A couple weeks ago I wrote a post about how to read scientific research papers. That covered what to do. Today I’m going to tell you what NOT to do as a consumer of research studies.

The following are bad practices that can cause you to misinterpret research findings, dismiss valid research, or apply scientific findings incorrectly in your own life.

1. Reading Only the Abstract

This is probably the BIGGEST mistake a reader can make. The abstract is, by definition, a summary of the research study. The authors highlight the details they consider most important—or those that just so happen to support their hypotheses.

At best, you miss out on potentially interesting and noteworthy details if you read only the abstract. At worst, you come with a completely distorted impression of the methods and/or results.

Take this paper, for example. The abstract summarizes the findings like this: “Consumption of red and processed meat at an average level of 76 g/d that meets the current UK government recommendation (less than or equal to 90g/day) was associated with an increased risk of colorectal cancer.”

Based on this, you might think:
1. The researchers measured how much meat people were consuming. This is only half right. Respondents filled out a food frequency questionnaire that asked how many times per week they ate meat. The researchers then multiplied that number by a “standard portion size.” Thus, the amount of meat any given person actually consumed might vary considerably from what they are presumed to have eaten.

2. There was an increased risk of colorectal cancers. It says so right there after all. The researchers failed to mention that there was only an increased risk of certain types of colon cancer (and a small one at that—more on this later), not for others, and not for rectal cancer.

3. The risk was the same for everyone. Yet from the discussion: “Interestingly, we found heterogeneity by sex for red and processed meat, red meat, processed meat and alcohol, with the association stronger in men and null in women.” Null—meaning not significant—in women. If you look at the raw data, the effect is not just non-significant, it’s about as close to zero as you can get. To me, this seems like an important detail, one that is certainly abstract-worthy.

Although it’s not the norm for abstracts to blatantly misrepresent the research, it does happen. As I said in my previous post, it’s better to skip the abstract altogether than to read only the abstract.

2. Confusing Correlation and Causation

You’ve surely heard that correlation does not imply causation. When two variables trend together, one doesn’t necessarily cause the other. If people eat more popsicles when they’re wearing shorts, that’s not because eating popsicles makes you put on shorts, or vice versa. They’re both correlated with the temperature outside. Check out Tyler Vigen’s Spurious Correlations blog for more examples of just how ridiculous this can get.

As much as we all know this to be true, the popular media loves to take correlational findings and make causal statements like, “Eating _______ causes cancer!” or “To reduce your risk of _______, do this!” Researchers sometimes use sloppy language to talk about their findings in ways that imply causation too, even when their methods do not support such inferences.

The only way to test causality is through carefully controlled experimentation where researchers manipulate the variable they believe to be causal (the independent variable) and measure differences in the variable they hypothesize will be affected (the dependent variable). Ideally, they also compare the experimental group against a control group, replicate their results using multiple samples and perhaps different methods, and test or control for confounding variables.

As you might imagine, there are many obstacles to conducting this type of research. It’s can be expensive, time consuming, and sometimes unethical, especially with human subjects. You can’t feed a group of humans something you believe to be carcinogenic to see if they develop cancer, for example.

As a reader, it’s extremely important to distinguish between descriptive studies where the researchers measure variables and use statistical tests to see if they are related, and experimental research where they assign participants to different conditions and control the independent variable(s).

Finally, don’t be fooled by language like “X predicted Y.” Scientists can use statistics to make predictions, but that also doesn’t imply causality unless they employed an experimental design.

3. Taking a Single Study, or Even a Handful of Studies, as PROOF of a Phenomenon

When it comes to things as complex as nutrition or human behavior, I’d argue that you can never prove a hypothesis. There are simply too many variables at play, too many potential unknowns. The goal of scientific research is to gain knowledge and increase confidence that a hypothesis is likely true.

I say “likely” because statistical tests can never provide 100 percent proof. Without going deep into a Stats 101 lesson, the way statistical testing actually works is that you set an alternative hypothesis that you believe to be true and a null hypothesis that you believe to be incorrect. Then, you set out to find evidence to support the null hypothesis.

For example, let’s say you want to test whether a certain herb helps improve sleep. You give one experimental group the herb and compare them to a group that doesn’t get the herb. Your null hypothesis is that there is no effect of the herb, so the two groups will sleep the same.

You find that the group that got the herb slept better than the group that didn’t. Statistical tests suggest you can reject the null hypothesis of no difference. In that case, you’re really saying, “If it was true that this herb has no effect, it’s very unlikely that the groups in my study would differ to the degree they did.” You can conclude that it is unlikely—but not impossible—that there is no effect of the herb.

There’s always the chance that you unwittingly sampled a bunch of outliers. There’s also a chance that you somehow influenced the outcome through your study design, or that another unidentified variable actually caused the effect. That’s why replication is so important. The more evidence accumulates, the more confident you can be.

There’s also publication bias to consider. We only have access to data that get published, so we’re working with incomplete information. Analyses across a variety of fields have demonstrated that journals are much more likely to publish positive findings—those that support hypotheses—than negative findings, null findings (findings of no effect), or findings that conflict with data that have been previously published.

Unfortunately, publication bias is a serious problem that academics are still struggling to resolve. There’s no easy answer, and there’s really nothing you can do about it except to maintain an open mind. Never assume any question is fully answered.

4. Confusing Statistical Significance with Importance

This one’s a doozy. As I just explained, statistical tests only tell you whether it is likely that your null hypothesis is false. They don’t tell you whether the findings are important or meaningful or worth caring about whatsoever.

Let’s take that study we talked about in #1. It got a ton of coverage in the press, with many articles stating that we should all eat less red meat to reduce our cancer risk. What do the numbers actually say?

Well, in this study, there were 2,609 new cases of colorectal cancer in the 475,581 respondents during the study period—already a low probability. If you take the time to download the supplementary data, you’ll see that of the 113,662 men who reported eating red or processed mean four or more times per week, 866 were diagnosed. That’s 0.76%. In contrast, 90 of the 19,769 men who reported eating red and processed meat fewer than two times per week were diagnosed. That’s 0.45%.

This difference was enough to be statistically significant. Is it important though? Do you really want to overhaul your diet to possibly take your risk of (certain types of) colorectal cancer from low to slightly lower (only if you’re a man)?

Maybe you do think that’s important. I can’t get too worked up about it, and not just because of the methodological issues with the study.

There are lots of ways to make statistical significance look important, a big one being reporting relative risk instead of absolute risk. Remember, statistical tests are just tools to evaluate numbers. You have to use your powers of logic and reason to interpret those tests and decide what they mean for you.

5. Overgeneralizing

It’s a fallacy to think you can look at one piece of a jigsaw puzzle and believe you understand the whole picture. Any single research study offers just a piece of the puzzle.

Resist the temptation to generalize beyond what has been demonstrated empirically. In particular, don’t assume that research conducted on animals applies perfectly to humans or that research conducted with one population applies to another. It’s a huge problem, for example, when new drugs are tested primarily on men and are then given to women with unknown consequences.

6. Assuming That Published Studies are Right and Anecdotal Data is Wrong

Published studies can be wrong for a number of reasons—author bias, poor design and methodology, statistical error, and chance, to name a few. Studies can also be “right” in the sense that they accurately measure and describe what they set out to describe, but they are inevitably incomplete—the whole puzzle piece thing again.

Moreover, studies very often deal with group-level data—means and standard deviations. They compare the average person in one group to the average person in another group. That still leaves plenty of room for individuals to be different.

It’s a mistake to assume that if someone’s experience differs from what science says it “should” be, that person must be lying or mistaken. At the same time, anecdotal data is even more subject to biases and confounds than other types of data. Anecdotes that run counter to the findings of a scientific study don’t negate the validity of the study.

Consider anecdotal data another piece of the puzzle. Don’t give it more weight than it deserves, but don’t discount it either.

7. Being Overly Critical

As I said in my last post, no study is meant to stand alone. Studies are meant to build on one another so a complete picture emerges—puzzle pieces, have I mentioned that?

When conducting a study, researchers have to make a lot of decisions:

  • Who or what will their subjects be? If using human participants, what is the population of interest? How will they be sampled?
  • How will variables of interest be operationalized (defined and assessed)? If the variables aren’t something discrete, like measuring levels of a certain hormone, how will they be measured? For example, if the study focuses on depression, how will depression be evaluated?
  • What other variables, if any, will they measure and control for statistically? How else will they rule out alternative explanations for any findings?
  • What statistical tests will they use?

And more. It’s easy as a reader to sit there and go, “Why did they do that? Obviously they should have done this instead!” or, “But their sample only included trained athletes! What about the rest of us?”

There is a difference between recognizing the limitations of a study and dismissing a study because it’s not perfect. Don’t throw the baby out with the bathwater.

That’s my top seven. What would you add? Thanks for reading today, everybody. Have a great week.

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The post 7 Mistakes to Avoid When You’re Reading Research appeared first on Mark’s Daily Apple.

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Scientific journal articles can be incredibly intimidating to read, even for other scientists. Heck, I have a Ph.D. in a research science and have authored scientific papers, but sometimes I look at a research report outside my field of study and just go, “Nope, can’t decipher this.”

Learning to read them is an important skill, however, in today’s environment of what I call “research sensationalism.” This is where the popular media gets hold of a scientific research report and blows the findings WAY out of proportion, usually while misrepresenting what the researchers actually did and/or found. You know what I’m talking about.

Unfortunately, you can’t trust popular media reports about scientific research studies. Too often, it’s shockingly evident that the people writing these reports (a) aren’t trained to evaluate scientific research, and (b) are just parroting whatever newswire release they got that morning with no apparent fact-checking.

Thus, if staying informed is important to you—or you just want to be able to shut down all the fearmongers in your life—you need to learn how to read the original journal articles and form your own judgments. You don’t have to become an expert in every scientific field, nor a statistician, to do so. With a little know-how, you can at least decide if the popular media reports seem accurate and if any given study is worth your time and energy.

Where to Begin

First things first, locate the paper. If it’s behind a paywall, try searching Google Scholar to see if you can find it somewhere else. Sometimes authors upload pdfs to their personal webpages, for example.

Ten years ago, I would have told you to check the journal’s reputation next. Now there are so many different journals with different publishing standards popping up all the time, it’s hard to keep up. More and more researchers are choosing to publish in newer open access journals for various reasons.

Ideally, though, you want to see that the paper was peer reviewed. This means that it at least passed the hurdle of other academics agreeing that it was worth publishing. This is not a guarantee of quality, however, as any academic can tell you. If a paper isn’t peer reviewed, that’s not an automatic dismissal, but it’s worth noting.

Next, decide what type of paper you’re dealing with:

Theoretical papers

  • Authors synthesize what is “known” and offer their own interpretations and suggestions for future directions.
  • Rarely the ones getting popular press.
  • Great if you want to know the new frontiers and topics of debates in a given field.

