clarified.  Here’s my version of the clarification:

Sorry … turns out we were wrong about the whole-grain thing.

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Okay, I was dishonest in the title of this post.  Not all Norwegians have heart disease.  But almost all Norwegian men are (if we believe the prevailing guidelines) at high risk for heart disease.

Like most Americans, I spend very little time thinking about Norwegians.  The great Chicago columnist Mike Royko once pointed that in the ethnic melting pot of Chicago, you can hear jokes about the Irish, Jews, Italians, Poles, African-Americans, Mexicans, Puerto Ricans, French, British, Russians and Germans.  He even remembered some jokes about Swedes.  But when he asked around, nobody could remember ever hearing a joke about Norwegians.  Royko even tracked down a Norwegian-American acquaintance who confirmed, “Naw, nobody tells jokes about us.  We’re too nice.”

I got thinking about the Norwegians this weekend while answering comments on my post about the Spanish Paradox.  I remembered logging a study about Norwegians and their risk of heart disease into my database and pulled it up.  Here are some quotes from the study:

Since the first US Framingham model for predicting heart disease risk was published in 1991, it has become ever more widely recommended that doctors in primary care carry out risk assessment by combining several risk factors for cardiovascular disease using algorithms. Until recently most risk equations have been derived from the Framingham study, but these calculations tended to overestimate risk in the European context.

Actually, the Framingham model is lousy at predicting heart disease in the American context as well.  But let’s move on.

A new European risk scoring system for cardiovascular disease, based on the first phase of the systematic coronary risk evaluation (SCORE) project, was presented in 2003. The system is based on a pooled dataset of cohort studies from 12 European countries, among these Norway, and offers a format for estimating fatal cardiovascular disease risk that is suitable for clinical practice.

After explaining those guidelines, the researchers report on the results of applying them to data collected from several thousand Norwegians.  Here’s what they found:

At age 40, 22.5% of women and 85.9% of men were at high risk of cardiovascular disease. Corresponding numbers at age 50 were 39.5% and 88.7%, and at age 65 were 84.0% and 91.6%.  At age 40, one out of 10 women and no men would be classified at low risk for cardiovascular disease.

Hmmm … people in Norway must be dropping like flies from heart disease, at least according to the prevailing guidelines for estimating heart-disease risk … you know, cholesterol levels and all that stuff.

Here again is the American Heart Association’s chart showing rates of cardiovascular disease around the world:

You’ll notice Norway is down toward the lower end of the scale – not as low as France or Spain, but lower than the U.S., U.K. or Germany.

For once, the researchers recognize that the current guidelines are poppycock.  They don’t put it quite that way, of course.  Their language is more academic and polite:

Implementation of European guidelines to prevent cardiovascular disease would label most people in an unselected Norwegian population at high risk of fatal disease from age 40

The validity of the evidence base of the guidelines is questionable and predicts practical and ethical dilemmas related to resource allocation and clinical counselling.

Any overestimation of a person’s risk for cardiovascular disease can have important implications. Apart from causing unnecessary concern, it undermines the patient’s informed choice for intervention. It is also likely to increase prescribing costs and affect life insurance premiums.

Yup.  First thing you know, your doctor is scaring the bejeezus out of you and talking you into taking statins.

Over the weekend, I also had a mini-debate on Twitter with someone who insisted the French paradox is probably a matter of genetics.  I pointed out that waves of French moved to England to become landowners after the Norman Conquest and that the French and English have been intermarrying for hundreds of years.  I doubt that there’s a big difference between French DNA and British DNA.  He didn’t buy it and tweeted a link to a document detailing the marked genetic differences among Europeans.  He apparently didn’t notice that the document he linked described differences among Europeans separated by the Alps for most of history.

Look at the AHA chart one more time.  Scotland and Ireland are near the top.  England and Wales are near the middle.  Now go find Australia.  I’ll give you minute …

… Find it?  Yup, Australia is near the bottom.  My Australian readers can correct me if I’m wrong, but I’m pretty sure we can’t explain away the “Australian Paradox” by suggesting Australians are genetically distinct from the Irish, Scots and Brits.

So we have the Spanish, who are in “poor cardiovascular health” according to current guidelines, but have a low rate of heart disease.  We have the Norwegians, nearly all of whom are at a high risk of heart disease according to current guidelines, but have a relatively low rate of heart disease.

I’m thinking the problem is with the current guidelines.  Nice to see some researchers say as much.

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Here’s one of the studies I’d saved and forgotten until I got organized over the holidays.  The researchers took a survey among doctors to determine their attitudes towards the obese.  Let’s look at the results:

Six hundred twenty physicians responded. They rated physical inactivity as significantly more important than any other cause of obesity. Two other behavioral factors — overeating and a high-fat diet — received the next highest mean ratings. More than 50% of physicians viewed obese patients as awkward, unattractive, ugly, and noncompliant.

So there’s the consensus medical opinion for you:  obese people are obese because they don’t move around enough and eat too much fat.  If you need more evidence that the average doctor doesn’t don’t know diddly about weight loss, there it is.

