Useful Info On Covid-19

For covid-19, data has been coming out. Two things to keep in mind are the incubation period and the latent period. The incubation period is the time from when the individual is infected to when they show symptoms, although there are asymptomatic cases where no symptoms are experienced at all.

The average incubation period is 3 days, but it can be as short as 2 days or maybe as long as 21 days or even 24 days. The upper end is rare. Quarantine for 14 days was assumed to be sufficient for nearly all patients. Even a quarantine of less than that, if implemented strictly and widely, presumably would eliminate most infections. Is that true?

More important is the latent period. This is how long it takes from being infected to the onset of symptoms. Keep in mind that, as I understand it, covid-19 is not more contagious than the common flu with any single exposure. Rather, there is a longer potential exposure period which translates as a higher infection rate.

It’s not clear how long one carries the virus and can pass it on to others. Doctors detected the RNA of the virus in the lungs 20 days after infection. And in a study, the pathogen was found in the respiratory tract for much longer, upwards of 37 days. However, carrying the virus doesn’t necessarily mean one is infectious.

For mild cases which is most cases, the infectious period following symptoms doesn’t likely last more than 10 days, even as the virus still can be detected. To demonstrate this, researchers used samples from patients (sputum, blood, urine, stool) to try to grow the virus. On day 8, they failed to do so with patients of mild infections.

So, the fact that some can test positive for weeks might be largely irrelevant. Most patients stop what is called viral shedding in the first 5 days, although in a minority of patients with severe sickness it can go some days beyond that. The extreme cases involved pneumonia and the viral shedding continued for 10-11 days. Still, generally speaking, the most infectious period is those first few days.

Also, keep in mind that not everyone is equally infectious. An elderly couple went on a cruise ship together for a couple of weeks. The wife got infected and presumably was sick for the entire two weeks and yet the husband remained free of infection.

Someone with symptoms may infect no one else while someone without symptoms could easily infect many. It is about 1.2% of covid-19 patients that show no symptoms. On the Diamond Princess cruise ship, 322 of 621 people tested positive with no symptoms. That makes containment difficult, especially with limited ability to do testing.

About symptoms, here is a key piece of info. In a small but significant number of cases, there are no symptoms at all. In many other cases, the symptoms are minor or even atypical. We mostly hear from the media about the respiratory problems, but it can be seen in other ways. Nearly half (48.5%) of patients had digestive issues such as diarrhea, vomiting, and abdominal pain. And about 7% showed no respiratory symptoms at all.

There are other symptoms as well. Most recently, it’s been found that loss of taste and smell can be a sign of infection. About half of patients, in one cluster from Germany, experienced a change in smell or taste. Sensory loss usually follows respiratory symptoms, although not always. Another symptom is redness around the eyes, as seen in some of the worst cases.

Those without the typical respiratory problems and higher temperature don’t see a doctor or only do so much later. This can actually make these cases more severe with a longer recovery period. Yet for some reason, few people are talking about the full spectrum of potential symptoms. In many lists of symptoms, gastrointestinal distress is not mentioned at all. And the loss of senses is only now being reported on.

Bonus info: A mouse study showed that ketosis has protectin against influenza (flu). Coronavirus is different in many ways, but the body deals with viruses through the same basic mechanisms. Ketosis causes the body to produce a special kind of T cell in the lungs and also a protective layer of mucose in the lungs. The survival rate of mice was higher for the mice on a keto diet.

This might be a similar reason why ketosis is inefficient in producing excess heat. Ben Bikman speculates this has to do with the time of year, winter, when ketosis tends to happen. While fasting or in dietary restriction during winter, it would be useful for both the body to produce extra heat and for the immune system to shift into higher functioning.

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Coronavirus may incubate for longer than we thought–which means quarantines may have been too short
by Joseph Guzman

A Person Can Carry And Transmit COVID-19 Without Showing Symptoms, Scientists Confirm
by Aria Bendix

Coronavirus Can Live in Patients for Five Weeks After Contagion
by Claire Che

People ‘shed’ high levels of coronavirus, study finds, but most are likely not infectious after recovery begins
by Helen Branswell

‘Covid-19 most infectious in early days’
by Sumitra Debroy & Malathy Iyer

Lost Sense of Smell May Be Peculiar Clue to Coronavirus Infection
by Roni Caryn Rabin

Study: Nearly half of COVID-19 patients experience digestive issues
by Joseph Guzman

Diarrhea Could Be First Sign Of Coronavirus Infection, Study Says
by Jan Cortes

Doctors say pink eye with other key symptoms may represent COVID-19 cases
from Chron

Plant-Based Nutritional Deficiencies

The purpose here is to highlight the nutritional deficiencies of plant-based diets but most specifically plant-exclusive diets such as veganism (important nutrients are listed below). Not all of these deficiencies involve essential nutrients, but our knowledge is limited on what is essential. There are deficiencies that will kill you quickly, others slowly, and still others that simply will cause deteriorating health or less than optimal functioning. Also, some of these nutrients or their precursors can be found in plant foods or otherwise produced by the body, but there can be several problems. The plant-based sources may be inadequate or not in the most bioavailable form, antinutrients in the plants may block the absorption of certain nutrients (e.g., phytates block mineral absorption), gut and microbiome problems related to a plant-based diet might interfere with absorption, and most people have severely limited capacity to turn certain precursors into the needed nutrients.

So, when eating a supposedly healthy diet, many vegans and vegetarians still have major deficiencies, even with nutrients that should be in their diet according to standard food intake calculations — in those cases, the nutrients are there in theory but for some reason not being absorbed or utilized. For example, raw spinach has a lot of calcium, but it is almost entirely unavailable to the body. Adding raw spinach to your smoothie or salad might be a net loss to your health, as the antinutrients will block the nutrients in other foods as well. Another factor is that, on a plant-based diet, nutrients can get out of ratio. Nutrients work together with some acting as precursors, others as catalysts, and still others like master hormones — such as vitamin K2 determining where calcium is transported to, preferably the bones as opposed to arteries, joints and the brain; or think about how the body can produce vitamin D3 but only if there is adequate cholesterol. As such, besides deficiencies, sometimes there can too much of a nutrient which interferes with another nutrient, as seen with copper in relation to zinc.

That is the advantage to an animal-based diet, which could even include a well-balanced vegetarian diet that emphasized dairy and eggs (Vegetarianism is an Animal-Based Diet), but unfortunately many vegetarians are near-vegan in limiting even those non-meat animal foods. Here is the reason why animal foods are so important. Other animals have similar nutritional needs as humans and so, when we eat animal foods, we are getting not only the nutrients our bodies need but in the required form and ratio for our own optimal functioning. Without animal foods, one has to study nutrition to understand all of this and then try to artificially re-create it through careful calculations in balancing what one eats and supplements, an almost impossible task that requires someone to have a scientific mindset. Even then, one is likely to get it wrong. Regular testing of nutritional levels would be absolutely necessary to ensure everything is going according to plan.