Original research, aka empirical research

  • Report the findings of one of more studies where the researchers gather data, analyze it, and present their findings.
  • Encompasses a wide variety of methods, including ethnographic and historical data, observational research, and laboratory-based studies.

Meta-analyses & systematic reviews

  • Attempt to pool or summarize the findings of a group of studies on the same topic to understand the big picture.
  • Combining smaller studies increases the number of people studied and the statistical power. It can also “wash out” minor problems in individual studies.
  • Only as good as the studies going into them. If there are too few studies, or existing studies are of poor quality, pooling them does little. Usually these types of reports include a section describing the quality of the data.

Since popular media articles usually focus on empirical research papers, that’s what I’ll focus on today. Meta-analyses and reviews tend to be structured in the same way, so this applies to them as well.

Evaluating Empirical Research

Scientists understand that even the best designed studies will have issues. It’s easy to pick apart and criticize any study, but “issues” don’t make studies unreliable. As a smart reader, part of your job is to learn to recognize the flaws in a study, not to tear it down necessarily, but to put the findings in context.

For example, there is always a trade-off between real-world validity and experimental control. When a study is conducted in a laboratory—whether on humans, mice, or individual cells—the researchers try to control (hold constant) as many variables as possible except the ones in which they are interested. The more they control the environment, the more confident they can be in their findings… and the more artificial the conditions.

That’s not a bad thing. Well-controlled studies, called randomized control trials, are the best method we have of establishing causality. Ideally, though, they’d be interpreted alongside other studies, such as observational studies that detect the same phenomenon out in the world and other experiments that replicate the findings.

NO STUDY IS EVER MEANT TO STAND ON ITS OWN. If you take nothing else from this post, remember that. There is no perfect study. No matter how compelling the results, a single study can never be “conclusive,” nor should it be used to guide policy or even your behavioral choices. Studies are meant to build on one another and to contribute to a larger body of knowledge that as a whole leads us to better understand a phenomenon.

Reading a Scientific Journal Article

Most journal articles follow the same format: Abstract, Introduction, Methods, Results, Discussion/Conclusions. Let’s go through what you should get out of each section, even if you’re not a trained research scientist.

The Abstract succinctly describes the purpose, methods, and main findings of the paper. Sometimes you’ll see advice to skip the abstract. I disagree. The abstract can give you a basic idea of whether the paper is interesting to you and if it is likely to be (in)comprehensible.

DO NOT take the abstract at face value though. Too often the abstract oversimplifies or even blatantly misrepresents the findings. The biggest mistake you can make is reading only the abstract. It is better to skip it altogether than to read it alone.

The Introduction describes the current research question, i.e., the purpose of the study. The authors review past literature and set up why their study is interesting and needed. It’s okay to skim the intro.

While reading the introduction:

  • Make a note of important terms and definitions.
  • Try to summarize in your own words what general question the authors are trying to address. If you can, also identify the specific hypothesis they are testing. For example, the question might be how embarrassment affects people’s behavior in social interactions, and the specific hypothesis might be that people are more likely to insult people online when they feel embarrassed.
  • You might choose to look up other studies cited in the introduction.

The Methods should describe exactly what the researchers did in enough detail that another researcher could replicate it. Methods can be dense, but I think this is the most important section in terms of figuring out how much stock you should be putting in the findings.

While reading the methods, figure out:

  • Who/what were the subjects in this study? Animals, humans, cells?
  • If this is a human study, how were people selected to participate? What are their demographics? How well does the sample represent the general population or the population of interest?
  • What type of study is this?
    • Observational: observing their subjects, usually in the natural environment
    • Questionnaire/survey: asking the subject questions such as opinion surveys, behavioral recall (e.g., how well they slept, what they ate), and standardized questionnaires (e.g., personality tests)
    • Experimental: researchers manipulate one or more variables and measure the effects
  • If this is an experiment, is there a control condition—a no-treatment condition used as a baseline for comparison?
  • How were the variables operationalized and measured? For example, if the study is designed to compare low-carb and high-carb diets, how did the researchers define “low” and “high?” How did they figure out what people were eating?

Some red flags that should give you pause about the reliability of the findings are:

  • Small or unrepresentative sample (although “small” can be relative).
  • Lack of a control condition in experimental designs.
  • Variables operationalized in a way that doesn’t make sense, for example “low-carb” diets that include 150+ grams of carbs per day.
  • Variables measured questionably, as with the Food Frequency Questionnaire.

The Results present the statistical analyses. This is unsurprisingly the most intimidating section for a lot of people. You don’t need to understand statistics to get a sense of the data, however.

While reading the results:

  • Start by looking at any tables and figures. Try to form your own impression of the findings.
  • If you aren’t familiar with statistical tests, do your best to read what they authors say about the data, paying attention to which effects they are highlighting. Refer back to the tables and figures and see if what they’re saying jibes with what you see.
  • Pay attention to the real magnitude of any differences. Just because two groups are statistically different or something changes after an intervention doesn’t make it important. See if you can figure out in concrete terms how much the groups differed, for example. If data are only reported in percentages or relative risk, be wary of drawing firm conclusions.

It can take a fair amount of effort to decipher a results section. Sometimes you have to download supplementary data files to get the raw numbers you’re looking for.

The Discussion or Conclusions summarize what the study was about. The authors offer their interpretation of the data, going into detail about what they think the results actually mean. They should also discuss the limitations of the study.

While reading the discussion:

  • Use your own judgment to decide if you think the authors are accurately characterizing their findings. Do you agree with their interpretation? Are they forthcoming about the limitations of their study?

Red flags:

  • Concrete statements like “proved.” Hypotheses can be supported, not proven.
  • Talking in causal terms when the data is correlational! As I said above, well-controlled experimental designs are the only types of research that can possibly speak to causal effects. Questionnaire, survey, and historical data can tell you when variables are potentially related, but they say nothing about what causes what. Anytime authors use words like “caused,” “led to,” or “_[X]_ increased/decreased _[Y]_” about variables they didn’t manipulate in their study, they are either being sloppy or intentionally misleading.

What about Bias?

Bias is tricky. Even the best intentioned scientists can fall victim to bias at all stages of the research process. You certainly want to know who funded the study and if the researchers have any conflicts of interest. That doesn’t you should flatly dismiss every study that could potentially be biased, but it’s important to note and keep in mind. Journal papers should list conflicts of interest.

Solicit Other Opinions

Once you feel like you have your own opinion about the research, see what other knowledgeable people you trust have to say. I have a handful of people I trust for opinions—Mark, of course, Chris Kresser, and Robb Wolf being a few. Besides fact-checking yourself, this is a good way to learn more about what to look for when reading original research.

To be clear, I don’t think it’s important that you read every single study the popular media grabs hold of. It’s often okay just to go to your trusted experts and see what they say. However, if a report has you really concerned, or your interest is particularly piqued, this is a good skill to have.

Remember my admonition: No study is meant to stand alone. That means don’t put too much stock in any one research paper. It also means don’t dismiss a study because it’s imperfect, narrow in scope, or you can otherwise find flaws. This is how science moves forward—slowly, one (imperfect) study at a time.

That’s it for today. Share your questions and observations below, and thanks for reading.

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The post A Beginner’s Guide to Reading Scientific Research appeared first on Mark’s Daily Apple.

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For today’s edition of Dear Mark, I’m answering three questions. First, what’s the deal with the new Harvard study claiming that eating more red meat increases the death rate? Does it actually prove this? Second, how about the one claiming that reduced carb diets also increase death? Should you worry? And finally, why do I recommend eating locally farmed farmer’s market produce, even if it isn’t organic?

Let’s go:

Hi Mark,

What’s your take on this Harvard study? www.hsph.harvard.edu/news/press-releases/increasing-red-meat-consumption-linked-with-higher-risk-of-premature-death/

“those who increased their daily servings of red meat over an eight-year period were more likely to die during the subsequent eight years”

It’s total nonsense with very little applicability to MDA readers.

Red meat eaters were more likely to be smokers.

Red meat eaters weighed more.

What else did people change as they added or removed red meat from their diets over the eight years?

The study doesn’t say much.

What we know:

Those who ate more red meat as time wore on also ate more calories per day—roughly 400 more. Those who ate less red meat as time wore on tended to reduce their overall calorie intake.

Those who ate more red meat as time wore on also gained more weight.

The simplistic urge is to assign blame for these changes to the increase in red meat, since that’s what the study is studying and that’s what they keep mentioning throughout the paper. But there are a million other variables that could have caused it, that likely did cause it, because that’s how cause-and-effect works in this world. Or rather, causes-and-effect.

And remember: this wasn’t an interventional study where one group was told to avoid red meat and one group was told to eat more red meat. This was data pulled from two different studies done decades ago, gathered by asking people what they ate on a typical day and then following up with them at a late date to see who died, who got cancer, who gained weight. It wasn’t explicitly about red meat. So, this is a mishmash of remembrances of what some people think they might have eaten, and the researchers from today’s particular paper homed in on the red meat and tuned out everything else.

This isn’t about individual people. These are abstract numbers.

One of the more interesting notes in the discussion section of the paper was this line:

Unprocessed meat consumption was only associated with mortality in the U.S. populations, but not in European or Asian populations.

I’ll be revisiting that line in the near future. For now, though, any ideas what could be going on?

Mark, do low-carb diets increase all-cause mortality? Hearing from lots of people about this latest one…

He’s talking about this one.

This is another piece of nonsense. Instead of studying legitimate low-carb diets like keto, Atkins, or basic Primal Blueprint, it separated people into four tiers of “low-carb” intake.

  • Tier one got 66% of their energy from carbohydrates.
  • Tier two got 57% of energy from carbohydrates.
  • Tier three got 49% of energy from carbohydrates.
  • Tier four—the one with the highest mortality risk—got 39% of energy from carbohydrates.

Now, I could probably hit “send” and stop the post right now. I mean, that about says it all. In what world is 39% of calories from carbohydrates a low-carb diet? How is that the “lowest-carb” diet? Pure madness.

The study also didn’t discuss diet quality. What kind of fats, carbs, and protein are these people eating? What exactly are they omitting and including? How’s their omega-3 intake? They eating mostly chicken, mostly beef, or plants?

All we know, in addition to their macronutrient ratios, is that people in the “low-carb”/39% carb group:

  • Smoked the second most.
  • Ate the least saturated fat.
  • Drank the most alcohol.
  • Exercised the least.

Really what this study is saying is that eating the high-fat, high-carb Standard American Diet will increase your mortality. This is no surprise.

As I’ve said before, you should pick a macronutrient—fat or carbs—to focus on and go with it. Sure, Michael Phelps could eat 10k calories of McDonald’s and maintain optimal performance, body comp, and health because he’s burning through it all, but you’re not him and you’re not training at an Olympic level for five hours a day. Trying to hang out in no-man’s land where you’re kinda high-carb, kinda high-fat is a bad idea for most people. You could make a 39% carb diet “better” by going with Perfect Health Diet principles, sticking to healthy Primal sources of starches and fats, but that doesn’t work for everyone.

