Which Cancers Does Exercise Prevent?

Needs a bit more hormetic stress

“Would you spot me, bro?”

I’ve always assumed that exercise reduces the risk of cancer, contributing to the well-established fact that folks who exercise live longer than others.

But a recent study found a positive association between exercise and two cancers: melanoma and prostate. “Positive association” means the more you exercise, the higher your risk of melanoma and prostate cancer (if you have a prostate).

The good news is that exercise was linked to lower risk of 13 other cancers.

Here’s a quote for the New York Times Well blog:

The researchers found a reduced risk of breast, lung and colon cancers, which had been reported in earlier research. But they also found a lower risk of tumors in the liver, esophagus, kidney, stomach, endometrium, blood, bone marrow, head and neck, rectum and bladder.

And the reductions in risk for any of these 13 cancers rose steeply as people exercised more. When the researchers compared the top 10 percent of exercisers, meaning those who spent the most time each week engaging in moderate or vigorous workouts, to the 10 percent who were the least active, the exercisers were as much as 20 percent less likely to develop most of the cancers in the study.

I’m surprised the protective effect of exercise against cancer wasn’t stronger.

Action Plan

So how much physical activity does it take to prevent cancer? And what type of exercise? We await further studies for specific answers.

I’m hedging my bets with a combination of aerobic and strength training two or three times a week.

Steve Parker, M.D.

PS: If you think cancer’s bad, read one of my books. Wait, that didn’t come out right.

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From The Low Carb Diabetic: Drug Makers Accused of Fixing Prices on Insulin

“A lawsuit filed Monday accused three makers of insulin of conspiring to drive up the prices of their lifesaving drugs, harming patients who were being asked to pay for a growing share of their drug bills.The price of insulin has skyrocketed in recent years, with the three manufacturers — Sanofi, Novo Nordisk and Eli Lilly — raising the list prices of their products in near lock step, prompting outcry from patient groups and doctors who have pointed out that the rising prices appear to have little to do with increased production costs.”

Source: The Low Carb Diabetic: Drug Makers Accused of Fixing Prices on Insulin

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Dr Stefan Guyenet’s Critique of Gary Taubes’ Sugar Hypothesis

An unregulated poison?

An unregulated poison?

Gary Taubes argues that sugar is the likely cause of the Western world’s epidemics of obesity, type 2 diabetes, had heart disease.

I agree it’s a strong contributor to those maladies, if only via it’s contribution to overweight and obesity. I wouldn’t say it’s the sole cause.

Here’s an excerpt from Guyenet’s response to Taubes to whet your appetite:

“A Slow-Acting Toxin

According to Taubes, sugar may be a “toxin” and “the primary cause of diabetes, independent of its calories, and perhaps of obesity as well.” Elsewhere in the essay, coronary heart disease is added to the list. Yet Taubes asserts that this speculative hypothesis cannot currently be tested because there is so little existing research on sugar, and so little interest in conducting such research, that “the research necessary to nail it down would take years to decades to complete and is not even on the radar screen of the funding agencies.

”This belief is remarkable in light of the fact that a Google Scholar search returns hundreds of scientific papers on the health impacts of sugar, many of them human randomized controlled trials, and many funded by the U.S. National Institutes of Health. In reality, the health impacts of sugar are of considerable interest to the scientific community, and as such, they have been studied extensively. Having established that this research exists, let’s take a look at it.

The hypothesis that sugar is the primary cause of coronary heart disease is easily refuted. In the United States, coronary heart disease mortality has plummeted by more than 60 percent over the last half century, despite a 16 percent increase in added sugar intake.[9] Roughly half of this decline can be attributed to better medical care, while the other half is attributed to underlying drivers of disease such as lower cholesterol and blood pressure levels and an impressive drop in cigarette use.[10]This striking inverse relationship is incompatible with the hypothesis that sugar is the primary cause of coronary heart disease, although it doesn’t exonerate sugar.