As for supplements and fortification, the nutrients aren’t always in the best form and so wouldn’t be as bioavailable nor would likely have all the needed cofactors in just the right amounts. Besides, a diet dependent on supplementation and fortification is not healthy by definition, in that the food itself in natural form lacksing those nutrients. The fact that most vegans in particular and vegetarians as well have to be extremely obsessive about nutrition just to maintain a basic level of health is not high praise to the health-giving benefits of such a plant-based diet — and hence the reason even vegetarians should emphasize the allowed animal foods (there are even vegans who will make exceptions for some animal foods, such as fish). This is probably why most people quit these diets after a short period of time and why most people who quit, including those who quit after years or decades, do so for health reasons. Among those who remain on these diets, their responses on surveys show that most of them cheat on occasion and so are getting some minimal level of animal-based nutrition, and that is a good thing for their health even as it calls into question the validity of health claims about plant-based diets (Being “mostly vegan” is like being “a little pregnant.”).

There has long been a bias against meat, especially red meat. It goes back to the ancient Greek thought of Galen and how it was adapted to Medieval society in being Christianized for purposes of maintaining social hierarchy and social control. This Galenic bias was carried forward in the Christian tradition and then modernized within nutrition studies through the surprisingly powerful influence of the Seventh Day Adventists who continue to fund a lot of nutritional studies to this day. This has had practical consequences. It has long been assumed, based on a theology of a sinful world, that eating animals would make us beastly. It’s similar to the ancient idea that eating the muscles or heart of a fallen warrior would make one strong or courageous. A similar logic was applied to plants, that they have inherent qualities that we can imbibe.

So, it has been long believed that plant foods are somehow healthier for both body and soul, somehow more spiritual and so would bring humans closer to God or else closer to their divine natural state before the Fall of Man. That has been the moral concern of many Christians, from Medieval Catholics to modern Seventh Day Adventists. And in secularized form, it became internalized by mainstream nutrition studies and dietary guidelines. Part of the purpose of eating plants, according to Christianized Galenism, was that a strong libido was considered bad and it was understood that a plant-based diet suppressed libido, which admittedly doesn’t sound like a sign of health but their idea of ‘health’ was very different. It was also worried that, along with firing up the libido, meat would heat up the entire body and would lead to a shorter lifespan. Pseudo-scientific explanations have been used to rationalize this theological doctrine, such as concerns about mTOR and IGF-1, although this requires contorting the science and dismissing other evidence.

The problem is this simply became built into mainstream nutritional ideology, to such an extent that few questioned it until recently. This has led to most researchers, nutritionists, dieticians, and other health experts to obsess over the nutrients in plants while overlooking the nutrients in animal foods. So, you’ll hear something along the lines of, “meat is not an important source of vitamin E and with the exception of liver, is not a particularly good source of fat-soluble vitamins” (Nutrients in Meat, from the Meat We Eat). Keep in mind that assertion comes from a project of the American Meat Science Association — not likely to be biased against meat. It’s sort of true, depending on how one defines meat. From Galenic thought, the notion of meat is still associated with red meat. It is true that muscle meat, particularly lean muscle meat, from beef, pork and veal doesn’t have much vitamin E compared to plant foods (M. Leonhardt et al, Vitamin E content of different animal products: influence of animal nutrition). This is why some vegetarians and even vegans see no contradiction or conflict, much less hypocrisy, in eating fish and fowl — culturally, these have for millennia been considered a separate category from meat.

Yet adequate amounts of vitamin E are found in many animal foods, whether or not we label them as ‘meat’: chicken, goose meat, fish, seafood, crayfish, butter, and cheese; and some vitamin E is also found in liver and eggs (Atli Anarson, 20 Foods That Are High in Vitamin E). We have to be clear what we mean by ‘meat’. On a meat-based diet, even to the degree of being carnivore, there are plentiful good sources of every essential nutrient, including vitamin E, and many that aren’t essential but highly conducive to optimal health. Besides animal foods, there is no other source of such immense nutrient-density and nutrient-biavailability. Plant foods don’t come close in comparison.

Also, as vitamin E is an antioxidant, it’s important to note that animal foods contain many other antioxidants that play a similar role in maintaining health, but animal-sourced antioxidants have been mostly ignored because they don’t fit the dominant plant-based paradigm. Plant foods lack these animal-sourced antioxidants. So why do so few talk about a deficiency in them for vegans and vegetarians? And why have researchers so rarely studied in depth the wide variety of nutrients in animal foods to determine their full health benefits? This is particularly odd when considering, as I already stated, every known essential nutrient can be found in animal foods but not in plant foods. Isn’t that an important detail? Why is there a collective silence among mainstream health experts?

Think about how plant antinutrients can block the absorption of nutrients, both in plant foods and animal foods, and so require even more nutrients to counteract this effect which might simply further increase the antinutrient intake, unless one is careful in following the food selection and preparation as advised by those like Steven Gundry (The Plant Paradox). Or think about how glucose competes with the antioxidant vitamin C causing an increase of scurvy if vitamin C is not increased, and yet a low-carb diet with far lower intake of vitamin C is not linked to scurvy — maybe the reason ancient Vikings and Polynesians could remain healthy at sea for months, but once a high-carb diet was introduced modern sailors were plagued by scurvy (Sailors’ Rations, a High-Carb Diet). Similarly, a plant-based diet in general might require greater amounts of vitamin E: “Plant-based foods have higher concentrations of vitamin E. And for good reason. A plant-based diet requires additional protection from oxidation of PUFA which Vitamin E helps provide through its antioxidant properties. It’s still found in adequate supply in meat” (Kevin Stock, Vitamins and Minerals – Plants vs Animals).

What is adequate depends on the diet. A diet low in carbs, seed oils, and other plant foods may require fewer plant-based antioxidants, especially if this is countered by an increase of animal-based antioxidants. It is reminiscent of the fiber debate. Yes, fiber adds bulk that supposedly will increase regularity, ignoring the fact that the research is divided on this topic. No doubt bulking up your poop makes you have larger poops and more often, but is that really a good thing? People on a low-residue carnivore diet more easily digest and absorb what the eat, and so they don’t have bulky poops — then again they don’t usually have constipation either, not if they’re getting enough dietary fat. The main cause of constipation is plant foods. So, why are people advised to eat more plant foods in the hope of resolving this issue caused by plant foods? It’s absurd! We keep looking at problems in isolation, as we look at nutrients in isolation (Hubris of Nutritionism). This has failed us, as demonstrated by our present public health crisis.