You mentioned going to Farmers Markets every week. I would love someone to explain to me the push for buying local and going to Farmers Markets. Every time I hear them mentioned I cringe a little. I certainly understand buying local, and I agree with that, IF the fruits and vegetables are organic. Usually they are not, so I stay away from local and avoid the toxins/pesticides.
I can only assume that those who buy local don’t mind the pesticides, and if they juice, drinking a glass of chemicals.
What am I missing here? I would love to buy local, but sadly it’s rarely organic. I’d rather buy non-local organic.

Have you ever talked to the supposedly non-organic farmers?

In my experience, the vast majority of vendors at the farmers markets are using organic methods even if they aren’t certified. Reason being, organic certification is quite stringent to attain. It’s a multi-year process.

They have to go chemical-free for years. If they’re at year three of the conversion to organic, they can’t advertise “organic” but for all intents and purposes they’re there.

It costs money. Farming is a hard way to make a living. Going legit might represent a big chunk of cash that they can’t quite justify at the moment.

Go to a market, and go frequently. Get to know the people there. Look the farmer in the eyes and ask how they grow. The majority of the ones I’ve met are doing things right. They’re small operations. They’ve got their kids pitching in and helping out. They’re using man/womanpower and precision and know-how. They aren’t flying crop dusters to carpet bomb the entire field with chemicals.

Another (big) advantage of local produce is the freshness. Fruit and vegetables that travel fifty miles after being picked the day before are a world of difference from produce picked last week and shipped halfway across the country (let alone world sometimes).

That’s it for today, folks. If you have any questions or comments about today’s questions and answers, write in down below.

The post Dear Mark: Increased Red Meat, Reduced Carb, Increased Death? appeared first on Mark’s Daily Apple.

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A couple months ago, a study came out that seemed to show that cheating on your keto diet with a high-carb meal opened you up to severe blood vessel damage. Nine healthy, normal weight adults followed a keto diet (70% fat, 20% protein, 10% carbs). Then they ate a high-carb “cheat meal,” measured their blood sugar, and measured their endothelial microparticles—a marker of damage to the endothelial lining and potential harbinger of impaired vascular function. Their blood sugar went way up, and so did their endothelial microparticle count, leading researchers to conclude that keto dieting makes people more susceptible to hyperglycemia-induced endothelial damage.

So, is keto cheating unhealthy? Let’s take a closer look….

My Analysis Of the Study:

Here’s why I don’t think this study applies to most of you:

These people were on keto diets, but they weren’t keto-adapted (let alone fat-adapted). They’d only been doing the diet for a week. Bare minimum, it takes three weeks to a month for full keto-adaptation to occur—and often longer. We’d have to see what happens to endothelial microparticle count when someone who is fully keto-adapted is exposed to higher carb intakes.

The “cheat meal” was 75 grams of pure glucose. This is the oral glucose tolerance test—the disgusting, cloyingly sweet drink they give people to test for diabetes. It measures your ability to handle pure glucose. It’s not a meal. It’s not actually food even. There are no mitigating micronutrients. There are no other macronutrients included. It’s just a shot of pure sugar, down the hatch. I don’t know about you, but that’s not my preferred method of a high-carb cheat meal.

However, it does illustrate the importance of sticking with the diet—any diet—for way longer than a week before assessing the effects or stepping out to indulge.

Look at the big picture. Acute perturbations to endothelial homeostasis can look bad in the short term and good over time. Hell, when you ask overweight women to engage in a single bout of high intensity exercise, their endothelial microparticle count goes up just like it went up for the guys in this study who drank the glucose water. They “damage” their vascular function. But if they keep training regularly, their endothelial microparticle count goes down. Acute stressors can look bad when applied once and awesome when applied consistently. That’s not to say that drinking 75 grams of glucose consistently will suddenly become healthy. I’m just showing how looking at a single short term reaction doesn’t give the entire story, or even accurately portray the effects of the same stimulus applied consistently over the long term.

A Better Perspective On Cheat Meals

Cheat meals can actually help you lose more weight. In one study, women were placed on a cyclic diet consisting of three phases. For each phase, they reduced calories for 11 days followed by 3 days of ad libitum (i.e. at one’s pleasure) eating. After the three phases, they’d lost an average of 8 kg (about 17 lbs) of pure body fat. This surpassed the amount predicted by calories in, calories out. This study didn’t employ all-out cheat days, or call them cheat days, but the concept of “ad libitum” is pretty similar.

If you cycle in high carb days or high carb meals into your keto diet, and you end up getting leaner and performing better in the gym because of it, are you really hurting yourself? Are you really setting your vascular system up for impending doom? I doubt it. One of the best ways to improve endothelial function is to lose excess body fat. Whatever helps you get to that goal should also improve vascular function.

If You’re Going To Cheat On Keto:

Get fully adapted.

The people in this study were not keto-adapted. They’d only been eating the diet for a week before taking the test. Stay with the diet for two months—strictly—before venturing out with cheat days.

Don’t cheat with an oral glucose tolerance test.

While some folks undoubtedly get off on drinking 75 grams of pure glucose, there are better ways to cheat. Like with food. Also, food tends to include mitigating factors—phytonutrients, fiber, vitamins, minerals—that improve the metabolic response to the macronutrients contained therein. For instance, including some natural cocoa in the cheat meal can drop your endothelial microparticles by 60% alone.

Be relatively lean and experienced.

Cheat days are more effective for fairly lean-ish people to kickstart the loss of those last few pounds. They’re designed for long-time keto eaters to replenish glycogen stores and improve training. They’re designed for people who have been strict for long enough that they just need a break. They just aren’t going to work the same for obese people who’ve been keto for a little while who still have a lot of easy weight to lose on strict keto.

Cheat after a big workout.

Exercising increases insulin sensitivity. And if you lift heavy things, you increase something called non-insulin dependent glucose uptake in the muscles. That means your muscles can actually refill their glycogen content without using insulin to do it. If you’re keto and want to incorporate high carb meals/days or cheat meals, legitimate training is pretty much required. After all, why do you need the carbs if you’re not training?

Cheat if you need it.

If things are stalling, and you’ve tried being even stricter to no avail, perhaps momentarily loosening up with a cheat meal is exactly what you need. Read this post to get the lowdown on why carb refeeds can help break weight loss stalls and how to do them.

This study shouldn’t be ignored. Big boluses of sugar are never a good idea, especially when you’ve only been eating low-carb or keto for a week and have yet to adapt. I find it plausible that such excursions can induce acute damage to the vascular system in anyone with impaired glucose tolerance—even if that glucose intolerance is transient, as it is in short term keto dieters—but I don’t think it means much for people with good heads on their shoulders who do keto the right way.

What do you think, folks? Do you cheat on your diet, whether you’re keto or just Primal? What steps do you take to make sure you’re getting the most out of your dietary excursions?

Thanks for reading, everyone. Take care!

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References:

Durrer C, Robinson E, Wan Z, et al. Differential impact of acute high-intensity exercise on circulating endothelial microparticles and insulin resistance between overweight/obese males and females. PLoS ONE. 2015;10(2):e0115860.

Mcfarlin BK, Venable AS, Henning AL, et al. Natural cocoa consumption: Potential to reduce atherogenic factors?. J Nutr Biochem. 2015;26(6):626-32.

The post Is Keto Cheating Unhealthy? appeared first on Mark’s Daily Apple.

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Have you heard? There’s a new “red meat will kill you” study. This time, it’s colorectal cancer.

Here’s the press release.

Here’s the full study.

I covered this a couple Sundays ago in “Sunday with Sisson.” If you haven’t signed up for that, I’d recommend it. SWS is where I delve into my habits, practices, and observations, health-related and health-unrelated—stuff you won’t find on the blog. Anyway, I thought I’d expand on my response to that study here today.

How the Study Was Conducted

It’s the basic story you see with most of these observational studies. Around 175,000 or so people were asked to recall what they ate on a regular basis—a food frequency questionnaire. This is the exact questionnaire, in fact. The research team took the answers, measured some baseline characteristics of all the subjects—socioeconomic status, exercise levels, whether they smoked, education level, occupation, family history of colorectal cancer, and a few others—and then followed up with participants an average of 5.7 years later to see how many had developed colorectal cancer.

What the Study “Showed”

Those who had moderate amounts of red meat had a 20% higher chance of getting cancer.

And in the end, the increased risk was a relative risk. It wasn’t a 20% absolute increase in risk. It was a relative increase in risk. The subjects started with a 0.5% risk of getting bowel cancer. In those who ate the most processed meat and red meat, that risk increased 20%—to 0.6%!

From 0.5 to 0.6%. Sure, that’s an increase, but is it something to overhaul your entire diet for? To give up the best sources of zinc, iron, B vitamins, protein, carnosine, creatine? All that for a measly 0.1% that hasn’t even been established as causal?

Study Findings Most News Outlets Won’t Include

One head scratcher that leaps out: the link between unprocessed red meat and colon cancer was not actually statistically significant. Only processed meat was significantly linked to colon cancer.

Another head scratcher: red meat, whether processed or unprocessed, had no significant association with colorectal cancer in women. Why didn’t they highlight the fact that in women, eating red meat was completely unrelated? That’s half the world’s population. That’s you or your mom, your daughter, your grandmother, your girlfriend. And unless they were to look at the full study and read the fine print, they’d never know that red meat actually had the opposite relationship. You’d think the authors would want to mention that in the abstract or see that the press releases and media treatments highlighted that fact.

It’s probably because mentioning that red meat was neutral in women and had no statistically significant link to colon cancer in men and women would have destroyed their case for red meat as an independent carcinogen. See, carcinogens are supposed to be carcinogens. There are many meaningful differences between men and women, but a poison is a poison.

What’s the proposed mechanism for red meat triggering colon cancer in men but not in women? If they didn’t have one (and I imagine they wouldn’t have mentioned it if they did), then there’s probably something else going on.

Besides, the literature is far from unequivocal.

What Other Research Says About Red Meat and Bowel Cancer

In analyses that include consideration of cooking methods and other mitigating factors, red meat has no relationship with colon cancer.

Or what about this study, where colon cancer patients were more likely to eat red meat, but less likely to have type 2 diabetes? Should people avoid red meat and work toward getting diagnosed with type 2 diabetes?

Or how about this study, which found no difference in colorectal cancer rates between people who ate red meat-free diets and people who ate diets containing red meat? Shouldn’t the diet without any red meat at all have some effect?

Or this classic study, where rats on a bacon-based diet had the lowest rates of colon cancer. In fact, bacon protected them from colon cancer after they were dosed with a colon cancer promoter, while rats on normal “healthy” chow were not.