Is sugar the primary cause of diabetes, “independent of its calories”? Research suggests that a high intake of refined sugar may increase diabetes risk, in large part via its ability to increase calorie intake and body fatness, but it is unlikely to be the primary cause.[11] An immense amount of research, including several large multi-year randomized controlled trials, demonstrates beyond reasonable doubt that the primary causes of common (type 2) diabetes are excess body fat, insufficient physical activity, and genetic susceptibility factors.[12]

The ultimate test of the hypothesis that sugar is the primary cause of obesity and diabetes would be to recruit a large number of people—perhaps even an entire country—and cut their sugar intake for a long time, ideally more than a decade. If the hypothesis is correct, rates of obesity and diabetes should start to decline, or at the very least stop increasing. Yet this experiment is far too ambitious to conduct.

Or is it? In fact, this experiment has already been conducted—in our very own country. Between 1999 and 2013, intake of added sugar declined by 18 percent, taking us back to our 1987 level of intake. Total carbohydrate intake declined as well.[13] Over that same period of time, the prevalence of adult obesity surged from 31 percent to 38 percent, and the prevalence of diabetes also increased.[14]”

Source: Americans Eat Too Much Cake, but the Government Isn’t To Blame | Cato Unbound

Enjoy the view:

Well below room temp here

Not much sugar in this environment except for berries in spring and summer

Taubes partial response:

“In stopping an epidemic, nothing is more important than correctly identifying its cause. Where we are today with obesity and diabetes reminds me of where infectious disease specialists were through most of the 19th century, when they blamed malaria and other insect-born diseases on miasma, or the bad air that came out of swamps. That was mildly effective, in that it was an explanation for why the rich in any particular town preferred to build their homes on hills, high above the miasma and, incidentally, away from the swamps and lowlands and slums where the vectors of these diseases were breeding. But only by identifying the vectors and the actual disease agents do we help everyone avoid them and eradicate the diseases. Only by unambiguously identifying the cause can we effectively design treatments to cure it. The kinds of explanations that Dr. Guyenet and Freedhoff put forth – highly palatable foods or ultra-processed foods – are the nutritional equivalents of the miasma explanation. They sound good; they might help some people incidentally eat the correct diets or offer a description of why other people already do, but they’re not the proximate cause of these epidemics. And there is a proximate cause. We have to find it. I can guarantee it’s not saturated fat, regardless of the effect of that nutrient on heart disease risk. What is it?

Now I am going to focus primarily on Dr. Guyenet’s response, as his was by far the most antagonistic, questioning both the history I present in the lead essay as well as the conclusions I’ve derived from the history and the science. While Dr. Guyenet does indeed challenge “specific and testable assertions” related to my lead essay, the one assertion he does manage to refute successfully is not, regrettably, an assertion I made in the article. As for the rest, the evidence against is not nearly as compelling as he presents it.

First, Dr. Guyenet examined “the 1980 Dietary Guidelines to determine if they condemn fat and take a weak stance on sugar as suggested.” He then set out to determine whether the 1980 Guidelines contributed to obesity, diabetes, and coronary heart disease. He concluded that they didn’t.

I was under the impression when I wrote the essay, though, and still am upon re-reading it, that I do not make such a simplistic assertion. The point that I made is not about the 1980 USDA Guidelines alone – Dr. Guyenet and I both note that they urged readers to avoid too much sugar – but rather the entire movement of the research community to demonize fat, and the journalistic coverage of it, and the series of government documents, and the consensus conferences that followed along because of it—all part of the same concerted public health effort that led us by the late 1980s to believe that the essence of a healthy diet is its relative absence of fat and saturated fat. As an unintended consequence, this ill-conceived dogma-building directed attention away from the possibility that sugar has deleterious effects independent of its calories.