Let me throw in a last thought about antioxidants. It’s like the fiber issue. People on plant-based diets have contipation issues and so they eat more plant foods in the form of fiber in trying to solve the problem plant foods cause, not realizing that constipation generally resolves itself by eliminating or limiting plant foods. So, in relation to antioxidants, we have to ask ourselves what is it about our diet in the first place that is causing all the oxidative stress? Plant foods do have antioxidants, but some plant foods also cause oxidative stress (e.g., seed oils). If we eliminate these plant foods, our oxidative stress goes down and so our requirement of antioxidants to that degree also lessens. Our body already produces its own antioxidants and, combined with what comes from animal foods, we shouldn’t such excess amounts of antioxidants. Besides, it’s not clear from studies that plant antioxidants are always beneficial to health. It would be better to eliminate the need for them in the first place. Shawn Baker explained this in terms of vitamin C (interview with Shan Hussain, The Carnivore Diet with Dr. Shawn Baker MD):

“The Carnivore diet is deficient in carbohydrates and essential vitamins like Vitamin C, how do we make up for that? When I wanted to do this I was curious about this as well. You will see a number of potential deficiencies around this diet. There is no role of fibre in this diet. With Vitamin C we know there are some transporters across different cell membranes. In a higher glucose environment, Vitamin C is competitively inhibited and therefore we see less absorption of Vitamin C. We also see that interestingly human red blood cells do have the capacity to actually recycle Vitamin C which is something that not many people are aware of. One of the major function of Vitamin C is that it is an antioxidant. In low carbohydrate states our antioxidants systems particularly things like glutathione are regulated. We may obviate some of the need of antioxidants of the Vitamin C by regulating around systems in a low carb diet. Also, Vitamin C is very important in the function of carnitine which is part of the fat cycle. When we are ingesting carnitine we have actual transporters in the gut which can take up full carnosine. It is a misconception that we can only take amino acids, a number of di and tripeptide transporters that are contained within our gut. The other function of Vitamin C is when we don’t have sufficient Vitamin C relative to our needs, we start to develop symptoms of scurvy, bleeding gum problems, teeth falling out, sores and cuts won’t heal. This is all due to the collagen synthesis. If we look at Vitamin C’s role in collagen synthesis, it helps to take proline and lysine, hydroxyproline and hydroxylysine. In meat-based diet, we are getting that in ample amount. Even a steak has 3% of its content as collagen. There are all kinds of compensatory mechanisms.”

I’ll end on an amusing note. Chris Kresser wrote about the carnivore diet (Everything You Need to Know about the Carnivore Diet and How It Can Affect Your Health). Athough an advocate of low-carb diets and nutrient-dense animal foods, he is skeptical that carnivory will be healthy for most humans long-term. One worry is that there might be nutritional deficiencies, but the argument he makes is funny. He basically saying that if all one eats is muscle meat then key nutrients will get missed. Then he goes onto point out that these nutrients can be found in other animal foods, such as liver and dairy. So, his main concern about a carnivore diet is actually that people might not eat enough animal foods or rather not enough of certain animal foods. So, make sure you eat lots of a wide variety of animal foods if going full carnivore and apparently even critics like Kresser agree you’ll be fine, at least nutritionally. The problem isn’t too much animal foods but potentially too little. That made me smile.

Now to the whole point of this post. Below is a list of nutrients that are commonly deficient in those on plant-based diets, especially those on plant-exclusive diets (i.e., vegans). I won’t explain anything about these nutrients, as there is plenty of info online. But you can look to the linked articles below that cover the details.

  • Vitamin K2 (MK-4)
  • Vitamin D3 (Cholecalciferol)
  • Vitamin A (Retinol)
  • Vitamin B12 (Cobalamin)
  • Vitamin B6 (Pyridoxine)
  • B3 (Niacin)
  • B2 (Riboflavin)
  • Calcium
  • Heme Iron
  • Zinc
  • Selenium
  • Iodine
  • Sulfur
  • Creatine
  • Beta-Alanine
  • Carnosine
  • Beta-Alanine (Precursor to Carnosine)
  • L-Carnitine
  • Taurine
  • Choline
  • Coenzyme Q10 (CoQ10)
  • Phytanic Acid
  • DHA Omega-3 (Docosahexaenoic Acid)
  • EPA Omega-3 (Eicosapentaenoic Acid)
  • DPA Omega-3 (Docosapentaenoic Acid)
  • ARA Omega-6 (Arachidonic Acid)
  • CLA (Conjugated Linoleic Acid)
  • Phosphatidylserin
  • Cholesterol
  • Collagen
  • Complete Protein
  • Glutathione
  • Glycine
  • Essential Amino Acids (Methionine, Tryptophan, Lysine, Leucine, Cysteine, Proline, Tyrosine, Phenylalanine, Serine, Alanine, Threonine, Isoleucine and Valine)

Just for the sake of balance, I’ll also share a list of plant compounds that are problematic for many people — from Joe Cohen (20 Nutrients that Vegans & Vegetarians are Lacking):

  1. Lectins
  2. Amines
  3. Tannins
  4. Trypsin Inhibitors
  5. FODMAPS
  6. Salicylates
  7. Oxalates
  8. Sulfites, Benzoates, and MSG
  9. Non-protein amino acids
  10. Glycosides
  11. Alkaloids [includes solanine, chaconine]
  12. Triterpenes
  13. Lignins
  14. Saponins
  15. Phytic Acid [Also Called Phytate]
  16. Gluten
  17. Isoflavones

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Are ‘vegetarians’ or ‘carnivores’ healthier?
Gundry’s Plant Paradox and Saladino’s Carnivory
Dr. Saladino on Plant and Animal Foods
True Vitamin A For Health And Happiness
Calcium: Nutrient Combination and Ratios
Vitamin D3 and Autophagy

The Vegetarian Myth: Food, Justice, and Sustainability
by Lierre Keit

Vegan Betrayal: Love, Lies, and Hunger in a Plants-Only World
by Mara J. Kahn

The Meat Fix: How a lifetime of healthy eating nearly killed me!
by John Nicholson

The Fat of the Land/Not By Bread Alone
by Vilhjalmur Stefansson

Sacred Cow: The Case for (Better) Meat: Why Well-Raised Meat Is Good for You and Good for the Planet
by Diana Rodgers and Robb Wolf

The Carnivore Code: Unlocking the Secrets to Optimal Health by Returning to Our Ancestral Diet
by Paul Saladino

Primal Body, Primal Mind: Beyond Paleo for Total Health and a Longer Life
by Nora Gedgauda

Paleo Principles
by Sarah Ballantyn

 
The Queen of Fats: Why Omega-3s Were Removed from the Western Diet and What We Can Do to Replace Them
by Susan Allport

The Omega Principle: Seafood and the Quest for a Long Life and a Healthier Planet
by Paul Greenberg

The Omega-3 Effect: Everything You Need to Know About the Super Nutrient for Living Longer, Happier, and Healthier
by William Sears and James Sear

The Missing Wellness Factors: EPA and DHA: The Most Important Nutrients Since Vitamins?
by Jorn Dyerberg and Richard Passwater

Could It Be B12?: An Epidemic of Misdiagnoses
by Sally M. Pacholok and Jeffrey J. Stuar

What You Need to Know About Pernicious Anaemia and Vitamin B12 Deficiency
by Martyn Hooper

Living with Pernicious Anaemia and Vitamin B12 Deficiency
by Martyn Hoope

Pernicious Anaemia: The Forgotten Disease: The causes and consequences of vitamin B12 deficiency
by Martyn Hooper

Healing With Iodine: Your Missing Link To Better Health
by Mark Sircus

Iodine: Thyroid: The Hidden Chemical at the Center of Your Health and Well-being
by Jennifer Co

The Iodine Crisis: What You Don’t Know About Iodine Can Wreck Your Life
by Lynne Farrow

L-Carnitine and the Heart
by Stephen T. Sinatra and Jan Sinatra

Food Politics: How the Food Industry Influences Nutrition and Health
by Marion Nestle

Unsavory Truth: How Food Companies Skew the Science of What We Eat
by Marion Nestle

Formerly Known As Food: How the Industrial Food System Is Changing Our Minds, Bodies, and Culture
by Kristin Lawless

Death by Food Pyramid: How Shoddy Science, Sketchy Politics and Shady Special Interests Have Ruined Our Health
by Denise Minge

Nutrition in Crisis: Flawed Studies, Misleading Advice, and the Real Science of Human Metabolism
by Richard David Feinman

Nutritionism: The Science and Politics of Dietary Advice
by Gyorgy Scrinis

Measured Meals: Nutrition in America
by Jessica J. Mudry

(Although more about macronutrients, also see the work of Gary Taubes and Nina Teicholz. They add useful historical context about nutrition studies, dietary advice, and public health.)