The Blind Spot In Red Meat Research

I don’t need to go into all the confounding factors that might predispose conventional red meat lovers to bowel cancer. Nor will I mention that it’s impossible to fully control for variables like the buns and bread and fries you eat the red meat with and the industrial seed oils it’s cooked in.

That last bit is crucial: the seed oils. It’s what nearly every cancer researcher misses. It’s not just a minor variable; it’s quite possibly the most important determinant of whether meat is carcinogenic in the colon or not. Heme iron—the compound unique to red meat that usually gets the blame for any increase in cancer—is most carcinogenic in the presence of the omega-6 fatty acid linoleic acid.

In one studyfeeding heme iron to rats promoted colon cancer only when fed alongside high-linoleic acid safflower oil. Feeding MUFA-rich and far more oxidatively-stable olive oil alongside the heme prevented the colon carcinogenesis.

Another study had similar results, finding that meats containing medium to high amounts of heme—beef and beef blood sausage—promoted carcinogenic conditions in the colon when the fat sources were linoleic acid-rich corn and soybean oil.

And most recently is this paper. Mice were split into three groups. One group got heme iron plus omega-6 PUFA (from safflower oil). One group got heme iron plus omega-3 PUFA (from fish oil). The third group got heme iron plus saturated fat (from fully hydrogenated coconut oil, which contains zero PUFA). To determine the carcinogenicity of each feeding regimen, the researchers analyzed the effect the animals’ fecal water (which is exactly what it sounds like) had on colon cells. The fecal water of both PUFA groups was full of carcinogenic indicators and lipid oxidation byproducts, and exposing colonic epithelial cells to fecal water from PUFA-fed mice was toxic. The coconut oil-derived fecal water had no markers of toxicity or lipid oxidation.

I never see these (animal) studies cited in observational studies of meat and colon cancer. I think that’s a huge blindspot, and it’s one of the reasons I rarely put any stock in these scary-sounding studies.

That’s it for today, folks. Thanks for reading. Now go enjoy a steak.

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References:

Bylsma LC, Alexander DD. A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer. Nutr J. 2015;14:125.

Alsheridah N, Akhtar S. Diet, obesity and colorectal carcinoma risk: results from a national cancer registry-based middle-eastern study. BMC Cancer. 2018;18(1):1227.

Rada-fernandez de jauregui D, Evans CEL, Jones P, Greenwood DC, Hancock N, Cade JE. Common dietary patterns and risk of cancers of the colon and rectum: Analysis from the United Kingdom Women’s Cohort Study (UKWCS). Int J Cancer. 2018;143(4):773-781.

The post Does Red Meat Give You Colon Cancer? appeared first on Mark’s Daily Apple.

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Have you tried hemp oil?

After almost a century of being outlawed, hemp—a form of cannabis with extremely low levels of psychoactive THC—is now legal in the United States. This is big news for people interested in the therapeutic effects of cannabidiol (or CBD) because—while hemp doesn’t contain enough THC, the compound that provides the “high” of cannabis, or any other psychoactive compounds—it does contain cannabidiol (CBD).

For years, all anyone talked about when they talked about cannabis was the THC content. Breeders focused on driving THC levels as high as possible and ignored the other compounds. Even pharmaceutical companies interested in the medical applications of cannabis focused on the THC, producing synthetic THC-only drugs that performed poorly compared to the real thing. It turns out that all the other components of cannabis matter, too, and foremost among them is CBD.

CBD doesn’t get you high, but it does have big physiological impacts. These days, researchers are exploring CBD as a treatment for epilepsy, anxiety, and insomnia. They’ve uncovered potential anti-inflammatory, anxiolytic, and immunomodulatory properties. And now that it’s quasi legal, hundreds of CBD-rich hemp oil products are appearing on the market.

What are the purported benefits of using CBD-rich hemp oil, and what does the evidence say?

Although CBD research is growing, it’s still understudied and I expect I’ll have to update this post in the near future with more information. But for now, here’s a rundown of what the research says.

The Health Benefits of CBD In Hemp Oil

CBD For Anxiety Reduction

Anxiety can be crippling. I don’t have generalized social anxiety, but I, like anyone else, know what it feels like to be anxious about something. It happens to everyone. Now imagine feeling that all the time, particularly when it matters most—around other people. The average person doesn’t consider the import and impact of anxiety on a person’s well-being. If CBD can reduce anxiety, that might just be its most important feature. Does it?

Before a simulated public speaking event, people with generalized social anxiety disorder were either given 600 mg of CBD or a placebo. Those who received CBD reported less anxiety, reduced cognitive impairment, and more comfort while giving the speech. Seeing as how people without social anxiety disorder claim public speaking as their biggest fear, that CBD helped people with social anxiety disorder give a speech is a huge effect.

This appears to be legit. A placebo-controlled trial is nothing to sniff at.

CBD For Sleep

A 2017 review provides a nice summary of the effects of CBD on sleep:

In insomnia patients, 160 mg/day of CBD increased sleep time and reduced the number of arousals (not that kind) during the night.

Lower doses are linked to increased arousals and greater wakefulness.

High dose CBD improved sleep; adding THC reduced slow wave sleep.

In preliminary research with Parkinson’s patients, CBD reduced REM-related behavioral disorder—which is when you basically act out your dreams as they’re happening.

More recently, a large case series (big bunch of case studies done at once) was performed giving CBD to anxiety patients who had trouble sleeping. Almost 80% had improvements in anxiety and 66% had improvements in sleep (although the sleep improvements fluctuated over time).

Mental Health

While its psychoactive counterpart THC has been embroiled in controversial links with psychosis and schizophrenia for decades, CBD may be an effective counterbalancing force for mental health.

In patients with schizophrenia, six weeks of adjunct treatment with cannabidiol resulted in lower rates of psychotic symptoms and made clinicians more likely to rate them as “improved” and made researchers more likely to rate them as “improved” and not “severely unwell.” There were also improvements in cognitive performance and overall function. It seems the “adjunct” part of this study was key, as other studies using cannabidiol as the only treatment mostly failed to note improvements.

This was placebo controlled, so it makes a good case for CBD hemp oil as adjunct treatment (in addition to regular therapy) in people with schizophrenia.

Among 11 PTSD patients who took an average of 50 mg of CBD per day for 8 weeks, 10 (90%) experienced a 28% improvement in symptoms. No one dropped out or complained about side effects. CBD seemed to particularly benefit those patients who had issues with nightmares.

This is promising but preliminary. This was an 11-person case study, not a placebo-controlled trial.

Epilepsy

A recent review of four human trials lays out the evidence: More than a third of all epilepsy patients experienced 50% or greater seizure reductions with just 20 mg of CBD. The effect of CBD on seizure activity is so widely acknowledged and understood that the only FDA-approved CBD-based product is Epidiolex, a plant-based CBD extract used to treat seizures in patients with Dravet syndrome and Lennox-Gastaut syndrome.

CBD for epilepsy is legit. Side note: I wonder how CBD would combine with ketogenic dieting for epilepsy control.

Pain

By far the biggest draw for medical consumers of CBD is its supposed ability to nullify pain.

In one study, researchers induced arthritis in rats with intra-articular injections, then gave them CBD. Rats given CBD were able to put more weight on their joints and handle a heavier load before withdrawing. Local CBD reduced nerve damage.

That’s great for pet rats. What about people?

There actually isn’t a lot of strong data on pain management using CBD by itself. Far more robust is the evidence for using CBD with THC for pain. According to this group of researchers, the two compounds exert “constituent synergy” against neuropathic pain. One study found that low doses of each were more effective combined than high doses of either alone in neuropathic cancer-related pain. Another gave a THC/CBD oromucosal spray to otherwise treatment-resistant neuropathy patients, finding that the spray reduced pain, improved sleep, and lessened the severity of symptoms.

Anything Else?

Anecdotal evidence for pain relief and other benefits with CBD is vast. Chris Kresser, a practitioner and researcher I trust, swears by it. I have employees who use it quite frequently, reporting that it improves their sleep, hones their focus, reduces pain, speeds recovery, and reduces anxiety. These things are always hard to evaluate, but I can say that my people do great work, and I have zero reason to distrust them.

In later posts, I’ll probably revisit some of these other, more theoretical or anecdotal potential benefits to see if there’s any evidence in support.

Is It Safe?

A recent study gave up to 6000 mg of CBD to healthy subjects, finding it well tolerated and the side effects mild and limited to gastrointestinal distress, nausea, somnolence, headaches, and diarrhea. For comparison’s sake, keep in mind that a typical dose of CBD is 20 mg.

Mouse research indicate that extended high-dose CBD (15-30 mg/kg of bodyweight, or 1200-2400 mg per day for an 80 kg man) might impair fertility. Male mice who took high-dose CBD for 34 days straight experienced a 76% reduction in testosterone, reduced sperm production, and had dysfunctional weird-looking sperm. In the 30 mg/kg group, the number of Sertoli cells—testicular cells where sperm production takes place and sperm is incubated—actually dropped. Male mice taking CBD also were worse at mounting females and had fewer litters.

Those are really high doses. For epilepsy, a common dose is 600 mg/day, and that’s for a severe condition. Most other CBD therapies use much smaller doses in the range of 20-50 mg/day. Long term safety may still be an issue at these lower doses, but we don’t have any good evidence that this is the case.

There’s some evidence that the dosages of CBD required to achieve anti-inflammatory effects are also high enough to induce cytotoxicity in healthy cells, though that’s preliminary in vitro (petri dish) research and as of yet not applicable to real world applications. Time will tell, though, as the legal environment opens up and we accumulate more research.

Is Isolated CBD the Same As Whole Plant Extracts?

As we’ve learned over the past dozen years of reading about nutrition and human health, whole foods tend to be more effective than isolated components. Whole foods have several advantages:

  • They contain all the components related to the compound, especially the ones we haven’t discovered and isolated. Supplements only contain the isolated compounds we’ve been able to quantify.
  • They capture all the synergistic effects of the multiple components working together. Isolated supplements miss that synergy unless they specifically add it back in, and even then they’ll probably miss something.

It’s likely that whole plant hemp extracts high in CBD are superior to isolated synthetic CBD for the same reason. Is there any evidence of that?

A high-CBD cannabis whole plant extract reduces gut inflammation and damage in a mouse model of inflammatory bowel disease. Purified CBD does not.

Even at a 2:1 CBD:THC ratio, co-ingesting isolated CBD with isolated THC using a vaporizer fails to reduce the psychotic and memory-impairing effects of THC. In another study, however, smoking cannabis naturally rich in both CBD and THC completely prevented the memory impairment.

And as we saw in the pain section above, THC combined with CBD seems more effective against pain than either alone.

