Episode 86: Grokking

On this week’s show: Learn cooking science for free; preview of a GMO debate; baby food found to lack nutrients; deconstructing Doritos; athletes sponsoring junk food and buying grassfed beef; the salmonella outbreak; and why walking burns fat. In the Moment of Paleo segment: Waiting is. After the Bell: a mom talks about feeding her baby naturally and Jared Diamond talks about aging in Western civilization versus Hunter-gatherer civilizations.

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Episode 87: Your Stomach, Your Mind

On this week’s show, we explore stories that connect the gut and the mind. First a couple of documentary suggestions with trailers. In the news: addictive Oreos, popcorn as advertising defense, sleep cleans the brain (literally), and grocery store surveillance is coming. In the Moment of Paleo segment, we discuss creating a healthy feedback system to achieve your goals. After the Bell features clips from Dr. Yoni Freedhoff and Dr. Natasha Campbell-McBride.

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A Ketogenic Diet is Effective for Treating Type 2 Diabetes, New Study Shows

The number of people with diabetes has quadrupled since 1980. The CDC estimates that over 30 million Americans live with diabetes, and it is among the leading causes of death. Although diet and weight loss can improve type 2 diabetes (T2D), few people achieve this with the current standard of care. Long-term results are especially poor.

But a new long-term study has shown dramatic improvement and, in fact, reversal of T2D. The treatment protocol was revolutionary because it used diet rather than medication.

The study included 262 adults with T2D. They had a mean age of 54 years, 92 percent were obese, and 88 percent were on prescription diabetes medication. A control group of similar demographics received the usual T2D care model. The primary outcome measures were glycosylated hemoglobin (HbA1c), weight, and medication use.

The treatment protocol for the study was nutritional ketosis (i.e., a ketogenic diet). Subjects also received remote medical monitoring and biometric feedback. The study length was one year.

The biometric feedback included monitoring of body weight, blood glucose, and blood ketones. Subjects received education and communication with their telemedicine healthcare providers by app. These healthcare providers included a health coach (i.e. dietitian or other nutrition-trained provider) and a physician. The healthcare team monitored and adjusted diet and medication. Social support was provided by an online support community.

Subjects received individualized nutrition recommendations for achieving ketosis. Specific goals for blood ketones (beta-hydroxybutyrate) were adjusted within the range of 0.5-3.0 mmol/L based on biomarkers as well as hunger, cravings, energy, and mood. Typically, dietary carbohydrate intake was less than 30g/day. Protein and fat intake was also monitored and adjusted. The diet also included three to five daily servings of non-starchy vegetables, adequate mineral and fluid intake, a multivitamin, vitamin D3, and supplemental omega-3. Electrolytes were supplemented as needed.

The results were unprecedented. The control group reached significant improvement at 70 days. Then they continued to improve over the duration of the study. At the one-year point, the study group had lowered their HbA1c from 7.6 percent to 6.3 percent, while the control group had no change. The study group lost 12 percent of their body weight, an average of 30.4 lb (13.8 kg). The control group did not lose weight. Among the study group subjects who began on insulin, 94 percent were able to stop. All subjects on sulfonylurea medications were able to stop. Overall medication use (excluding metformin) dropped from 57 percent to 30 percent of subjects. On the other hand, the control group had no change in total medication use. In fact, their average insulin use increased.

Importantly, the control group experienced no adverse outcomes. Adherence was high, with a 16.8 percent dropout rate. Other improvements enjoyed by the control group included improved blood lipids, lower inflammation, and improved liver function.

This study showed that nutritional ketosis combined with medical monitoring, support, and biofeedback is incredibly effective for D2M treatment. It is significantly more effective than the standard treatment model. Importantly, this treatment modality is safe and sustainable over the long term. Of course, medical advice and monitoring is critical for T2D patients attempting a ketogenic diet, since medication dosing will need to be adjusted.

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Episode 88: Is Fat Good?