20 Nutrients that Vegans & Vegetarians are Lacking
by Joe Cohen

8 Nutrients You May Be Missing If You’re Vegetarian or Vegan
by Tina Donvito

7 Nutrients That You Can’t Get from Plants
by Atli Anarson

7 Supplements You Need on a Vegan Diet
by Alina Petre

The Top 5 Nutrient Deficiencies on a Plant Based Diet
by Kate Barrington

5 Brain Nutrients That You Can’t Get From Plants
by Kris Gunnars

Vitamin Supplements for Vegetarians
by Jeff Takacs

Health effects of vegan diets
by Winston J Craig

Nutritional Deficiencies and Essential Considerations for Every Vegan (An Evidence-Based Nutritional Perspective)
from Dai Manuel

Why You Should Think Twice About Vegetarian and Vegan Diets
by Chris Kresser

Three Big Reasons Why You Don’t Want to be a Vegetarian
by Alan Sears

How to Avoid Common Nutrient Deficiencies if You’re a Vegan
by Joseph Mercola

What is Glutathione and How Do I Get More of It?
by Mark Hyman

Could THIS Be the Hidden Factor Behind Obesity, Heart Disease, and Chronic Fatigue?
by Joseph Mercola

Vegetarianism produces subclinical malnutrition, hyperhomocysteinemia and atherogenesis
by Y. Ingenbleek Y and K. S. McCully

Vegan Diet is Sulfur Deficient and Heart Unhealthy
by Larry H. Bern

Heart of the Matter : Sulfur Deficits in Plant-Based Diets
by Kaayla Daniel

Copper-Zinc Imbalance: Unrecognized Consequence of Plant-Based Diets and a Contributor to Chronic Fatigue
by Laurie Warner

Vegan diets ‘risk lowering intake of nutrient critical for unborn babies’ brains’
by Richard Hartley-Parkinson

The Effects of a Mother’s Vegan Diet on Fetal Development
by Marc Choi

Vegan–vegetarian diets in pregnancy: danger orpanacea? A systematic narrative review
by G. B. Piccoli

Is vegetarianism healthy for children?
by Nathan Cofnas

Clinical practice: vegetarian infant and child nutrition
by M. Van Winckel, S. Vande Velde, R. De Bruyne, and S. Van Biervliet

Dietary intake and nutritional status of vegetarian and omnivorous preschool children and their parents in Taiwan
C. E. Yen, C. H. Yen, M. C. Huang, C. H. Cheng, and Y. C. Huang

Persistence of neurological damage induced by dietary vitamin B-12 deficiency in infancy
by Ursula von Schenck, Christine Bender-Götze, and Berthold Koletzko

Severe vitamin B12 deficiency in an exclusively breastfed 5-month-old Italian infant born to a mother receiving multivitamin supplementation during pregnancy
by S. Guez et al

Long-chain n-3 PUFA in vegetarian women: a metabolic perspective
by G. C. Burdge, S. Y. Tan, and C. J. Henry

Signs of impaired cognitive function in adolescents with marginal cobalamin status
by M. W. Louwman et al

Transient neonatal hypothyroidism due to a maternal vegan diet
by M. G. Shaikh, J. M. Anderson, S. K. Hall, M. A. Jackson

Veganism as a cause of iodine deficient hypothyroidism
by O. Yeliosof and L. A. Silverman

Do plant based diets deprive the brain of an essential nutrient?
by Ana Sandoiu

Suggested move to plant-based diets risks worsening brain health nutrient deficiency
from BMJ

Could we be overlooking a potential choline crisis in the United Kingdom?
by Emma Derbyshire

How a vegan diet could affect your intelligence
by Zaria Gorvett

Vitamins and Minerals – Plants vs Animals
by Kevin Stock

Health effects of vegan diets
by Winston J Craig

Comparing Glutathione in the Plasma of Vegetarian and Omnivore Populations
by Rachel Christine Manley

Vegan diets are adding to malnutrition in wealthy countries
by Chris Elliott, Chen Situ, and Claire McEvoy

What beneficial compounds are primarily found in animal products?
by Kamal Patel

The Brain Needs Animal Fat
by Georgia Ede

The Vegan Brain
by Georgia Ede

Meat, Organs, Bones and Skin
by Christopher Masterjohn

Vegetarianism and Nutrient Deficiencies
by Christopher Masterjohn

Adding milk, meat to diet dramatically improves nutrition for poor in Zambia
from Science Daily

Red meat plays vital role in diets, claims expert in fightback against veganism
by James Tapper

Nutritional Composition of Meat
by Rabia Shabir Ahmad, Ali Imran and Muhammad Bilal Hussain

Meat and meat products as functional food
by Maciej Ostaszewski

Meat: It’s More than Protein
from Paleo Leap

Conjugated Linoleic Acid: the Weight Loss Fat?
from Paleo Leap

Nutritional composition of red meat
by P. G. Williams

How Red Meat Can ‘Beef Up’ Your Nutrition
by David Hu

Endogenous antioxidants in fish
by Margrét Bragadóttir

Astaxanthin Benefits Better than Vitamin C?
by Rachael Link

Astaxanthin: The Most Powerful Antioxidant You’ve Never Heard Of
from XWERKS

Antioxidants Are Bullshit for the Same Reason Eggs Are Healthy
by Sam Westreich

We absolutely need fruits and vegetables to obtain optimal antioxidant status, right?
by Paul Saladino

Hen Egg as an Antioxidant Food Commodity: A Review
Chamila Nimalaratne and Jianping Wu

Eggs’ antioxidant properties may help prevent heart disease and cancer, study suggests
from Science Daily

The Ultimate Superfood? Milk Offers Up a Glass Full of Antioxidants
by Lauren Milligan Newmark

Antioxidant properties of Milk and dairy products: a comprehensive review of the current knowledge
by Imran Taj Khan et al

Antioxidants in cheese may offset blood vessel damage
from Farm and Dairy

Identification of New Peptides from Fermented Milk Showing Antioxidant Properties: Mechanism of Action
by Federica Tonolo

Bioavailability of iron, zinc, and other trace minerals from vegetarian diets
by Janet R Hunt