That’s not to say isolated (even synthetic in some cases—see note below) CBD isn’t helpful. We saw it improve joint pain and reduce nerve damage in arthritic rats. It’s just that full-spectrum hemp oil containing multiple naturally-occurring compounds is probably ideal for general health applications. Specific conditions requiring high doses may be another question entirely. Again, we’ll find out as more research comes out.

A word about synthetics: this is fodder for a follow-up, but it appears there may be additional concerns with synthetic CBD, and even supposedly “natural” CBD companies have in some cases allegedly added ingredients to their formulas without letting consumers know.

Is It Legal?

CBD-rich hemp oil lies in a legal grey area. The recently passed Farm Bill allows people to grow and make products from industrial hemp, as long as it contains less than 0.3% THC. That means CBD derived from industrial hemp is legal at a federal level. But because the Farm Bill has provisions that allow states to set their own rules, legality at a state level is more complicated.

States where hemp is still illegal—South Dakota, Idaho, and Nebraska—do not permit the sale or use of hemp-derived CBD oil.

In states that permit recreational cannabis—California, Vermont, Massachusetts, Maine, Oregon, Colorado, Washington, Nevada, Michigan, and Alaska—CBD derived from both hemp and psychoactive cannabis is legal.

In all other states, hemp-derived CBD is legal.

The FDA has yet to approve of CBD, so most of the big online retailers like Amazon and Walmart don’t allow CBD products to be advertised. However, Amazon sells a ton of “hemp extract” tinctures and oils with “hemp extract content” listed in milligram dosages—a workaround for listing the CBD content.

If you’re looking for CBD-rich hemp oil, watch out for culinary hemp oil, which comes in larger quantities and has no discernible CBD content. CBD-rich hemp oil will come in dropper bottles, not liters.

You can also buy directly from manufacturers online who proudly advertise their CBD content. I’ve heard good things about Ojai Energetics and Sabaidee, though I haven’t used either.

Many health food stores sell it. Surprisingly, I’ve seen it in every pet store I’ve entered in the last half year.

Word of Caution: Because it isn’t regulated by the FDA yet, there’s no telling exactly what you’re getting. Choose a product with verifiable lab tests. Many CBD hemp oil products have far less CBD than advertised. In addition to CBD content, the most reputable manufacturers also test for pesticides, heavy metals, mycotoxins, and bacteria and advertise their results.

CBD-rich hemp oil is a hot topic these days, and it’s only going to get hotter. I think the compound shows great promise in promoting health and wellness, and I’ll look forward to doing more research as it unfolds.

For now, what about you? Do you use CBD? Have you noticed any benefits? Any downsides? Share your questions and feedback down below.

Thanks for reading, everyone. Take care.

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References:

Bergamaschi MM, Queiroz RH, Chagas MH, et al. Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naïve social phobia patients. Neuropsychopharmacology. 2011;36(6):1219-26.

Lattanzi S, Brigo F, Trinka E, et al. Efficacy and Safety of Cannabidiol in Epilepsy: A Systematic Review and Meta-Analysis. Drugs. 2018;78(17):1791-1804.

Elms L, Shannon S, Hughes S, Lewis N. Cannabidiol in the Treatment of Post-Traumatic Stress Disorder: A Case Series. J Altern Complement Med. 2018;

Serpell M, Ratcliffe S, Hovorka J, et al. A double-blind, randomized, placebo-controlled, parallel group study of THC/CBD spray in peripheral neuropathic pain treatment. Eur J Pain. 2014;18(7):999-1012.

Silva RL, Silveira GT, Wanderlei CW, et al. DMH-CBD, a cannabidiol analog with reduced cytotoxicity, inhibits TNF production by targeting NF-kB activity dependent on A receptor. Toxicol Appl Pharmacol. 2019;368:63-71.

Carvalho RK, Souza MR, Santos ML, et al. Chronic cannabidiol exposure promotes functional impairment in sexual behavior and fertility of male mice. Reprod Toxicol. 2018;81:34-40.

Morgan CJA, Freeman TP, Hindocha C, Schafer G, Gardner C, Curran HV. Individual and combined effects of acute delta-9-tetrahydrocannabinol and cannabidiol on psychotomimetic symptoms and memory function. Transl Psychiatry. 2018;8(1):181.

Morgan CJ, Schafer G, Freeman TP, Curran HV. Impact of cannabidiol on the acute memory and psychotomimetic effects of smoked cannabis: naturalistic study: naturalistic study [corrected]. Br J Psychiatry. 2010;197(4):285-90.

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I have a confession to make: I, Mark Sisson, suffer from keto crotch.

It’s embarrassing, really. I thought maybe it was just the change in climate moving from Malibu to Miami—the humidity, the heat, the fact that I’m paddling and swimming more often now. There’s a whole lot of moisture down there. Perpetual steaminess.

But then I met up with my writing partner and good pal Brad Kearns, who’s been working with me on my upcoming book. Brad lives in Northern California, which is far from hot or humid right now. He’s also a staunch keto guy most of the time, and, well, let’s just say I could smell him before I could see him. We met up at a coffee shop and cleared out everyone in a fifteen foot radius. We sampled a new exogenous ketone product he’s been trying and not one, not two, but three separate individuals approached to inquire if we were salmon fishermen.

Okay, let’s get serious. Does “keto crotch” really exist? And, if it does, what can you do to prevent it?

I’m writing this not because of overwhelming demand from loyal followers of the Keto Reset plan. In fact, I hadn’t ever heard of “keto crotch” before last week. There’s a good chance almost no one heard of it before March 2019, if Google Trend data for “keto crotch” searches is any indication. I’m writing this post because the barrage of news articles, Twitter hashtag campaigns, and extremely serious warnings from people with lots of acronyms after their name has led people to ask me if it’s a legitimate phenomenon. A few acquaintances have brought it up in social situations. Our marketing director found herself fielding keto crotch questions at a dinner for Expo West last week.

So, are women following a ketogenic diet experiencing an epidemic of stinky vaginas?

Probably not.

Is Keto Crotch Even Physiologically Plausible?

Vaginal odor does change. It fluctuates naturally, and sometimes it can get worse. The most common cause of unpleasant changes to vaginal odor is bacterial vaginosis, which occurs when something upsets the balance between the beneficial lactobacilli bacteria that normally live in the vagina and pathogenic bacteria. What can upset the balance?

The vagina is supposed to be an acidic environment; that’s how the healthy lactobacilli thrive. If something upsets that pH balance, tilting it toward alkalinity, unhealthy bacteria gain a foothold and become predominant, and begin producing unpleasant-smelling amines like putrescine, tyramine, and cadaverine. This is bacterial vaginosis. As it turns out, the lactobacilli bacteria normally present in the vagina are instrumental in maintaining an acidic pH. They consume glycogen, spit out lactic acid, and exert antimicrobial and antifungal effects that block common vaginal pathogens like candida, e. coli, and gardnerella from taking hold and causing trouble.

The interaction between diet and vaginal biome is understudied. To my knowledge, there exist no direct controlled trials that address the issue. It’d be great to have a study take a cohort of women, split them up into different dietary groups, and follow them for a year,  tracking their vaginal pH and bacterial levels. Alas, we do not.

We do have a study that provides a hint. In 2011, researchers looked for correlations between dietary patterns and bacterial vaginosis in a cohort of nearly 2000 non-pregnant mostly African-American women aged 15-44. While there probably weren’t many keto dieters, and the diets as a whole were of the standard American variety, glycemic load—which basically boils down to carb load—was the strongest predictor of bacterial vaginosis. Other markers of food quality, like a person’s adherence to “healthy eating guidelines,” initially seemed to reduce the chance of bacterial vaginosis, but those relationships were almost abolished after controlling for other factors. Only glycemic load remained highly significant.

This connection between dietary glycemic load and bacterial vaginosis starts looking more causal when you realize that diabetes—a disease where one’s “glycemic load” is perpetually elevated and exaggerated—is another risk factor for bacterial vaginosis.

There’s also a 2007 study that found “high” intakes of dietary fat, particularly saturated and monounsaturated fat, were a significant predictor of bacterial vaginosis. In this study, “high fat” meant around 39% of energy from fat. That leaves 61% of energy from carbohydrate and protein, the kind of “high-fat, high-carb” Standard American No-Man’s-Land that’s landed the country in the current metabolic predicament. High-fat intakes in the presence of high-carb intakes may very well be bad for your vagina, but it says nothing about the likelihood of keto crotch.

At any rate, neither study was a controlled trial, so we can’t say anything about causality.

What about a yeast infection? The most common offender is candida, which usually favors sugar for fuel, but there’s also evidence that it can metabolize ketones. Could keto make a latent yeast infection worse and lead to smelly “keto crotch”?

Perhaps keto can make candida worse (that’s for another day), but that’s not the cause of “keto crotch.” Candida vagina infections don’t smell very much, if at all, and they certainly don’t smell “fishy.” That’s only caused by bacteria and the aforementioned amines they can produce.

Free glycogen levels in vaginal fluid are a strong predictor of bacterial vaginosis. If ample glycogen is available, the good lactic acid bacteria have plenty of food and produce plenty of lactic acid to maintain the acidic pH conducive to vaginal health. If inadequate glycogen is present, the lactic acid bacteria have less food and produce less lactic acid, increasing the chances of the pH tilting toward alkalinity. An alkaline vagina is a vagina where pathogenic bacteria—the ones that produce stinky amines—can establish themselves.

The question then is if ketogenic diets lower free glycogen in the vaginal fluid. That’s a fair question. I wasn’t able to find any solid answers. I guess “ketosis effect on vaginal glycogen” isn’t the most lucrative avenue of scientific inquiry.

Should I Worry?

Even assuming this is a real phenomenon, it’s a rare one. The vast, vast majority of people following a ketogenic diet aren’t coming down with keto crotch. Other than a few Reddit posts from the past 5 years, I haven’t seen anyone at all in our neck of the woods complain.

Maybe people doing Primal keto are eating more nutrient-dense ketogenic diets than people doing conventional (or caricature) keto. Salads, steaks, eggs, and lots of non-starchy veggies are a great way to stay keto and obtain micronutrients. And there are links between micronutrient status and bacterial vaginosis. The most common relevant deficiencies include vitamin D (correcting the deficiency can cure the vaginosis) and folate. Hard to get adequate folate if your diet is based on salami and cream cheese.

We also know that the health of your skin biome tracks closely with that of your gut, and that eating plenty of non-starchy veggies, fermented foods (yogurt, kefir, sauerkraut, kimchi, etc), and colorful produce can provide prebiotic fiber, prebiotic polyphenols, and probiotic bacteria that nourish your gut biome. If the vaginal biome is also connected to the gut biome (and it is), tending to the latter should also have positive effects on the former.

The Primal brand of keto tends to emphasize micronutrients and gut health a bit more than some other types of keto I see floating around. If—and it’s a very big “if”—keto crotch is legit, that may explain some of the discrepancy.

