Best. Yogurt. Ever.

As I mentioned in my last post, Dr. William Davis has recommended a particular strain of bacteria, Lactobacillis reuteri, as having many health benefits.

He discussed those benefits in the video I embedded in that post, and now as promised here’s a video I produced that demonstrates how to make it.

You can read Dr. Davis’ instructions for making the yogurt (and read more about its benefits) on The Undoctored Blog, but I think the video above is helpful to show you step-by-step how to make it consistently and flawlessly.

Dr. Davis suggests you can make the yogurt by putting the liquid in a pan in the oven. He says you can just turn the oven up to 350ºF for 90 seconds, and then shut it off, repeating the cycle every few hours to keep the temperature between 100-110ºF.

In my experience that’s way too much work, and is susceptible to failure. If you forget to turn off the oven, you kill the bacteria. If you fail to turn on the oven at least once in the middle of the night, the whole mix can sour. I had a couple of flops in my first five batches using that method.

That’s why I decided to get a yogurt maker, which keeps the mix at a constant temperature with no need to pay attention to it. Since then I would guess I have made 50 batches or more, and haven’t had a single failure.

After getting the BioGaia tablets, which contain the bacteria, and inulin powder as a source of prebiotic fiber on which they feed, all you need is the liquid that will be turned into yogurt.

Dr. Davis says he uses half-and-half as his base, and also has made yogurt from almond milk or coconut milk. If you use almond milk, he says you need to add some sugar to your mix, in addition to the inulin.

Whole milk is another option, but my choice is a mix of half-and-half with heavy whipping cream, as you’ll see in the video. This is definitely not low-fat yogurt.

I have gotten great results by keeping the mix at 104ºF for 36 hours, and by putting some water in the yogurt maker it keeps the temperature more even throughout the jars. After they’re done, I put them in the refrigerator.

As you can see, this is the thickest yogurt you’re likely to find. It stands up straight.

When it’s time to eat, I take one of the jars from the refrigerator and spread it out in a dish, adding three more teaspoons of the inulin both to sweeten the yogurt and to provide some prebiotic fiber to feed the bacteria in my GI tract.

I think it tastes great plain, but I typically also top it with some fresh raspberries or blackberries.

This is a delicious dessert, and I think the benefits Dr. Davis cites seem to hold true for me. He says it has a powerful appetite-suppressant effect, and while I think my low-carb diet has helped me not experience cravings during my typical 18-hour fasting window, the yogurt could definitely be a contributing factor.

Dr. Davis also touts the skin-thickening and collagen-increasing properties of L. reuteri and this yogurt, which supposedly results in a more youthful appearance and faster wound healing. I found a picture that isn’t necessarily definitive in this regard, but it might give a clue.

The picture on the left is from January 2019, when I was just starting to make and eat the yogurt. I tried to duplicate the angle in the one on the right this evening, 16 months later. The horizontal forehead creases seem less pronounced to me, but you be the judge:

I think the oxytocin-enhancement benefits are real too, as I’ve been able to put on muscle mass through weightlifting.

Since I find it so delicious, and because research suggests benefits that my own experience tends to support, I plan to keep making this for Lisa and me for the long term.

If you try it, I’d love to hear about your experience.

See the whole series about my health journey. Follow along on FacebookTwitter and LinkedIn.

Weekend Watching: Another Look at Dietary Guidelines

Conventional dietary wisdom tells us that we should limit intake of fat, and that saturated fat is the worst!

Right at the top of the Nutrition Facts panel on any of the processed food we buy is a declaration of its fat content: Total Fat, Saturated Fat, Trans Fat, Polyunsaturated Fat and Monounsaturated Fat.

Total Carbohydrate doesn’t even get second billing: it’s below both Cholesterol and Sodium.

There was a time when I was extremely grateful for the product at right, when I had recently been diagnosed with celiac disease.

Other cereals I had tried were gluten free, but that was the most you could say for them. They were not at all tasty. Chex cereals were the first ones made for the mass market that also were gluten-free, and Corn Chex was my favorite variety.

I ate it for breakfast almost every day, and as you can see on the label I definitely wasn’t getting too much fat, even with 2% milk. But each serving did have 33g of carbohydrates, even when I didn’t add any extra sugar.

Over just a few years it played a significant role in me gaining 40 lbs. and getting to Peak Lee.

Knowing that I had been on a diet that was rich in so-called “healthy whole grains” and yet was anything but healthy, when I started to run across messages challenging this dietary consensus I was open to at least trying a different approach.

Of course it was not without a bit of concern: after all, if I lost a bunch of weight but was setting myself up for heart disease, that wouldn’t be a net benefit.

That’s why I found it really helpful to have serious scientists like Dr. Peter Attia review the literature and outline what the research on diet and heart disease really says.

I think you’ll find this video fascinating, as I did. Watch it for yourself and let me know what you think in the comments.

If you doubt that it’s worth the 79 minutes to watch, I’ll provide a few bullet point highlights below.