Dietary iron intake and iron status of German female vegans: results of the German vegan study.
by A. Waldmann, J. W. Koschizke, C. Leitzmann, and A. Hahn

Mechanisms of heme iron absorption: Current questions and controversies
by Adrian R. West and Phillip S. Oates

Association between Haem and Non-Haem Iron Intake and Serum Ferritin in Healthy Young Women
by Isabel Young et al

Pork meat increases iron absorption from a 5-day fully controlled diet when compared to a vegetarian diet with similar vitamin C and phytic acid content.
by M. Bach Kristensen, O. Hels, C. Morberg, J. Marving, S. Bügel, and I. Tetens

Do you need fiber?
by Kevin Stock

Ketosis, Epigenetics, and the Brain

It’s long been understood that ketones, specifically beta-hydroxybutyrate (BHB), are a brain superfuel. It’s easy to explain the evolutionary reasons for this. Hunter-gatherers spent much more time in ketosis. This metabolic state tends to occur during periods of low food access. That happens in winter but also throughout the year, as hunter-gatherers tend toward a feast and fast pattern.

After a period of plenty, it might be a while until the next big kill. Some hunting expeditions could take days or weeks. They needed their brains working in top form for a successful hunt. Many hunter-gatherer tribes purposely fast on a regular basis as a demonstration of their toughness, to show that they can go long periods without food, a very important ability for hunters. Even tribal people living amongst food abundance will fast for no particular reason other than it’s part of their culture.

The Piraha, for example, can procure food easily and yet will go without, sometimes simply because they’d rather socialize around the village or are in the middle of communal dancing that can go on for days. They have better things to do than eat all the time. Besides, on a low-carb diet that is typical among hunter-gatherers, it takes little effort to fast. That is one of the benefits of ketosis, one’s appetite is naturally suppressed and so it effortlessly promotes caloric restriction.

Along with improving brain function, ketosis increases general health, probably including extending lifespan and certainly extending healthspan. Some of this could be explained by creating the conditions necessary for autophagy, although there are many other factors. An interesting example of this was shown in a mouse study.

The researchers exposed the rodents to influenza (E. L. Goldberg et al, Ketogenic diet activates protective γδ T cell responses against influenza virus infection). Most of the mice on a high-carb diet died, whereas most on the keto diet lived. In this case, it wasn’t the ketones themselves but other processes involved. Giving exogenous ketones as a supplement did not have the same effect as the body producing its own ketones. We typically think of ketosis only in terms of ketones, but obviously there is much more going on.

Still, in the case of neurocognitive functioning, the ketones themselves are key. It’s not only that they act as a superfuel but simultaneously alter epigenetic expression of specific genes related to memory. On the opposite side, research shows that feeding people sugar literally makes them dumber. Ketosis also decreases inflammation, including inflammation in the brain. Through multiple causal mechanisms, ketosis has been medically used as an effective treatment for numerous neurocognitive conditions: mood disorders, schizophrenia, autism, ADHD, Alzheimer’s, etc.

If ketosis is a biological indicator of food scarcity, why does the body expend extra energy that is limited? This seems counter-intuitive. Other species deal with food scarcity by shutting the body down and slowing metabolism, some going into full hibernation or semi-hibernation during winter. But humans do the opposite. Food scarcity increases physiological activity. In fact, ketosis is actually inefficient, as it burns more energy than is needed with the excess being put off as heat.

Benjamin Bikman, an insulin researcher, speculates this is because ketosis often happens in winter. Hibernating creatures lower their body temperature, but humans don’t have this capacity. Neither do we have thick fur. Humans need large amounts of heat to survive harsh winters. In ketosis, everything goes into overdrive: metabolism, immune system, and brain. This alters the epigenome itself that can be passed onto following generations.

* * *

You Are What Your Mother and Father (and Grandmothers and Grandfathers) Ate
by Mark Sisson

Epigenetic Explanations For Why Cutting Sugar May Make You Feel Smarter
by Caitlin Aamodt

High Fat, Low Carb Diet Might Epigenetically Open Up DNA and Improve Mental Ability
by Bailey Kirkpatrick

Epigenetics May Provide Relief for Fragile X Syndrome and Intellectual Disorders
by Tim Barry

To Empathize is to Understand

What is empathy as a cognitive ability? And what is empathy as an expansion of identity, as part of awareness of self and other?

There is a basic level of empathy that appears to be common across numerous species. Tortoises, when seeing another on its back, will help flip it over. There are examples of animals helping or cooperating with those from an entirely different species. Such behavior has been repeatedly demonstrated in laboratories as well. These involve fairly advanced expressions of empathy. In some cases, one might interpret it as indicating at least rudimentary theory of mind, the understanding that others have their own experience, perspective, and motivations. But obviously human theory of mind can be much more complex.

One explanation about greater empathy has to do with identity. Empathy in a way is simply a matter of what is included within one’s personal experience (Do To Yourself As You Would Do For Others). To extend identity is to extend empathy to another individual or a group (or anything else that can be brought within sphere of the self). For humans, this can mean learning to include one’s future self, to empathize with experience one has not yet had, the person one has not yet become. The future self is fundamentally no different than another person.

Without cognitive empathy, affective empathy is limited to immediate experience. It’s the ability to feel what another feels. But lacking cognitive empathy as happens in the most severe autism, theory of mind cannot be developed and so there is no way to identity, locate and understand that feeling. One can only emotionally react, not being able to differentiate one’s own emotion from that of another. In that case, there would be pure emotion, and yet no recognition of the other. Cognitive empathy is necessary to get beyond affective reactivity, not all that different than the biological reactivity of a slug.

It’s interesting that some species (primates, rats, dolphins, etc) might be able to have more cognitive empathy and theory of mind than some people at the extreme ends of severe autism, not necessarily being an issue of intelligence. On the other hand, the high functioning on the autistic spectrum, if intervention happens early enough, can be taught theory of mind, although it is challenging for the. This kind of empathy is considered a hallmark of humanity, a defining feature. This is what leads to problems of social behavior for those with autism spectrum disorder.

Someone entirely lacking in theory of mind would be extremely difficult to communicate and interact with beyond the most basic level, as is seen in the severest cases of autism and other extreme developmental conditions. Helen Keller asserts she had no conscious identity, no theory of her own mind or that of others, until she learned language.* Prior to her awakening, she was aggressive and violent in reacting to a world she couldn’t understand, articulate, or think about. That fits in with the speculations of Julian Jaynes. What he calls ‘consciousness’ is the addition of abstract thought by way of metaphorical language, as built upon concrete experience and raw affect. Keller discusses how her experience went from from the concreteness of touch to the abstraction of language. In becoming aware of the world, she became aware of herself.

Without normal development of language, the human mind is crippled: “The “black silence” of the deaf, blind and mute is similar in many respects to the situation of acutely autistic children where there are associated difficulties with language and the children seem to lack what has been called “a theory of mind” ” (Robin Allott, Helen Keller: Language and Consciousenss). Even so, there is more to empathy than language, and that might be true as well for some aspects or kinds of cognitve empathy. Language is not the only form of communication.