Finally, be sure to check out this very interesting Twitter thread where the author lays out his suspicions that the whole “keto crotch” phenomenon might be a manufactured stunt designed to vilify the ascendant ketogenic diet. Nothing definitive, but it’s certainly food for thought.

If You’re Concerned…

Okay. Say you’ve recently gone keto and your vagina is smellier than usual. (And you’ve ruled out other, more obvious potential causes like changes in soaps, etc.) It’s hard to ignore, and I wouldn’t want you to. What can you do?

  • Confirm that you have bacterial vaginosis. Seriously, get it checked out.
  • Make sure you’re getting enough folate and vitamin D. Supplement if need be.
  • Eat prebiotics and probiotics. Fermented food and/or a good probiotic supplement.
  • Try a carb refeed. If ketosis depletes vaginal glycogen and increases pH, the occasional carb refeed could restore glycogen by 30-50 grams and should do the trick. Note that this is entirely theoretical; I’m not saying it’s a “problem” on keto.
  • Hang out in the keto zone. I’ve written about the keto zone—that metabolic state where you’ve reached full keto and fat-adaptation and find yourself shifting in and out of ketosis as you please due to increased metabolic flexibility. A few carbs here, a fasting day there, a few more days of keto. Again, if full keto is theoretically depleting vaginal glycogen, maybe relaxing your restrictions will solve the issue while maintaining your fat adaptation. This is actually where I hang out most of the time.

That’s it for today, folks. Do you have “keto crotch”? Do you know anyone who does? Or did your vaginal health improve on keto? I’m curious to hear what everyone’s experiences have been, so don’t be shy.

Take care and be well.

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References:

Thoma ME, Klebanoff MA, Rovner AJ, et al. Bacterial vaginosis is associated with variation in dietary indices. J Nutr. 2011;141(9):1698-704.

Kalra B, Kalra S. Vulvovaginitis and diabetes. J Pak Med Assoc. 2017;67(1):143-145.

Taheri M, Baheiraei A, Foroushani AR, Nikmanesh B, Modarres M. Treatment of vitamin D deficiency is an effective method in the elimination of asymptomatic bacterial vaginosis: A placebo-controlled randomized clinical trial. Indian J Med Res. 2015;141(6):799-806.

Dunlop AL, Taylor RN, Tangpricha V, Fortunato S, Menon R. Maternal vitamin D, folate, and polyunsaturated fatty acid status and bacterial vaginosis during pregnancy. Infect Dis Obstet Gynecol. 2011;2011:216217.

The post The Curious Phenomenon of “Keto Crotch” appeared first on Mark’s Daily Apple.

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One thing I’ve realized being in this game for so long is that if you’re convinced that meat truly is deadly, you’re not going to stop looking for reasons why. They’ve tried blaming just about every part of meat over the years, including the protein itself, the saturated fat, the cholesterol, the methionine, the char on BBQ, and even the obscure compounds like TMAO or Neu5gc. The latest component of meat they’ve zeroed in on is iron—the essential mineral responsible for energy production and a host of other vital functions.

The experts’ track record with all the other “evil meat components” has many of my readers skeptical, so they asked me to weigh in on iron.

Iron is an essential mineral, integral in the production of energy and the creation of blood cells. If pregnant women don’t get it, they can’t deliver oxygen and nutrients to their growing babies. If kids don’t get it, they shortchange their mental and physical development. If adults don’t get it, their basic day-to-day physiological function falls apart. Without adequate iron, our antioxidant defenses, our immunity, and our metabolic function all suffer. Hell, most countries even mandate the fortification of refined flour with large amounts of iron to prevent these tragedies.

Iron also has a dark side. A large body of observational evidence links elevated iron levels to diseases and disease states like type 2 diabetesheart diseaseinsulin resistanceinflammation, Alzheimer’s disease, hypertension, fatty liver, hypothyroidism, arthritis, and cancer. You name it, it’s probably linked to elevated iron. And as much as I’d like to, I can’t dismiss these connections as non-causal.

For one, iron is inherently reactionary: The very same proclivity for electron exchange that makes iron so integral in biochemical reactions that address stress and support health means it can also create free radicals that damage DNA, cells, blood lipids, and increase stress and harm health.

Two, there’s a little something called hereditary hemochromatosis.

Hereditary hemochromatosis is a genetic condition increasing a person’s absorption and retention of dietary iron. This has benefits in certain contexts—carriers have a natural resistance to the bubonic plague, as one effect of hemochromatosis is to render white immune cells iron-deficient and thus resistant to the plague virus which feeds on iron—but it’s mostly negative in today’s relatively plague-free world. Most of the hemochromatosis literature focuses on homozygotes (carriers of two copies of the gene) and specific “iron overload-related diseases,” which include cirrhosis, liver fibrosis, liver cancer, elevated liver enzymes, “physician-diagnosed symptomatic hemochromatosis,” or finger arthritis. Those are bad conditions to have, to be sure, but that’s not even a complete list. Homozygous carriers of the mutation also have greater risks for diabetes, arthritis, fatigue, liver disease, and frailty and muscle loss. They’re more likely to experience neurodegenerative diseases like Parkinson’s and Alzheimer’s. Even heterozygous carriers (those who carry just one copy of the variant) have an elevated risk of iron overload compared to the general population.

Okay, okay. But couldn’t it be that the hemochromatosis gene is increasing disease risk through another, non-iron route? Perhaps high iron is just a marker of disease, not a cause. After all, most genes are pleiotropic—they have more than one effect.

Probably not. The most reliable treatment for hereditary hemochromatosis is phlebotomy. Literally removing iron from the body by draining blood is the first (and often only necessary) line of defense against hereditary iron overload. And it works really well.

Besides, phlebotomy may also be beneficial in people without clinical iron overload or hemochromatosis. It’s the most effective way to reduce iron stores and tends to increase insulin sensitivity. In insulin resistant men with fatty liver, blood donation normalized insulin sensitivity and liver enzymes. In meat eaters, blood donation reduced ferritin levels to match those of lacto-ovo-vegetarians and improved insulin sensitivity. One study even tested the effect of randomized phlebotomy on cancer incidence. After four and a half years, those subjects placed in the phlebotomy group lived longer, had less cancer, and had lower ferritin levels than the subjects who didn’t donate blood.

I can’t argue with the research, but the idea that a primary component of a food we’ve been eating for millions of years and to which we may even owe much of our brainpower—the iron in meat—still rankles. Is iron truly inherently “bad,” or is there anything about our modern environment that makes it so?

Possible Modern Influences On Iron Levels

Less Bleeding

One factor is that we don’t shed as much blood as before. Most men engage in far fewer bouts of direct violent conflict. Most people have fewer parasites feasting on their blood. And when’s the last time you exchanged blood oaths with anyone? We have fewer opportunities to bleed, in other words. That’s why regular phlebotomy can be such a useful tool for men (and some women) with too much iron in their bodies—it emulates all the bloodletting we used to do in a controlled, safe fashion.

Less Intense Activity

We use iron to generate energy. The more physical activity in which we engage, the more iron we utilize. This is usually couched in warnings for female athletes engaged in intense training, but it can also explain the beneficial effects of exercise in people with iron overload. There are even cases of “mild exercise” causing iron deficiency, so everything that increases energy expenditure—walking, gardening, hiking—will at least subtly reduce iron stores. More activity, less iron sitting around idle getting into trouble.

Too Many Seed Oils

I strongly suspect that the unprecedented dissemination of high-omega-6 seed oils throughout our food systems, our body fat, and our cellular membranes are exacerbating—if not causing—the relationship between excess iron and various diseases. Take the supposedly ironclad (pun intended) relationship between heme iron and colon cancer, which is mediated by iron’s peroxidative alteration of fatty acids in the colon. In animal studies that seek to show this relationship, you can’t get the colon cancer to “take” unless you feed the animal high-PUFA oils along with their heme iron. In one studyfeeding heme iron to rats promoted colon cancer only when fed alongside high-PUFA safflower oil. Feeding MUFA-rich and far more oxidatively-stable olive oil alongside the heme prevented the colon carcinogenesis. In another paper, only mice consuming fish oil-based and safflower oil-based diets exhibited carcinogenic fecal peroxides after eating heme iron; a coconut oil-based group of mice had no negative reaction to heme.

Among a cohort of US nurses, where PUFA intake is around 7% of calories and comes from seed oil, iron intake has moderate links to colon cancer. Among a cohort of Swedish women, where PUFA intake is under 5% of calories with a greater proportion coming from fish, the association is far weaker.

What To Do About All This?

First, men and postmenopausal women should figure out their hemochromatosis status. Both men and women with hereditary hemochromatosis have elevated risks of iron overload-related diseases, but they are much higher for men. (Premenopausal women have a handy built-in mechanism for shedding excess iron—menstruation.) Modern men and older women, with our absence of intestinal parasites and our lower tendency to engage in bloody hand-to-hand fighting, have few opportunities to shed iron. Your doctor will be able to order the test, or you can go through a genetic testing service and look for positive hits on C282Y and H63D.

Do it earlier rather than later. Studies indicate that one of the biggest predictors of whether someone with genetic iron overload develops liver cancer is their age at diagnosis of hemochromatosis. Those who wait risk incurring more damage.

Even if you’re negative for hereditary hemochromatosis, you can still have iron overload. Determine this by asking your doctor for a ferritin test. According to the Mayo Clinic, for men, the ferritin reference range is 24 to 336 ng/ml, and for women, it is 11 to 307. That is a wide range, and levels that your doctor would probably classify as technically normal have been associated with insulin resistance, atherosclerosis, and reduced telomere length (a marker of aging).

From what I can tell, levels approaching 200 ng/ml in men should definitely be classified as “high.” And lower may be even better. In one study, egg-and-dairy-eating vegetarian men had ferritin levels of 35 ng/ml and better insulin sensitivity than meat-eating men with ferritin levels of 72 ng/ml. After donating enough blood to hit 35 ng/ml, the meat eaters insulin sensitivity improved.

Dr. F. S. Facchini has used blood donation to induce “near iron deficiency”—the lowest body iron store that allows normal red blood cell production—in his gout patients, clearing them of gout attacks for as long as they maintained it. His patients at high risk for heart disease also saw major benefits from hitting very low ferritin levels (“to levels commonly seen in premenopausal females”), including increased HDL and lower blood pressure, even if they started with normal ferritin.

What seems safe is to stay on the low end of normal—say, from 50-150 ng/ml—as long as no symptoms of low iron arise.

As for women? Higher levels don’t seem to correlate with the same health issues in women. Lucky.

Now, say you have high iron, whether it’s hereditary hemochromatosis or just high normal ferritin levels….

What Should You Do About High Iron Levels?

Donate Blood

The quickest, safest way that also does the most social good (if you care about that sort of thing) is to donate blood. When you donate blood, your body must upregulate hemoglobin production to replace the lost blood. That requires iron, which is taken from body stores.