On today’s show, we tackle the big question about fat by taking a look at recent worldwide reporting and media coverage of dietary fat. First, Nick Offerman offers his prose on the beauty of bacon. Then, we bounce from The Dr. Oz show and CBS News in America to the BBC in the UK to ABC’s Catalyst in Australia — they’re all chiming in about fat. Sweden’s government is making some changes to their dietary recommendations. And, we’ll wrap up the show with 13 Nutritional Lies that have made people sick and overweight. After the Bell it’s Dr. Aseem Malhotra and Arthur Haines.

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Episode 89: Criminals

This week’s show is full of hard-hitting information about the pharmaceutical industry, including coverage of the ABC’s Heart of the Matter, Part 2, which focuses on statin drugs. Also, DNA barcoding shows that many herbal supplements are not what they seem. We also cover the updated Nordic Dietary Recommendations. The Moment of Paleo covers rigid versus intuitive approaches. After the Bell: Alan Watts; Herbal Supplements; and the Nordic Dietary Recommendations press conference.

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Can Pro-Inflammatory Gut Bacteria Cause Obesity?

The microbiome and the brain are the chief regulators of adiposity and eating behavior in humans. In many respects, the microbiome is even more influential than the brain. While the many processes occurring in the brain ultimately shape our thoughts and behavior, they are in turn heavily influenced by signals issuing from other areas—like the gastrointestinal microbiome and adipose tissue.

Some experts even characterize the brain as a puppet controlled by the body’s microbial colonists. This is obviously a stretching the truth a bit. Still, it does reinforce the important point that the brain is not an isolated organ; it’s significantly affected by what goes on in the rest of the body.

This fact is unfortunately under-recognized within conventional medical circles, including among mental- and behavioral-health specialists. Over the past decade, as the research on the gut-brain axis has taken off, this has gradually started to change; however, an astonishingly large number of medical professionals still seem to perceive the brain as an independent actor.

My intention here is not to take an in-depth look at the science on the gut-brain axis. Instead, I want to address the implications of a single study published a few years back that has lingered in the back of my mind since I first discovered it. This study makes a potent statement about the influence wielded by our bacterial inhabitants.

Microbes: More Powerful Than Most People Think

The study to which I refer was fairly simple. During clinical research, the two authors discovered—via gut-microbiome testing—that a morbidly obese, diabetic man harbored significant dysbiosis: a bacterial community rich in Enterobacter, a microbial genus rife with opportunistic, endotoxin-producing pathogens. At the start of the experiment, Enterobacter comprised 35 percent of the man’s gut bacteria.

When the man was put on a whole-foods diet rich in whole grains, traditional Chinese medical foods, and prebiotics, his body started to change. Various metabolic and inflammatory variables gradually tapered down to normal levels, and the man lost 30.1 kg (66.22 lb) in 9 weeks—and 51.4 kg (113.08 lb) in 23 weeks. Even more interestingly, at 9 weeks, the Enterobacter population of the subject’s gut had shrunk markedly. It now made up only 1.8 percent of his total gut bacteria. Moving forward, it kept shrinking. At 23 weeks, it was completely undetectable.

Now, it would be irresponsible to conclude from this that the gradual disappearance of Enterobacter from the participant’s gut caused his weight loss and improved health markers. Correlation does not equal causation; many factors are at play here. It is unclear which occurred first: the metabolic improvements and weight loss, or the loss of Enterobacter from the gut. Perhaps there is no causal link at all.

Still, it’s well-established that our gut bugs greatly affect our immunity, circulating endotoxin levels, metabolism, and appetite, among other markers.Hence, it seems highly plausible that the dietary intervention exerted such strong health effects because it altered the man’s gut microbiota, which mediated some of the various effects.

In order to assess whether this had indeed been the case, the researchers isolated a bacterial strain, Enterobacter cloacae, from the Enterobacter population found in the study participant’s gut. They then transferred this strain into the guts of germ-free mice.