These government reports, as I noted, included the FDA GRAS report on sugar in 1986, the Surgeon General’s Report on Nutrition and Health in 1988, the National Academy of Sciences Diet and Health report in 1989, the British COMA report on food policy the same year, and others. I could have also mentioned the 1984 NIH consensus conference on “lowering blood cholesterol to prevent heart disease” that followed on this legendary Time Magazine cover – “Cholesterol, And Now the Bad News” – and the founding in 1986 of the National Cholesterol Education Program, which published its guidelines for cholesterol lowering the following year. All focused on dietary fat and serum cholesterol as the agents of heart disease and all mostly or completely ignored the evolving science on insulin resistance and metabolic syndrome that implicated sugar and other processed carbohydrates.

Indeed, if anything, the more relevant of the two USDA Dietary Guidelines, the one that Dr. Guyenet does not address, is the 1985 version that declared without a caveat, as I noted, that “too much sugar in your diet does not cause diabetes.” This is, of course, remains the critical question and the one that yet has to be rigorously tested (ignoring the tautology implied by the use of the words “too much”).

Dr. Guyenet, Dr. Freedhoff, and I all agree that had Americans eaten as the guidelines cautioned (and just as Michael Pollan would have preferred as well), we’d all very likely be healthier. But we didn’t. The question is whether the dietary fat/serum cholesterol/heart disease obsession directed attention away from the hypothesis that sugar causes heart disease, diabetes, and perhaps obesity as well through its effect on insulin resistance. The secondary question is whether this obsession in government documents, programs, journalistic coverage, and (pseudo)scientific reviews explains why we continued to eat such high sugar diets. As Dr. Guyenet notes, Americans still consume a significant amount of our calories from grain-based desserts and sugary beverages. But why? By focusing on the straw man of the 1980 guidelines, Dr. Guyenet fails to address that question. That he’s taking on a straw man makes me thinks he’s more interested in appearing to win an argument than in dealing with what may be the single most important public health issue of our era.

A key point to make, as Professor Kealey does, is that Americans did indeed respond to the dietary dogma of the 1970s and 1980s by changing their diets. Dr. Freedhoff and Dr. Guyenet are wrong in this regard when they attend only to the total percentage and amounts of fats, carbohydrates, and protein in our diets, and not the type of fats, carbohydrates, and even protein. Looking at what we ate instead of how much we ate supports the supposition that Americans heard the advice on fat and acted on it, even as we were ignoring the sugar advice. As the USDA reports, between 1970 and 2005, we cut down on our use of butter (-17%) and lard (-66%), while almost doubling vegetable oil consumption (from 38.5 pounds per capita yearly to 73.7); we more than doubled how much chicken we ate (33.8 pounds per capita yearly to 73.6, probably skinless white meat, but I’m speculating), while reducing our red meat consumption by 17 percent, and beef by 22 percent. We cut back on eggs, too. So while total fat consumption decreased only marginally, as Drs. Freedhoff and Guyenet note, that marginal decrease is accompanied by a reduction in animal fats and their replacement by vegetable oils, which were thought to be heart healthy and still are (perhaps also erroneously). The type of fats we consumed and the type of foods we consumed changed significantly, and this change was very much in accord with what we were being told.

The post-1980 focus on dietary fat also led to the creation and sale of thousands, perhaps tens of thousands, of non-fat and low-fat food-like substances (credit for the terminology once again to Mr. Pollan). In this instance, the CDC’s publication Healthy People 2000 is informative: Healthy People 2000 included multiple “nutrition objectives” aimed at reducing dietary fat consumption, including the creation of 5,000 low-fat or low-saturated fat products. It included nutrition objectives to reduce salt intake and increase complex carbohydrate and fiber consumption, but included no such objective for sugar or sugar-rich foods. Why not? Indeed, I find that the words “sugar” or “sugars” appear only five times in the almost 400-page final review of how well the guidelines were met. In 1995, the American Heart Association counseled in one of its pamphlets that Americans could control the amount and kind of fat consumed by “choos[ing] snacks from other food groups such as…..low-fat cookies, low-fat crackers,…unsalted pretzels, hard candy, gum drops, sugar, syrup, honey, jam, jelly, marmalade (as spreads).” In 2000, the AHA published this cookbook of low-fat and luscious sugar-rich “soul-satisfying” desserts. I don’t know if Dr. Guyenet would describe this as a “weak stand” on sugar or not, but it does shed light on our failure to limit sugar consumption during a period in which all public health advice was focused on reducing fat.