Rats are a great example in comparing to humans. We think of them as pests, as psychologically inferior. But anyone who has kept rats knows how intelligent and social they are. They are friendlier and more interactive than the typical cat. And research has shown how cognitively advanced they are in learning. Rats do have the typical empathy of concern for others. For example, they won’t hurt another rat in exchange for a reward and, given a choice, they would rather go hungry. But it goes beyond that.

It’s also shown that “rats are more likely and quicker to help a drowning rat when they themselves have experienced being drenched, suggesting that they understand how the drowning rat feels” (Kristin Andrews, Rats are us). And “rats who had been shocked themselves were less likely to allow other rats to be shocked, having been through the discomfort themselves.” They can also learn to play hide-and-seek which necessitates taking on the perspective others. As Ed Yong asks in The Game That Made Rats Jump for Joy, “In switching roles, for example, are they taking on the perspective of their human partners, showing what researchers call “theory of mind”?”

That is much more than mere affective empathy. This seems to involve active sympathy and genuine emotional understanding, that is to say cognitive empathy and theory of mind. If they are capable of both affective and cognitive empathy, however limited, and if Jaynesian consciousness partly consists of empathy imaginatively extended in space and time, then a case could be made that rats have more going on than simple perceptual awareness and biological reactivity. They are empathically and imaginatively engaging with others in the world around them. Does this mean they are creating and maintaining a mental model of others? Kristin Andrews details the extensive abilities of rats:

“We now know that rats don’t live merely in the present, but are capable of reliving memories of past experiences and mentally planning ahead the navigation route they will later follow. They reciprocally trade different kinds of goods with each other – and understand not only when they owe a favour to another rat, but also that the favour can be paid back in a different currency. When they make a wrong choice, they display something that appears very close to regret. Despite having brains that are much simpler than humans’, there are some learning tasks in which they’ll likely outperform you. Rats can be taught cognitively demanding skills, such as driving a vehicle to reach a desired goal, playing hide-and-seek with a human, and using the appropriate tool to access out-of-reach food.”

To imagine the future for purposes of thinking in advance and planning actions, that is quite advanced cognitive behavior. Julian Jaynes argued that was the purpose of humans developing a new kind of consciousness, as the imagined metaphorical space that is narratized allows for the consideration of alternatives, something he speculates was lacking in humans prior to the Axial Age when behavior supposedly was more formulaic and predetermined according to norms, idioms, etc. Yet rats can navigate a path they’ve never taken before with novel beginning and ending locations, which would require taking into account multiple options. What theoretically makes Jaynesian consciousness unique?

Jaynes argues that it’s the metaphorical inner space that is the special quality that created the conditions for the Axial Age and all that followed from it, the flourishing of complex innovations and inventions, the ever greater extremes of abstraction seen in philosophy, math and science. We have so strongly developed this post-bicameral mind that we barely can imagine anything else. But we know that other societies have very different kinds of mentalities, such as the extended and fluid minds of animistic cultures. What exactly is the difference?

Australian Aborigines give hint to something between the two kinds of mind. In some ways, the mnemonic systems represent more complex cognitive ability than we are capable with our Jaynesian consciousness. Instead of an imagined inner space, the Songlines are vast systems of experience and knowledge, culture and identity overlaid upon immense landscapes. These mappings of externalized cognitive space can be used to guide the individual across distant territories the individual has never seen before and help them to identify and use the materials (plants, stones, etc) at a location no one in their tribe has visited for generations. Does this externalized mind have less potential for advanced abilities? Upon Western contact, Aborigines had farming and ranching, kept crop surpluses in granaries, used water and land management.

It’s not hard to imagine civilization having developed along entirely different lines based on divergent mentalities and worldviews. Our modern egoic consciousness was not an inevitability and it likely is far from offering the most optimal functioning. We might already be hitting a dead end with our present interiorized mind-space. Maybe it’s our lack of empathy in understanding the minds of other humans and other species that is an in-built limitation to the post-bicameral world of Jaynesian consciousness. And so maybe we have much to learn from entirely other perspectives and experiences, even from rats.

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* Helen Keller, from Light in My Darkness:

I had no concepts whatever of nature or mind or death or God. I literally thought with my body. Without a single exception my memories of that time are tactile. . . . But there is not one spark of emotion or rational thought in these distinct yet corporeal memories. I was like an unconscious clod of earth. There was nothing in me except the instinct to eat and drink and sleep. My days were a blank without past, present, or future, without hope or anticipation, without interest or joy. Then suddenly, I knew not how or where or when, my brain felt the impact of another mind, and I awoke to language, to knowledge, to love, to the usual concepts of nature, good, and evil. I was actually lifted from nothingness to human life.

And from The Story of My Life:

As the cool stream gushed over one hand she spelled into the other the word water, first slowly, then rapidly. I stood still, my whole attention fixed upon the motions of her fingers. Suddenly I felt a misty consciousness as of something forgotten–-a thrill of returning thought; and somehow the mystery of language was revealed to me. I knew then that ‘w-a-t-e-r’ meant the wonderful cool something that was flowing over my hand. That living word awakened my soul, gave it light, hope, joy, set it free! There were barriers still, it is true, but barriers that could in time be swept away.

And from The World I Live In:

Before my teacher came to me, I did not know that I am. I lived in a world that was a no-world. I cannot hope to describe adequately that unconscious, yet conscious time of nothingness. I did not know that I knew aught, or that I lived or acted or desired. I had neither will nor intellect. I was carried along to objects and acts by a certain blind natural impetus. I had a mind which caused me to feel anger, satisfaction, desire. These two facts led those about me to suppose that I willed and thought. I can remember all this, not because I knew that it was so, but because I have tactual memory. It enables me to remember that I never contracted my forehead in the act of thinking. I never viewed anything beforehand or chose it. I also recall tactually the fact that never in a start of the body or a heart-beat did I feel that I loved or cared for anything. My inner life, then, was a blank without past, present, or future, without hope or anticipation, without wonder or joy or faith. […]

Since I had no power of thought, I did not compare one mental state with another. So I was not conscious of any change or process going on in my brain when my teacher began to instruct me. I merely felt keen delight in obtaining more easily what I wanted by means of the finger motions she taught me. I thought only of objects, and only objects I wanted. It was the turning of the freezer on a larger scale. When I learned the meaning of “I” and “me” and found that I was something, I began to think. Then consciousness first existed for me. Thus it was not the sense of touch that brought me knowledge. It was the awakening of my soul that first rendered my senses their value, their cognizance of objects, names, qualities, and properties. Thought made me conscious of love, joy, and all the emotions. I was eager to know, then to understand, afterward to reflect on what I knew and understood, and the blind impetus, which had before driven me hither and thither at the dictates of my sensations, vanished forever.”