  • Studies of Benedictine and Trappist monks, Navajo Indians, Irish immigrants to Boston, Swiss Alpine farmers and Maasai and other African pastoralists report no association of saturated fat to heart disease.
  • A 1957 study of 5,400 male employees of Western Electric Company compared the 15 percent who ate the most fat to the 15 percent who ate the least. “Worthy of comment, is the fact that of the 88 coronary cases, 14 have appeared in the high-fat intake group and 16 in the low-fat group.”
  • A follow-up study of the Western Electric cohort in 1981 found “The amount of saturated fatty acids in the diet was not significantly associated with the risk of death from CHD.”
  • The Minnesota Coronary Study, which involved 9,000 men and women whose diets could be strictly controlled because they were in mental institutions, found 269 deaths in the intervention group (with low saturated fat and cholesterol) and 206 deaths in the control group. The results, available in 1973, went unpublished for 16 years. Why? “We were disappointed in the way they turned out.”
  • 2001 Cochrane Collaboration meta-analysis involving 27 well-controlled randomized trials with 10,000 subjects followed for an average of three years each found No effect on longevity and No “significant effect on cardiovascular events.”
  • A second Cochrane Collaboration meta-analysis in 2006 “Multiple risk factor interventions for primary prevention for coronary heart disease” with 900,000 patient years of observation concluded: “The pooled effects suggest multiple risk factor intervention has no effect on mortality.”

OK, now go back and watch the video. It’s a pretty compelling story.

What do you think?

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Renewing a Connection, and a Call to Comment

My post yesterday on why A Calorie is NOT a Calorie — and why “eat less, move more” is a simplistic and harmful slogan masquerading as scientific weight-loss advice — led to a delightful reconnection with someone I first met more than a decade ago.

My good friend Dave deBronkart’s comment on my LinkedIn post drew Dr. Ted Eytan into the discussion, and it was a great pleasure to renew our acquaintance.

I first met Dr. Eytan in 2009 when we were on a panel together at a conference in Baltimore (which was also the day I met Ed Bennett for the first time after having interacted for several months on Twitter).

I was delighted to learn that he’s taken on a role as Associate Director with The Nutrition Coalition, and that he’s engaged in the effort to have U.S. Dietary Guidelines reflect sound science.

I had heard Nina Teicholz on a podcast talking about the Dietary Guidelines Advisory Commission and her work with The Nutrition Coalition, so it was cool to find out that Dr. Eytan is working so closely with her. As described earlier in this series, her book — The Big Fat Surprise — started me on this journey of dietary discovery.

The Nutrition Coalition is urging public comment as the U.S. Dietary Guidelines Advisory Commission is developing its 2020 Guidelines. This process happens every five years, and it has a huge impact. It affects everything from hospital meals to school lunches to what physicians and dietitians recommend to patients.

I submitted my comments last night. I hope you’ll check out all of the great information from The Nutrition Coalition and do likewise.

Tomorrow I’ll continue the series about my health journey. Follow along on FacebookTwitter and LinkedIn.

A Study is Not a Study

All scientific studies are not created equal.

Each type of scientific study has its uses and value, but when you make decisions on diet, exercise and other behaviors you are literally betting your life.

So it’s important to understand what different kinds of studies can tell us, and what they can’t.

The weakest evidence comes from observational studies. In a retrospective observational study, scientists compare outcomes in different populations or subgroups and compare characteristics of those populations.

They may note differences in outcomes, and then try to identify differences between the two populations that might explain the differing outcomes.

That’s an important and highly beneficial use of these kinds of studies: to generate hypotheses.

But those hypotheses need to be tested. Just because two factors are correlated doesn’t mean there is a causal relationship.

Sometimes the correlation is so strong that causation is highly likely. For cigarette smokers, for example, the incidence of lung cancer is 20-30 times higher than among nonsmokers. If the effect is large enough, an observational or epidemiological study can provide a good guide to decisions.

It would be foolish to think smoking is safe just because a controlled experiment in humans is impractical and unethical.

On the other end of the spectrum from observational studies is a randomized, double-blind and placebo-controlled trial.

  • A controlled study is one in which a group that is treated is compared with one that is not, the controls. If the outcomes of the treatment group are significantly better than the control group, it shows that the treatment has value.
  • Placebo-controlled means that some kind of intervention is done in each arm of the study. One group gets the pill that is hypothesized to be beneficial, while the other typically gets an identically appearing sugar pill. This is designed to overcome the placebo effect, in which people report feeling better because they think they’ve been treated. To be meaningful, the treatment arm needs to have results that are significantly better than placebo.
  • A randomized trial is one in which people are assigned by chance to either the treatment or the control.
  • A double-blind study is one in which neither the study subjects or the investigators know who is getting the treatment and who is a control. In addition to guarding against the placebo effect among subjects, this is designed to keep the investigators from imagining improvements in the treatment group.

This kind of study is often called a “gold standard” study. In the best of them, the treatment and control groups will be as identical as possible. You wouldn’t want one to have 60% tobacco smokers while the other has 30%, for example. Ideally, the only relevant difference between the groups will be that one got the treatment while the other didn’t.