Don’t Manage Iron Overload With Diet

By that I mean stuff like:

  • Don’t give up red meat.
  • Don’t stop eating liver every week.
  • Keep eating oysters.
  • Don’t religiously adhere to reverse-kosher (only eating meat in the presence of dairy to inhibit iron absorption).

If you make dietary iron the focal point, you’ll miss out on all the incredible nutrients iron-rich foods like red meat and liver can offer. Besides, you’ll run yourself ragged following even more food restrictive rules that increase the chance of other nutrient deficiencies.

Don’t Manage an Iron Overload That Doesn’t Exist

I’ve seen people go down the rabbit hole of iron obsession without actually confirming they even had too much iron. They started giving blood (even self-administered), trying to reduce iron absorption by pairing dairy and calcium with their iron-rich foods, avoiding iron-rich foods—totally blind. Iron is an important nutrient. Deficiency is real. Anemia is no joke. Get tested before you start messing around with iron.

Follow a Healthy Primal Eating Plan

Whether it’s keto, low-carb, moderate-carb, or even vegetarian, going Primal will mitigate many of the potential effects of high iron by:

  • Avoiding Seed Oils and Excess Omega-6 Fats. Seed oils almost certainly make the “iron overload problem” worse, and may even be responsible for its negative effects and link to various diseases.
  • Including Phytonutrient-rich Fruits, Vegetables, Herbs, Teas, and Coffee. Polyphenols both inhibit iron absorption and reduce the oxidative interaction between iron and lipids.

So to sum up, get tested and be aware of the iron issue, but don’t let it rule you. It’s iron overload, not overlord.

Take care, everyone. What do you think of iron? Ever get tested? Ever give blood? See any benefits?

Let me know down below!

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References:

Tamosauskaite J, Atkins JL, Pilling LC, et al. Hereditary Hemochromatosis Associations with Frailty, Sarcopenia and Chronic Pain: Evidence from 200,975 Older UK Biobank Participants. J Gerontol A Biol Sci Med Sci. 2019;

Burke W, Imperatore G, Mcdonnell SM, Baron RC, Khoury MJ. Contribution of different HFE genotypes to iron overload disease: a pooled analysis. Genet Med. 2000;2(5):271-7.

Allen KJ, Gurrin LC, Constantine CC, et al. Iron-overload-related disease in HFE hereditary hemochromatosis. N Engl J Med. 2008;358(3):221-30.

Nowak A, Giger RS, Krayenbuehl PA. Higher age at diagnosis of hemochromatosis is the strongest predictor of the occurrence of hepatocellular carcinoma in the Swiss hemochromatosis cohort: A prospective longitudinal observational study. Medicine (Baltimore). 2018;97(42):e12886.

Larsson SC, Rafter J, Holmberg L, Bergkvist L, Wolk A. Red meat consumption and risk of cancers of the proximal colon, distal colon and rectum: the Swedish Mammography Cohort. Int J Cancer. 2005;113(5):829-34.

Liu B, Sun Y, Xu G, et al. Association between Body Iron Status and Leukocyte Telomere Length, a Biomarker of Biological Aging, in a Nationally Representative Sample of US Adults. J Acad Nutr Diet. 2018;

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Yesterday, I linked to a study showing that the beneficial effects of high levels of cardiorespiratory fitness—the kind you build with cardio/endurance training, HIIT, and sprints—have no upper limit. At first glance, this study appears to bust the “myth” of chronic cardio and the U-shaped curve of endurance training and prove that the more you train, the longer you’ll live. This appears to run counter to some of my central claims—that too much mid-to-high intensity endurance exercise leads to burnout, health issues, and diminishing returns.

A commenter wrote a great comment that got me wondering:

As far as “the more exercise the better” study I wonder if folks who had to drop out of long distance cardio training due to injuries or cortisol driven exhaustion are considered in the equation? In other words, if you can tolerate chronic cardio you may live longer, otherwise it might break you down. Everyone has a sweet spot for exercising is my gut feeling and you have to “listen to your body”. I still like the primal mantra along the lines of (if I may be so presumptuous as to paraphrase Mark) “walk a lot, do sprints once a week, lift heavy things once or twice a week, spend time outdoors, take part in sports or recreational activities that are fun for you”.

What do I think is going on? How do the results of this paper jibe with my take on Chronic Cardio?

First off, we have to acknowledge the basic structure of the study.

This study didn’t actually measure “hours spent training.” They gave subjects treadmill tests (stress tests) to determine their cardiovascular fitness, then divided everyone into different tiers of fitness based on the results. In fact, the authors of the study criticized the shortcomings of previous studies which used self-reported training data instead of objective measurements of cardiorespiratory fitness like the treadmill test. This makes the study far more accurate and useful. It also means you can’t make any ironclad proclamations about the connections between hours spent training and longevity. You can certainly make inferences—people who had better cardio fitness probably spent more time training to get it—but there are other interpretations. All you can say for certain is that higher levels of cardio fitness predict greater longevity.

I don’t see how anyone could argue with that. Of course being fitter is better.

But my criticism of chronic cardio isn’t a criticism of cardiovascular fitness. It’s a criticism of how most people go around obtaining that fitness—by destroying their bodies.

That doesn’t have to happen anymore. Tons of top guys these days are finally figuring out that you don’t have to log as many laps/miles/etc as possible to maximize your performance, but that wasn’t always the case. I grew up convinced that the more miles I ran, the healthier I’d be. That’s how I did it back in my marathon and triathlon days, and it almost destroyed me and an entire generation of my peers.

You can train twice as much as the next guy yet have worse fitness, either because you’re not training intelligently, you’re overtraining and hampering the adaptive process, or you’re not sleeping. That’s chronic cardio. You can train less and get better results, if you’re optimizing your recovery, nutrition, and sleep. That’s Primal Endurance.

As for these subjects, there is some serious genetic confounding occurring. Those dudes with elite fitness levels well into their 70s are often a different breed. They’re hard to kill. They’re tough. They can withstand the discomfort of grueling mile after mile. What other types of discomfort can they bear and even grow from? They’re just more robust than the average 70-year-old. It may not be the elite training itself that’s making them resist death. It’s just as likely they have the genetic capacity to excel in endurance training, and even if they didn’t exercise they’d still live longer than average.

There’s also the healthy user bias. The kind of lifestyle regular exercisers follow emphasizes sleep, plenty of rest and recuperation, smart supplementation and nutrition, and all sorts of other things that are also linked to longer, better health.

This paper makes a strong case for using something like Primal Endurance to build great cardiorespiratory fitness without risking chronic cardio territory.

Thanks for writing and reading, folks. Take care!

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The post Dear Mark: Is There No Upper Limit to Endurance Training? appeared first on Mark’s Daily Apple.

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Many of you have asked about prostate health in a Primal context. Men are interested because they know men have a decent chance of getting prostate cancer. Women are interested because they’re worried about the men in their lives getting prostate cancer. Today, I’m going to delve deep into the topic, exploring the utility (or lack thereof) of standard testing, the common types of treatment and their potential efficacy, as well as preventive and unconventional ways of reducing your risk and mitigating the danger of prostate cancer.

Let’s go.

First, what does the prostate do, anyway? Most people only think about it in terms of prostate cancer.

It’s a gland about the size of a small apricot that manufactures a fluid called prostatic fluid that combines with sperm cells and other compounds to form semen. Prostatic fluid protects sperm against degradation, improves sperm motility, and preserves sperm genetic stability.

What Goes Wrong With the Prostate?

There are a few things that can happen.

Prostatitis

Inflammation of the prostate, usually chronic and non-bacterial. A history of prostatitis is a risk factor for prostate cancer.

Benign Prostatic Hyperplasia

Non-cancerous enlargement of the prostate. As men age, the prostate usually grows in size. This isn’t always cancer but can cause similar symptoms.

Prostate Cancer

What most of us are interested in when we talk about prostate health… After skin cancer, prostate cancer is the most common cancer among men and the sixth most common cause of cancer death among men worldwide. Yet, most men diagnosed with prostate cancer do not die from it; they die with it. The 5-year survival rate in the US is 98%.

That said, there is no monolithic “prostate cancer.” Like all other cancers, there are different grades and stages of prostate cancer. Each grade and stage has a different mortality risk:

  • Low-grade prostate cancer grows more slowly and is less likely to spread to other tissues.
  • High-grade prostate cancer grows more quickly and is more likely to spread to other tissues.
  • Local prostate cancer is confined to the prostate. The 5-year relative survival rate (survival compared to men without prostate cancer) for local prostate cancer is almost 100%.
  • Regional prostate cancer has spread to nearby tissues. The 5-year relative survival rate for regional prostate cancer is almost 100%.
  • Distant prostate cancer has spread to tissues throughout the body. The 5-year relative survival rate for distant prostate is 29%. Distant prostate cancer explains most of the prostate-related mortality.

What Are Symptoms of Prostate Cancer?

The primary symptom is problems with urination. When the prostate gland grows, it has the potential to obstruct the flow of urine out of the bladder, causing difficulty urinating, weak urine flow, painful urination, or frequent urination. This can also be caused by benign prostatic hyperplasia, a non-cancerous enlargement of the prostate.

What Causes Prostate Cancer?

A big chunk is genetic. People with “knockout” alleles for BRCA, which codes for tumor suppression, have an elevated risk of some forms of prostate cancer. That’s the same one that confers added risks for breast cancer.

Ethnicity matters, too. Men of Sub-Saharan African descent, whether African-Americans in the U.S. or Caribbean men in the U.K., have the highest risk in the world for prostate cancer—about 60% greater than other ethnic groups. White men have moderate risks; South Asian, East Asian, and Pacific Islander men have lower risks.

Testosterone has a confusing relationship with prostate cancer. Conventional wisdom tends to hold that testosterone stimulates prostate cancer growth, and there’s certainly some evidence of a relationship, but it’s not that simple.

In one study, men with low free testosterone levels were less likely to have low-grade (less risk of spreading) prostate cancer but more likely to have high-grade (higher risk of spreading) prostate cancer.

In another, testosterone deficiency predicted higher aggressiveness in localized prostate cancers.

In Chinese men, those who went into treatment with low testosterone were more likely to present with higher-grade localized prostate cancers.

Other studies have arrived at similar results, finding that “hypogonadism represents bad prognosis in prostate cancer.”

Many prostate cancer treatments involve testosterone deprivation, a hormonal reduction of testosterone synthesis. This can reduce symptoms and slow growth of prostate tumors during the metastatic phase, but prostate cancer tends to be highly plastic, with the ability to adapt to changing hormonal environments. These patients often see the cancer return in a form that doesn’t require testosterone to progress.

What About Testing?

If you have a prostate, should you get tested starting at age 40?