In his book Fat Politics, Professor Eric Oliver (who appeared in Fat Head) wrote that obese people often avoid doctors – thus allowing treatable conditions to go untreated – because they’re afraid they’ll be criticized for their size.  Given the results of this survey, I’d say that’s a reasonable fear.

“Why aren’t you sticking to the low-fat diet and exercise program I prescribed?!”

“I am, Doctor.”

“No, you’re clearly not.  Just look at you.  You’re awkward, unattractive, ugly and noncompliant.  Now, when should we schedule you for a follow-up visit?”

Unfortunately, much if not most of the general public shares the same belief:  obesity is the result of laziness.  I was reminded of that in two emails I received this week from readers.  Here’s part of the first one:

Having watched Super Size Me I was, as I assume many others were, led to believe what the film intended: the vast majority of Americans are fat, lazy and (for lack of a better term) stupid — a belief I’ve pretty much held my entire life. Being athletic and “skinny,” I have done nothing but look down on those who didn’t match what I saw in the mirror.

I thought all you had to do to be like me is get your ass off the couch and do something. Burn more calories, lose weight, easy enough … or so I thought.  Having grown older and somewhat wiser, I’ve started realizing the faults of that mentality.

Put an M.D. after his name and take away the wisdom that came with maturity, and you’d have your average doctor looking at an obese patient.  Thank goodness he saw the light (and Fat Head.)

Here’s another email from a guy who also believed losing weight was all about being more active – until he gained weight himself:

I was always skinny as a child. I wrestled in high school at a lower weight (130), at 5’9″. The coach was a popular guy, so we often got graduates coming back to practice with the team a few times on their college winter break. Invariably, the graduates would be well over their old weights, leading to joking around about how “fat” they’d become. The coach would always tell us that, in time, we’d all develop paunches and be “fat old men.” We just accepted it, while we downed rice cakes and diet cola at lunch during the season to keep us in our weight class –by senior year, this was already difficult for me, despite the grueling practices.

Years passed (I’ve always wanted to write that)….

When I hit 30, I looked at my weight. Despite never being “fat”, I’d gone up to 170-175lbs (depending on whether I’d pigged out or not the last few days), which is overweight on the BMI scale.

I immediately started working out again like I did on the old squad, and pretty soon had a 2-3 times per week routine of distance running and weight training. I clocked a 7 minute mile in 6 months, and was lifting a substantial amount. Yet, despite all this hard work, I was still tipping the scales at 170lbs!

My diet was “extra healthy”: a glass of orange juice for breakfast, with perhaps some oatmeal; a meal of rice, beans, and cheese for lunch (easy on that fatty cheese, pile on the rice and beans!); and spaghetti for dinner, with 2-3 pieces of wheat bread to mop up the sauce. For a snack, an English muffin, or else three “reduced fat” Oreos. Yet, after months of this “healthy eating,” I still was at 170lbs on my best day! Who’d have thunk it, right?

And then the injuries started up. Plantar fascitis was a huge one—I’d wake up in the morning and feel a ton of pain just standing up. The podiatrist I saw gave me some painkillers and told me I’d need some inserts for my shoes, probably for most of my life. My back and neck ached too.

At first I just thought I was getting old. So I continued to work out. I hit 10 pullups, 100 situps, and 50 pushups, with my running at a 7 minute mile clip and lifting weights. But … more pain, no weight loss!

The reader saw Fat Head and decided to try a low-carb diet based on meats, eggs and vegetables with some full-dairy.  He hoped to lose 3-4 pounds in the first month.  He lost 10 instead.  He continues:

I nearly flipped out! As one person wrote on another website, low-carb dieting was like playing a video game with a God-mode-cheat-code. So easy! I didn’t count calories, never skimped on a meal, was always full and happy. And I hadn’t seen 160 since…well, I don’t know when I passed it to begin with, but certainly not since I passed 30.

Full, happy, no counting calories … that’s my life now.  I didn’t make a New Year’s resolution to lose weight this year and haven’t in three years. I don’t even own a scale.  My only diet resolution this year was to return to what I know works after indulging a bit over the holidays.

The “fluffy” picture (as one reader kindly put it) I posted earlier in the week was of me on a low-fat diet – and I was a regular jogger in those days.  (I once found a videotape of me jogging, looking quite fat in my jogging outfit.)  I also worked out at a Nautilus club two or three times per week.  An athletic, naturally-lean buddy of mine (who also believed people are fat because they eat too much and don’t move around enough) once joined me for a workout and admitted later he was surprised by how much I could out-lift him.

Despite the low-fat diet and all that physical effort (doctor approved!), I was fat.  I wasn’t morbidly obese, but I do remember a doctor pointedly telling me I should focus on losing some weight.  He likely thought I was lazy and sat around all the time.  Hardly.  I probably could have beaten him in either an arm-wrestling match or a 5k race.

It’s January, so millions of fat Americans are hitting the gyms and health clubs, hoping to sweat their way into leaner physiques.  Their doctors would approve.

Around April or so, many of them will become frustrated and give up — at least that’s the annual pattern Chareva and I have noticed at the rec center where we work out.  Their doctors will disapprove, labeling them as lazy and non-compliant.

Their doctors don’t know squat.

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