It’s also important to have a large enough number (or n) to enable statistical analysis of the likelihood that the result was not due to chance. As you read studies you’ll note that a p value is given, such as p<.05. That means the likelihood that a difference between the groups is due to chance is less than 5%: we’re 95% certain that the outcomes difference is a real one.

The strongest studies also have “hard” or objective endpoints, which are the outcomes being measured. Death or a heart attach are hard endpoints, while subjective measures like “feelings of well-being” are soft endpoints.

One of the big problems in scientific reporting is when headlines say, “Study shows….”

If it’s a gold standard study (randomized, double-blind, placebo-controlled), that’s legitimate.

If it’s an observational or epidemiological study, the more accurate headline would be “Study suggests ….” Those studies can only generate hypotheses to be tested in more rigorous gold standard studies.

So why even do these observational studies? They enable identification of promising lines of inquiry at lower cost. They can provide a good starting point.

One final type of study that is relevant for our consideration is animal studies. Because of common metabolic pathways, these also can suggest potential applications in humans.

Like observational studies, animal studies can point to areas for further investigation, but they aren’t definitive. Their major advantage is that with the shorter lifespans of animals and our ability to enforce compliance with the intervention, we’re able to get those preliminary answers in a shorter timeframe. And we don’t need to worry about the placebo effect in animals.

But lots of findings in mice have not borne out in human studies.

So how does this relate to dietary studies, and what should we do about it?

  1. It’s almost impossible to do a study of free-living humans for any length of time that truly isolates one variable.
  2. The effects identified in observational studies are typically not large enough to justify confident proclamations. An odds ratio of 20 or 30 meant cigarette smokers were 20-30x more likely than nonsmokers to develop lung cancer. If the odds ratio for developing colon cancer because of nitrates in bacon is 1.1, it’s a lot less clear that bacon is really a problem (see #1).
  3. The effects of diet accumulate over a lifetime. Even smoking seems to have its carcinogenic effects over a period of years, not weeks or months.
  4. It’s extremely hard to have a blinded study of diet, at least with normal foods. People know whether they’re eating eggs or pancakes, bacon or okra.
  5. Eating in a way that is radically different from what our ancestors ate, at least over the last several thousand years, is unlikely to be a prescription for health and vitality.

My main point is that it’s hard to determine precisely the health effects of different eating patterns and habits. It’s even harder when one hypothesis, the diet-heart hypothesis, becomes established and leads to confirmation bias driving out dissent, making it difficult to do and publish research that doesn’t align with prevailing thought.

And yet, we each are our own n of 1, and we need to decide what we’re going to eat today. Based on my reading and personal study and experimentation over the last few years, I’m convinced that the diet-heart hypothesis is seriously off track.

As I continue this series, which you can follow on Facebook, Twitter  or LinkedIn (or by just bookmarking and checking in regularly), I’ll introduce you to authors, physicians and scientists who have influenced me toward that position, as well as to some of the stronger studies that have led me to adjust my personal behaviors.

Even if you reach a different conclusion, it’s good to have explored the arguments so you’re making dietary decisions consciously instead of by default.

I’m an n of 1…and so are you

When physicians and scientists are confronted with a case that conflicts with what they understand to be true, particularly in the areas of diet and exercise, one typical response is, “Well…that’s an n of 1.”

What they’re saying is essentially this: I can’t prove that thing didn’t happen. But if it did happen, it was in this one case. And to rely on it, we need to see it replicated in studies of a larger population.

So the fact that my LDL and Triglyceride levels dropped 20-30 points and my HDL (good) cholesterol went up 17 points after I switched from cereal to eggs as my breakfast staple doesn’t prove anything.

I’m an n of 1.

Fair enough. The problem, however, as Gary Taubes (more on him in future posts) and Nina Teicholz have pointed out, is that dietary studies are among the least reliable ones in the scientific literature.

They’re either short-term, which by definition means they can’t reliably measure long-term effects, or they tend to rely on self-reported data on food consumption.

How many servings of fruits and vegetables did you have last week? How confident are you in that figure? Do you think the recollection accuracy of dietary study participants is markedly more reliable?

For more than 40 years Americans have been told to eat more whole grains and avoid saturated fat, and the weight of government has been placed behind these directives. As Teicholz and Taubes have suggested, however, these recommendations were made with an air of certainty that was far beyond what the study data could justify.

In their defense, the dietary experts felt a need to give some kind of direction to those who wanted to eat healthy. But the result has been our whole society has been subject to dietary experimentation on a massive scale.

You’re in the same position as those experts of a generation ago, except you don’t have to make recommendations for society as a whole.

You just need to decide how you’re going to eat.

Our twin epidemics of obesity and diabetes suggest that confidence in our current dietary guidelines is misplaced.

You’re an n of 1, too. We each have to reach our best judgment of what eating habits will best promote our health and vitality.

In future posts I’ll highlight some studies and perspectives you might find helpful. All studies are not created equal. More on that next time.

See the whole series about my health journey. Follow along on FacebookTwitter and LinkedIn.