Not necessarily. The value of early testing hasn’t been established. Some researchers even question whether early testing is more harmful than ignoring it, and most of the research finds middling to nonexistent evidence in favor of broad testing for everyone. Early testing has a small effect on mortality from prostate cancer, but no effect on all-cause mortality.

PSA testing can also be inaccurate. PSA is prostate specific antigen, a protein produced by the prostate. It’s normal to have low levels of PSA present in the body, and while high levels of PSA are a good sign of prostate cancer—even years before it shows up in imaging or digital probes—they can also represent a false positive. Those two other common yet relatively benign prostate issues—benign hyperplasia and prostatitis—can also raise PSA levels well past the “cancer threshold.”

Other causes of high levels of PSA include:

  • Urinary tract infections
  • Recent sex or ejaculation
  • Recent, vigorous exercise
  • Certain medications.

In fact, if you have a PSA reading of 4 (the usual threshold), there’s still just a 30% chance it actually indicates cancer.

What About Treatment?

Let’s say you do have prostate cancer, confirmed by PSA and a biopsy (or two, or three, as needle biopsies often miss cancers). What next? Should you definitely treat it?

It’s unclear whether treatment improves survival outcomes. One study took men aged 50-69 with prostate cancer diagnosed via PSA testing, divided them among three treatment groups, and followed them for ten years. One group got active monitoring—they continued to test and monitor the status of the cancer. One group received radiotherapy—radiation therapy to destroy the tumor. And the last group had the cancer surgically removed.  After ten years, there was no difference among the groups for all-cause mortality, even though the active-monitoring group saw higher rates of prostate cancer-specific deaths (8 deaths—in a group of 535 men— vs 5 in the surgery group and 4 in the radiotherapy group), cancer progression, and metastasis.

In another study of men with localized prostate cancer, removing the prostate only improved all-cause mortality rates among men with very high PSAs (more than 10). In men with lower PSAs, “waiting and seeing” produced similar outcomes as surgery.

Prostate removal also carries many unwanted side effects, like incontinence and sexual dysfunction. No one wants prostate cancer, but it’s no small thing to have problems with urination and sex for the rest of your life. Those are major aspects of anyone’s quality of life.

Before you make any decisions, talk to your doctor about your options, the relative mortality risk of your particular cancer’s stage and grade, and how the treatments might affect your quality of life.

How Can You Reduce the Risk of Prostate Cancer?

1. Inflammation is definitely an issue.

For one, there’s the relationship between prostatitis, or inflammation of the prostate, and prostate cancer that I already mentioned above.

Two, there’s the string of evidence linking anti-inflammatory compounds to reductions in prostate cancer incidence. For example, aspirin cuts prostate cancer risk. Low-dose aspirin (under 100 mg) reduces both the incidence of regular old prostate cancer and the risk of metastatic prostate cancer. It’s also associated with longer survival in patients with prostate cancer; other non-steroidal anti-inflammatories are not.

Third, anti-inflammatory omega-3 fatty acids (found in seafood and fish oil) are generally linked to lower rates of prostatic inflammation and a less carcinogenic environment; omega-6 fatty acids can trigger disease progression. A 2001 study of over 6,000 Swedish men found that the folks eating the most fish had drastically lower rates of prostate cancer than those eating the least. Another study from New Zealand found that men with the highest DHA (an omega-3 found in fish) markers slashed their prostate cancer risk by 38% compared to the men with the lowest DHA levels.

2. The phytonutrients you consume make a difference.

A series of studies on phytonutrient intake and prostate cancer incidence in Sicilian men gives a nice glimpse into the potential relationships:

The more polyphenols they ate, the less prostate cancer they got.

The more phytoestrogens they ate, the more prostate cancer they got. Except for genistein, an isoflavone found in soy and fava beans, which was linked to lower rates of prostate cancer. The Sicilians are eating more fava than soy, I’d imagine.

How about coffee, the richest source of polyphenols in many people’s daily diets? It doesn’t appear to reduce the incidence of prostate cancer, but it does predict a lower rate of fatal prostate cancer.

3. Your circadian rhythm and your sleep are important.

Like everything else in life, tumor suppression follows a circadian pattern. Nighttime melatonin—which is suppressed if your sleep hygiene is bad and optimal if your sleep hygiene is great—inhibits the growth of prostate cancer cells and reduces their ability to utilize glucose. One way to enhance nighttime melatonin is by getting plenty of natural, blue light during the day; this actually makes nighttime melatonin more effective at prostate cancer inhibition. On the other hand, getting that blue light at night is a major risk factor for prostate cancer.

4. Get a handle on your fasting blood sugar and insulin.

In one study, having untreated diabetic-level fasting blood sugar was a strong risk factor for prostate cancer. Another study found that insulin-lowering metformin reduced the risk, while an anti-diabetic drug that raised insulin increased the risk of prostate cancer. Metformin actually lowers PSA levels, which, taken together with the previous study, indicates a causal effect.

5. Keep moving, keep playing, keep lifting.

This has a number of pro-prostate effects:

It keeps you insulin sensitive, so neither fasting insulin, nor fasting glucose get into the danger zone.

If you’re doing testosterone suppression treatment, exercise can maintain (and even increase) your muscle mass, improve your quality of life, and increase your bone mineral density.

Oh, and do some deadlifts. Men with prostate cancer who trained post-surgery had better control over their bodily functions, as long as they improved their hip extensor strength. If you don’t know, hip extension is the act of standing up straight, of moving from hip flexion (hip hinging, bending over) to standing tall. It involves hamstrings, glutes, and the entire posterior chain. Deadlifts are the best way to train that movement pattern.

The prostate cancer issue is frightening because it’s so common. Almost all of us probably know someone who has or had it, even unknowingly. But the good news is that most prostate cancers aren’t rapidly lethal. Many aren’t lethal at all. So whatever you do, don’t rush into serious treatments or procedures without discussing the full range of options in a frank, honest discussion with your doctor.

That’s it for today, folks. Thanks for reading. If you have any questions, comments, or concerns about prostate cancer, feel free to chime in down below. I’d love to hear from you.

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References:

Perletti G, Monti E, Magri V, et al. The association between prostatitis and prostate cancer. Systematic review and meta-analysis. Arch Ital Urol Androl. 2017;89(4):259-265.

Ilic D, Djulbegovic M, Jung JH, et al. Prostate cancer screening with prostate-specific antigen (PSA) test: a systematic review and meta-analysis. BMJ. 2018;362:k3519.

Brawer MK, Chetner MP, Beatie J, Buchner DM, Vessella RL, Lange PH. Screening for prostatic carcinoma with prostate specific antigen. J Urol. 1992;147(3 Pt 2):841-5.

Castro E, Eeles R. The role of BRCA1 and BRCA2 in prostate cancer. Asian J Androl. 2012;14(3):409-14.

Watts EL, Appleby PN, Perez-cornago A, et al. Low Free Testosterone and Prostate Cancer Risk: A Collaborative Analysis of 20 Prospective Studies. Eur Urol. 2018;

Neuzillet Y, Raynaud JP, Dreyfus JF, et al. Aggressiveness of Localized Prostate Cancer: the Key Value of Testosterone Deficiency Evaluated by Both Total and Bioavailable Testosterone: AndroCan Study Results. Horm Cancer. 2018;

Dai B, Qu Y, Kong Y, et al. Low pretreatment serum total testosterone is associated with a high incidence of Gleason score 8-10 disease in prostatectomy specimens: data from ethnic Chinese patients with localized prostate cancer. BJU Int. 2012;110(11 Pt B):E667-72.

Teloken C, Da ros CT, Caraver F, Weber FA, Cavalheiro AP, Graziottin TM. Low serum testosterone levels are associated with positive surgical margins in radical retropubic prostatectomy: hypogonadism represents bad prognosis in prostate cancer. J Urol. 2005;174(6):2178-80.

Banerjee PP, Banerjee S, Brown TR, Zirkin BR. Androgen action in prostate function and disease. Am J Clin Exp Urol. 2018;6(2):62-77.

Zhou CK, Daugherty SE, Liao LM, et al. Do Aspirin and Other NSAIDs Confer a Survival Benefit in Men Diagnosed with Prostate Cancer? A Pooled Analysis of NIH-AARP and PLCO Cohorts. Cancer Prev Res (Phila). 2017;10(7):410-420.

Russo GI, Campisi D, Di mauro M, et al. Dietary Consumption of Phenolic Acids and Prostate Cancer: A Case-Control Study in Sicily, Southern Italy. Molecules. 2017;22(12)

Russo GI, Di mauro M, Regis F, et al. Association between dietary phytoestrogens intakes and prostate cancer risk in Sicily. Aging Male. 2018;21(1):48-54.

Discacciati A, Orsini N, Wolk A. Coffee consumption and risk of nonaggressive, aggressive and fatal prostate cancer–a dose-response meta-analysis. Ann Oncol. 2014;25(3):584-91.

Dauchy RT, Hoffman AE, Wren-dail MA, et al. Daytime Blue Light Enhances the Nighttime Circadian Melatonin Inhibition of Human Prostate Cancer Growth. Comp Med. 2015;65(6):473-85.

Kim KY, Lee E, Kim YJ, Kim J. The association between artificial light at night and prostate cancer in Gwangju City and South Jeolla Province of South Korea. Chronobiol Int. 2017;34(2):203-211.

Murtola TJ, Vihervuori VJ, Lahtela J, et al. Fasting blood glucose, glycaemic control and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Br J Cancer. 2018;118(9):1248-1254.

Haring A, Murtola TJ, Talala K, Taari K, Tammela TL, Auvinen A. Antidiabetic drug use and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Scand J Urol. 2017;51(1):5-12.

Park JS, Lee KS, Ham WS, Chung BH, Koo KC. Impact of metformin on serum prostate-specific antigen levels: Data from the national health and nutrition examination survey 2007 to 2008. Medicine (Baltimore). 2017;96(51):e9427.

Galvão DA, Taaffe DR, Spry N, Joseph D, Newton RU. Combined resistance and aerobic exercise program reverses muscle loss in men undergoing androgen suppression therapy for prostate cancer without bone metastases: a randomized controlled trial. J Clin Oncol. 2010;28(2):340-7.

Ying M, Zhao R, Jiang D, Gu S, Li M. Lifestyle interventions to alleviate side effects on prostate cancer patients receiving androgen deprivation therapy: a meta-analysis. Jpn J Clin Oncol. 2018;48(9):827-834.

Uth J, Fristrup B, Haahr RD, et al. Football training over 5 years is associated with preserved femoral bone mineral density in men with prostate cancer. Scand J Med Sci Sports. 2018;28 Suppl 1:61-73.

Park J, Yoon DH, Yoo S, et al. Effects of Progressive Resistance Training on Post-Surgery Incontinence in Men with Prostate Cancer. J Clin Med. 2018;7(9)

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