I cannot represent more clearly than any one else the gradual and subtle changes from first impressions to abstract ideas. But I know that my physical ideas, that is, ideas derived from material objects, appear to me first an idea similar to those of touch. Instantly they pass into intellectual meanings. Afterward the meaning finds expression in what is called “inner speech.”  […]

As my experiences broadened and deepened, the indeterminate, poetic feelings of childhood began to fix themselves in definite thoughts. Nature—the world I could touch—was folded and filled with myself. I am inclined to believe those philosophers who declare that we know nothing but our own feelings and ideas. With a little ingenious reasoning one may see in the material world simply a mirror, an image of permanent mental sensations. In either sphere self-knowledge is the condition and the limit of our consciousness. That is why, perhaps, many people know so little about what is beyond their short range of experience. They look within themselves—and find nothing! Therefore they conclude that there is nothing outside themselves, either.

However that may be, I came later to look for an image of my emotions and sensations in others. I had to learn the outward signs of inward feelings. The start of fear, the suppressed, controlled tensity of pain, the beat of happy muscles in others, had to be perceived and compared with my own experiences before I could trace them back to the intangible soul of another. Groping, uncertain, I at last found my identity, and after seeing my thoughts and feelings repeated in others, I gradually constructed my world of men and of God. As I read and study, I find that this is what the rest of the race has done. Man looks within himself and in time finds the measure and the meaning of the universe.

* * *

As an example of how language relates to emotions:

The ‘untranslatable’ emotions you never knew you had
by David Robson

But studying these terms will not just be of scientific interest; Lomas suspects that familiarising ourselves with the words might actually change the way we feel ourselves, by drawing our attention to fleeting sensations we had long ignored.

“In our stream of consciousness – that wash of different sensations feelings and emotions – there’s so much to process that a lot passes us by,” Lomas says. “The feelings we have learned to recognise and label are the ones we notice – but there’s a lot more that we may not be aware of. And so I think if we are given these new words, they can help us articulate whole areas of experience we’ve only dimly noticed.”

As evidence, Lomas points to the work of Lisa Feldman Barrett at Northeastern University, who has shown that our abilities to identify and label our emotions can have far-reaching effects.

Her research was inspired by the observation that certain people use different emotion words interchangeably, while others are highly precise in their descriptions. “Some people use words like anxious, afraid, angry, disgusted to refer to a general affective state of feeling bad,” she explains. “For them, they are synonyms, whereas for other people they are distinctive feelings with distinctive actions associated with them.”

This is called “emotion granularity” and she usually measures this by asking the participants to rate their feelings on each day over the period of a few weeks, before she calculates the variation and nuances within their reports: whether the same old terms always coincide, for instance.

Importantly, she has found that this then determines how well we cope with life. If you are better able to pin down whether you are feeling despair or anxiety, for instance, you might be better able to decide how to remedy those feelings: whether to talk to a friend, or watch a funny film. Or being able to identify your hope in the face of disappointment might help you to look for new solutions to your problem.

In this way, emotion vocabulary is a bit like a directory, allowing you to call up a greater number of strategies to cope with life. Sure enough, people who score highly on emotion granularity are better able to recover more quickly from stress and are less likely to drink alcohol as a way of recovering from bad news. It can even improve your academic success. Marc Brackett at Yale University has found that teaching 10 and 11-year-old children a richer emotional vocabulary improved their end-of-year grades, and promoted better behaviour in the classroom. “The more granular our experience of emotion is, the more capable we are to make sense of our inner lives,” he says.

Both Brackett and Barrett agree that Lomas’s “positive lexicography” could be a good prompt to start identifying the subtler contours of our emotional landscape. “I think it is useful – you can think of the words and the concepts they are associated with as tools for living,” says Barrett. They might even inspire us to try new experiences, or appreciate old ones in a new light.

* * *

And related to all of this is hypocognition, overlapping with linguistic relativity — in how language and concepts determine our experience, identity, and sense of reality — constraining and framing and predetermining what we are even capable of perceiving, thinking about, and expressing:

Hypocognition is a censorship tool that mutes what we can feel
by Kaidi Wu

It is a strange feeling, stumbling upon an experience that we wish we had the apt words to describe, a precise language to capture. When we don’t, we are in a state of hypocognition, which means we lack the linguistic or cognitive representation of a concept to describe ideas or interpret experiences. The term was introduced to behavioural science by the American anthropologist Robert Levy, who in 1973 documented a peculiar observation: Tahitians expressed no grief when they suffered the loss of a loved one. They fell sick. They sensed strangeness. Yet, they could not articulate grief, because they had no concept of grief in the first place. Tahitians, in their reckoning of love and loss, and their wrestling with death and darkness, suffered not from grief but a hypocognition of grief. […]

But the darkest form of hypocognition is one born out of motivated, purposeful intentions. A frequently overlooked part of Levy’s treatise on Tahitians is why they suffered from a hypocognition of grief. As it turns out, Tahitians did have a private inkling of grief. However, the community deliberately kept the public knowledge of the emotion hypocognitive to suppress its expression. Hypocognition was used as a form of social control, a wily tactic to expressly dispel unwanted concepts by never elaborating on them. After all, how can you feel something that doesn’t exist in the first place?

Intentional hypocognition can serve as a powerful means of information control. In 2010, the Chinese rebel writer Han Han told CNN that any of his writings containing the words ‘government’ or ‘communist’ would be censored by the Chinese internet police. Ironically, these censorship efforts also muffled an abundance of praise from pro-leadership blogs. An effusive commendation such as ‘Long live the government!’ would be censored too, for the mere mention of ‘government’.

A closer look reveals the furtive workings of hypocognition. Rather than rebuking negative remarks and rewarding praises, the government blocks access to any related discussion altogether, rendering any conceptual understanding of politically sensitive information impoverished in the public consciousness. ‘They don’t want people discussing events. They simply pretend nothing happened… That’s their goal,’ Han Han said. Regulating what is said is more difficult than ensuring nothing is said. The peril of silence is not a suffocation of ideas. It is to engender a state of blithe apathy in which no idea is formed.

Americans Fatter at Same Level of Food Intake and Exercise

Americans, to state the obvious, are unhealthier with each passing generation. And the most obvious sign of this is rising obesity rate. In one analysis, this was shown to be true even when controlling for levels of food intake and exercise (see article below). This is the kind of data that undermines conventional dietary advice based on Christian moralizing about the deadly sins of gluttony and sloth.

Heart attacks and obesity first became a public health concern in the 1940s and 1950s. That was following decades of seed oil and margarine consumption having mostly replaced lard in the American diet. We were told that saturated fat is dangerous and that seed oils were great for health. Americans were listening and they strictly followed this advice. Even restaurants stopped cooking their french fries in tallow.

In particular, olive oil has been sold as the best. Why is olive oil supposed to be so healthy? Because it has monounsaturated fat, the same as is primarily found in lard. Not too long ago, the healthiest population in the United States was in Roseto, Pennyslvania. Guess what was their main source of fat? Lard. They also ate massive loads of meat, as do other long-lived populations in the world such as in Hong Kong.

Red meat also decreased over that period and has continued to increase since then. Dairy has followed this pattern of decline. Americans are eating less animal fats now than ever before in American history or probably human existence. It’s true that Americans are eating more lean chicken and fish, but we were told those are healthy for us. Meanwhile, Americans are eating more fruits and vegetables, nuts and seeds than ever before.