The more important question, and a very different one, is whether our sugar consumption has uniquely deleterious effects on our health. To refute the claim that consuming sugar might cause heart disease, Dr. Guyenet points out that heart disease mortality has dropped precipitously over the years of the obesity and diabetes epidemics and during a period when sugar consumption clearly increased (technically “caloric sweeteners” since the increase was due primarily to high-fructose corn syrup). Professor Kealey makes a similar point but with a far more nuanced perspective about how mortality rates are confounded by what are, after all, a half-century’s worth of very concerted efforts by medical researchers, the pharmaceutical and medical industry, and public health authorities to reduce mortality. That these efforts succeeded in reducing mortality is indeed commendable, but it makes it far more difficult than Dr. Guyenet suggests to derive meaning from the mortality data. If it’s evidence against the sugar hypothesis, it’s very weak evidence.”

Dr. Michael Eades weighs in with words of wisdom, as usual.

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R.I.P., Mary Tyler Moore

Actress Mary Tyler Moore died today at the age of 80. She is probably the most famous type 1 diabetic of a certain generation, those watching TV in the 1960s and 1970s. According to her NYT obituary, her diabetes started in her 30s.

Average life expectancy in the U.S. is 78.8 years, based on 2014 data. It’s longer for women, shorter for men. That average is reduced by 10–12 years for those with type 1 diabetes.

It still amazes me that one of the very first users of insulin injections, Elizabeth Hughes, lived to be 73, having started insulin around age 22.

Steve Parker, M.D.

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Exposure to Cold May Help You With Weight Management

Well below room temp here

Should be well below room temp here

David Mendosa found a 2016 research report suggesting that cool temperatures may help with weight management by activating our brown fat, which burns more calories. Heat generated by brown fat is derived from glucose and triglycerides. Keep in mind as you read further that a comfortable environment temperature for a clothed human is about 23°C or 73°F. Those temps don’t stress our bodies by requiring us to either generate or dissipate extra body heat.

David writes:

Researchers have discovered that when we get mildly cold, which they define as being cool without shivering, our bodies burn more calories. As a result, managing our weight can be easier.
This is the conclusion of a recent review that two researchers at Maastricht University Medical Center in the Netherlands published in the November 2016 issue of the professional journal Diabetologia. The title of their article, “Combatting type 2 diabetes by turning up the heat,” puzzled me at first.

The title confused me because the study is about turning down the heat in the room we’re in. But then our bodies compensate by turning up their internal heat production.

When our body does this, its energy expenditure increases, ratcheting up our metabolism. Being mildly cold revs up our bodies’ brown fat, which unlike white fat, burns calories instead of storing them.

It’s not quite clear how much cold exposure it takes to turn on your brown fat. From the link above:

Cold acclimation by intermittent exposure to a cool (14–17°C) [57–63°F], or cold (10°C) [50°F] environment resulted in significant increases in NST [non-shivering thermogenesis or heat production] capacity. A 10 day cold acclimation study with 6 hour exposure to 14–15°C [57–59°F] per day was enough to significantly increase NST by 65% on average. A 6 week mild cold acclimation study (daily 2 hour cold exposure at 17°C [63°F]) also resulted in an increase in NST together with a concomitant decrease in body fat mass. The latter two studies also revealed significant increases in BAT [brown adipose tissue] presence and activation. All in all, cold-induced BAT activity is significant in adults and parallels NST. The actual quantitative contributions of BAT and of other tissues (e.g. skeletal muscle) to whole-body NST are, however, not elucidated and await further studies. Furthermore, more information is needed on the duration, timing and temperatures to find out which treatments are most effective with respect to increasing NST.