Over the course of a week, the Enterobacter cloacae strain was transferred into the guts of two groups of mice, one eating a high-fat diet (HFD) and the other eating a normal mouse-chow diet (NCD). Following this inoculation period, the mice in the HFD group started gaining a lot of weight, along with various other unfavorable metabolic shifts. Among other effects, the infected mice eating the HFD expressed an insulin- and leptin-resistant phenotype. The mice eating the NCD, on the other hand, remained lean throughout the experiment.  

The researchers also tested whether another bacterium, Bifidobacterium animalis, would induce the same obese phenotype as the Enterobacter cloacae strain in mice eating a HFD. It didn’t. Mice that were inoculated with Bifidobacterium animalis gained significantly less weight than mice inoculated with Enterobacter cloacae. This seems to suggest that obesity can’t be produced by just any bacterium.

Normal mice fed a HFD tend to become obese. Germ-free mice, on the other hand, have been shown to be resistant to HFD-induced obesity. This observation, and the aforementioned study, clearly suggest that microbes are involved in body-fat regulation processes in mice. They also highlight the fact that some types of bacteria are uniquely problematic in the context of obesity and body-fat regulation.

Reflections and Caveats

We must remember that the human gut microbiome is an extremely complex ecosystem, comprised of a wide variety of different microbes. In other words, no human gut is composed entirely of Bifidobacterium animalis, Enterobacter cloacae, or any other individual strain. Additionally, humans differ strikingly from mice in several important physiological aspects, and are not confined to standardized, high-fat diets designed for research.

Still, it seems we can learn a lot from the above study—which is only one among many indicating that microbes play a critical role in human body-fat regulation. I have little doubt that the current obesity epidemic is largely due to the fact that a lot of people harbor a gut terrain rich in proinflammatory bugs.

Diet is a major determinant of gut-microbial composition. This is clearly highlighted by the aforementioned study. If you eat a markedly different type of diet from that which we evolved to eat, you will promote a gut microbiome that differs markedly from that with which we evolved to corexist. This can encourage fat accumulation and metabolic derangement, in part because certain gut microbes will drive you to eat more of the food that they need to thrive (e.g., processed carbohydrates).

Many overweight and obese people may be able to “fix” their microbiomes simply by changing their diets; not everyone can, though. A person with severe gut dysbiosis may find that they have to incorporate additional microbiome-restoration strategies into their health regimen to reduce the levels of inflammatory mediators circulating in their blood. Eating fermented vegetables, undergoing fecal microbial transfer (FMT), and other interventions can be valuable in this regard. With time and care, they can cultivate a more weight-friendly gut terrain.


1 Alcock J, Maley CC, Aktipis CA. “Is Eating Behavior Manipulated by the Gastrointestinal Microbiota? Evolutionary Pressures and Potential Mechanisms.” Bioessays 36.10 (Oct 2014): 940-9.

2 Bradlow HL. “Obesity and the Gut Microbiome: Pathophysiological Aspects.” Horm Mol Biol Clin Investig 17.1 (Jan 2014): 53-61.

3 Cani PD, Amar J, Iglesias, MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmee E, Cousin B, Sulpice T, Chamontin B, Ferrieres J, Tanti, JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R. “Metabolic Endotoxemia Initiates Obesity and Insulin Resistance.” Diabetes 56.7 (Jul 2007): 1761-72.

4 Fei N, Zhao L. “An Opportunistic Pathogen Isolated from the Gut of an Obese Human Causes Obesity in Germ-free Mice.” Isme J 7.4 (Apr 2013): 880-4.

5 Fetissov SO. “Role of the Gut Microbiota in Host Appetite Control: Bacterial Growth to Animal Feeding Behaviour.” Nat Rev Endocrinol 13.1 (Jan 2017): 11-25.

6 Hartstra AV, Bouter KE, Backhed F, Nieuwdorp M. “Insights into the Role of the Microbiome in Obesity and Type 2 Diabetes.” Diabetes Care 38.1 (Jan 2015): 159-65.  