Furthermore, cold exposure over the course of 10 days increased insulin sensitivity in T2 diabetics by 43%. Eight study subjects, probably in the Netherlands, were exposed to temps of 14–15°C [57–59°F] but I don’t know for how many hours a day. Increased insulin sensitivity should help keep a lid on blood sugar levels and reduce the need for diabetes drugs.

In case you’re elderly, obese, or have type 2 diabetes, be aware that the activation of brown fat by cold exposure is not as robust as in others.

On the other hand, I found evidence that higher ambient temperatures (above 23°C) [73°F] may also help with weight management, regardless of what brown fat is doing. Science is hard.

Steve Parker, M.D.

PS: Check out my books for more ideas on weight management.

 

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Trick Question: Who’s Buried in Grant’s Tomb?

Thomas Twining started selling tea in London in 1706. His eponymous company has been doing it for 300 years, then. You’d think they know tea if anyone does. Here’s Twinings Green Tea:

Not to me

Green? Brown?  Golden brown? Tea-colored? Flax? Tannin? Purple? Polka-dotted?

Does that look green to you? I guess they specialize in black tea (which I bet isn’t black after brewing).

My quest for green “green tea” continues. I just ordered Kirkland Ito En Matcha Blend Japanese Green Tea from Amazon.

Steve Parker, M.D.

PS: If you don’t like green, you’ll find none of it inside my books.

PPS: The remains of Ulysses S. Grant and his wife are in a mausoleum referred to as Grant’s tomb. They are above ground, so technically they aren’t buried.

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Rutabaga / Swede/ Neeps : How will you serve this low-carb vegetable?

Jan over at The Low Carb Diabetic is getting me motivated to try a new vegetable: rutabaga.

Click the link below for Jan’s post for more photos and recipes.

“The picture above shows what Americans know as “rutabaga”. The Scottish call it “neeps” and serve it with haggis. I know it as swede, a fairly recent root vegetable, which is thought to have originated around the 17th century in Bohemia. In 1620 a Swiss botanist described the root vegetable, believed to be a hybrid of the cabbage and the turnip. By 1664 it was growing in England. A good source of vitamin.C, fibre, folate and potassium. It’s low in calories.”

Source: The Low Carb Diabetic: Swede / Rutabaga : How will you serve this low carb vegetable

Do you like rutabagas?

PS: If the copyright owner of the rutabaga photo wants me to take it down, contact Steve Parker, M.D., and it shall be done post haste.

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Prevent Kids’ Cavities with a Low-Carb Diet, Says DietDoctor

More that a few dentists agree that carbs cause cavities.

From DietDoctor:

“Roger W. Lucas, pediatric dentist, explains the link between carbs and cavities in his book More Chocolate, No Cavities: How Diet Can Keep Your Kid Cavity-Free. Simple carbohydrates such as flour and juice feed mouth bacteria that cause cavities. On the other hand, high fat and protein foods don’t.

Source: Prevent Kids’ Cavities with a Low-Carb Diet – Diet Doctor

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Men Hold the Line at 35%, But 40% of U.S. Women Now Obese

That excess weight can shorten your life

That excess weight can shorten your life

Yahoo has a brief article with a few more details. For $30 you can read the original scientific report from Journal of the American Medical Association.

Obesity in this context is defined as a body mass index of 30 or higher. Calculate your BMI here.

Is it your fault if you’re obese?

Steve Parker, M.D.

PS: If you want to buck the overweight/obesity trend, check out my books.

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Merry Christmas!

Credit: Zvonimir Atletic / Shutterstock.com

Credit: Zvonimir Atletic / Shutterstock.com

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