7 Neves AL, Coelho J, Couto L, Leite-Moreira A, Roncon-Albuquerque Jr. R. “Metabolic Endotoxemia: A Molecular Link between Obesity and Cardiovascular Risk.” J Mol Endocrinol 51.2 (11 Sep 2013): R51-64.

8 Norris V, Molina F, Gewirtz AT. “Hypothesis: Bacteria Control Host Appetites.” J Bacteriol 195.3 (Feb 2013): 411-6.

9 Ridaura VK, Faith JJ, Rey FE, Cheng J, Duncan AE, Kau AL, Griffin NW, Lombard V, Henrissat B, Bain JR, Muehlbauer MJ, Ilkayeva O, Semenkovich CF, Funai K, Hayashi DK, Lyle BJ, Martini MC, Ursell LK, Clemente JC, Van Treuren W, Walters WA, Knight R, Newgard CB, Heath AC, Gordon JI. “Gut Microbiota from Twins Discordant for Obesity Modulate Metabolism in Mice.” Science 341.6150 (6 Sep 2013): 1241214.     

10 Vrieze A, Van Nood E, Holleman F, Salojarvi J, Kootte RS, Bartelsman JF, Dallinga-Thie GM, Ackermans MT, erlie MJ, Oozeer R, Derrien M, Druesne A, Van Hylckama Vlieg JE, Bloks VW, Groen AK, Heilig HG, Zoetendal EG, Stroes ES, Vos WM, Hoekstra JB, Nieuwdorp M. “Transfer of Intestinal Microbiota from Lean Donors Increases Insulin Sensitivity in Individuals with Metabolic Syndrome.” Gastroenterology 143.4 (Oct 2012): 913-6.e7.   

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Vegetable Stew

Serves 4
Prep Time: 10 minutes
Cook Time: 50 minutes


2 TBSP coconut oil
12 baby onions, peeled but kept whole
1/2 medium red pepper, cut into large chunks
1/2 medium green pepper, cut into large chunks
2 medium sweet potatoes, peeled and cut into 1-inch cubes
1 small butternut squash, peeled and cut into 1-inch cubes
1 tsp ground coriander
1 tsp ground cumin
1/2 tsp ground cinnamon
Sea salt, to taste
1 (14 oz) can diced tomatoes
1 TBSP tomato paste
1 (14 oz) can vegetable stock
1 large zucchini, cut into large chunks
1/2 small head savoy cabbage, cored and sliced lengthways
2 TBSP coconut cream
2 TBSP fresh cilantro, chopped, for garnish
1 lime, cut into wedges, for garnish

The Method

  1. Heat the coconut oil in a large soup pot over medium-high heat. Add the onions and sauté for 5 minutes, or until they start to soften and turn brown in spots.
  2. Add the red and green peppers. Cook, stirring occasionally, for 4 minutes.
  3. Add the sweet potato, butternut squash, coriander, cumin, cinnamon, and a heaping pinch of salt. Cook, stirring occasionally, for 2 minutes
  4. Add the diced tomatoes, tomato paste, and vegetable stock. Stir to combine. Bring to a boil, cover, reduce heat to medium-low, and simmer for 30 minutes.
  5. Add the zucchini and cabbage. Cook, uncovered, an additional 10 minutes.
  6. Remove pot from heat and stir in the coconut cream. Season with additional salt, if desired. Spoon soup into serving bowls and garnish with chopped cilantro and lime wedges.

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Episode 90: Statins for Everyone!

On today’s show: Find out why I’m annoyed by the lack of journalistic excellence in reporting the new guidelines on statins; transfats may be banned all together; health benefits of vegetable oils questioned; red meat consumption linked to diabetes; and how saying no to McDonald’s can be dangerous. Sriracha lessons in the Moment of Paleo. After the Bell includes clips from Statin Nation, a sales rep turns Whistleblower, and the Triumphs of Experience from the TakeAway.

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