Calories-in/calories-out has been an utter failure. It’s not how much we are eating but what we are eating. That then determines how our metabolism functions, whether it burns fat or stores it. Exercise is largely irrelevant for fat loss. Fat people can exercise all the time and not lose weight, while some skinny people hardly move at all. Another study “demonstrated that there is no difference in total energy expenditure between traditional hunter-gathers, subsistence farmers and modern Westerners.”

One explanation is an increase of obesogens. These are chemicals that cause the body to create fat. In general, fat is where the body stores excess toxins that overwhelm the body. And indeed younger Americans are exposed to more toxins. Then this makes losing weight hard because all the toxins get released and make one feel like shit. It’s hard for the body to eliminate a lifetime of accumulated toxicity. On top of that, the young are prescribed more medications than ever before. Antidepressants and antipsychotics have been given out like candy for anyone with mild mental issues. What is a common side effect of these drugs? Yep, weight gain.

A third possibility is more complex. We know the gut microbiome has shrunk in number and diversity. It’s also changed in the profile of bacteria. Research is showing how important is the microbiome (see The Secrete Life of Your Microbiome by Susan L. Prescott and Alan C. Logan). Toxins and drugs, by the way, also alter the microbiome. So does diet. Even if total calorie intake hasn’t changed much relative to the increased height of the population, what has changed is what we are eating.

In place of animal fats, we are eating not only more seed oils but also more carbs and sugar. Animal fats are highly satiating and so food companies realized they needed to find something equally satiating. It turns out a high-carb diet is not only satiating but addictive. It knocks people out of ketosis and causes them to put on weight. It doesn’t matter if one tries to eat less. In processed foods, when carbs are combined with seed oils, the body is forced to burn the carbs immediately and so it has no choice but to turn the seed oils into fat.

By the way, what alters metabolism also alters the microbiome. This is seen when people go from a high-carb diet to a ketogenic diet. Ketosis is powerful in its impact on how the body functions in so many ways, even changing epigenetic expression of genes. Here is the worst part. Those epigenetic changes have been happening for generations with the loss of regular ketosis. Even epigenetics for obesity, following an environmental trigger like famine, have been shown to pass on across multiple generations. The microbiome, of course, also is inherited and each of those bacteria likewise have an epigenome that determines their genetic expression.

Everything we do as individuals, good and bad, doesn’t only affect us as individuals. People are getting fatter now not only because of what they are doing differently but because of everything that was done by their parents, grandparents, and great-grandparents. As I’ve said before, even if we reversed all these changes instantly, as we are unlikely to do, it would still require generations to fully reverse the consequences.

* * *

Why It Was Easier to Be Skinny in the 1980s
by Olga Khazan

A study published recently in the journal Obesity Research & Clinical Practice found that it’s harder for adults today to maintain the same weight as those 20 to 30 years ago did, even at the same levels of food intake and exercise. […]

Just what those other changes might be, though, are still a matter of hypothesis. In an interview, Kuk proffered three different factors that might be making harder for adults today to stay thin.

First, people are exposed to more chemicals that might be weight-gain inducing. Pesticides, flame retardants, and the substances in food packaging might all be altering our hormonal processes and tweaking the way our bodies put on and maintain weight.

Second, the use of prescription drugs has risen dramatically since the 1970s and ’80s. Prozac, the first blockbuster SSRI, came out in 1988. Antidepressants are now one of the most commonly prescribed drugs in the U.S., and many of them have been linked to weight gain.

Finally, Kuk and the other study authors think that the microbiomes of Americans might have somehow changed between the 1980s and now. It’s well known that some types of gut bacteria make a person more prone to weight gain and obesity. Americans are eating more meat than they were a few decades ago, and many animal products are treated with hormones and antibiotics in order to promote growth. All that meat might be changing gut bacteria in ways that are subtle, at first, but add up over time. Kuk believes that the proliferation of artificial sweeteners could also be playing a role.

Why Do Americans Keep Getting Fatter?
by Chris Bodenner

Notwithstanding the known errors of dietary assessment, it is interesting that we observe consistent trends over time in terms of how dietary intake relates with obesity and how this relationship has changed over time. This lends more confidence to our primary findings and suggests that there are either physiological changes in how diet relates with body weight or differences in how individuals are reporting their dietary intake over time. […]

[W]e observed that the BMI associated with a given leisure time physical activity frequency was still higher over time in men. This may be attributed to changes in non-leisure time physical activity such as reductions in occupational physical activity or increasing screen time. However, a study using doubly labelled water demonstrated that there is no difference in total energy expenditure between traditional hunter-gathers, subsistence farmers and modern Westerners. Thus, numerous other factors in addition to energy intake and physical activity may be important to consider when trying to explain the rise in obesity, and should be further evaluated in further studies.

Dr. Saladino on Plant and Animal Foods

Dr. Paul Saladino, a former vegetarian and present carnivore advocate, has a Youtube channel with many videos and he has done talks with numerous others. Following on the heels of Dr. Shawn Baker’s book on the carnivore diet, Dr. Saladino has just released his own book, The Carnivore Code. He discusses basic topics like fiber and nutrients, including nutrients that get less attention (carnitine, creatine, choline, taurine, etc; even cholesterol, necessary for brain function), but also more complex science such as IFG1, MTOR, methionine, and much else.

A major emphasis in his work is the contrast between nutrients from animal foods and antinutrients from plant foods, the latter specifically in terms of plant defense chemicals. There are many videos where he talks about this, but I’ll point to only a few of them: Do PLANT MOLECULES have SIDE EFFECTS?, AMA#2: Acid/base balance, APOE4/FTO, omega-3s, the problem with broccoli and more!, Dr Paul Saladino, Benefits of Eating Meat on The Carnivore Diet, Dangers of Lectins in Food, Are curcumin and sulforaphane good for you?, and How Broccoli is Destroying Your Thyroid! with Elle Russ.

Sally Norton is also a font of info on this topic. She likewise has tons of videos, but here is a good one: AHS17 Lost Seasonality and Overconsumption of Plants: Risking Oxalate Toxicity – Sally Norton. By the way, oxalates are just one type of antinutrient. There are many others. Dr. Saladino also goes far beyond only the antinutrients to show the research on what other plant chemicals do.

About fiber, there are several videos you could look at: Is Fiber NECESSARY for a HEALTHY Microbiome?, Paul Saladino MD on Why We Don’t Need Fiber for a Healthy MicrobiomeCarnivore Diet, Fiber, & Health, Dr. Paul Saladino: Statins, Fibre, and Mental Health, and The Great Fiber Myth – Dr. Shawn Baker, Paul Saladino MD, and Mark Sisson. By the way, you might check out some videos by others about fiber: Myths about fibre – how fibre causes constipation and bloating. and Dr. Zoë Harcombe – ‘What about fiber?’.

Maybe most interesting are his growing number of talks with those who are or were pushing plant-heavy diets. He seems to have persuaded Dr. Mercola that plants aren’t always a good thing, but there are many other great dialogues he has been involved with, such as with Dr. Terry Wahls, another former vegetarian.

Here are some of those videos: “The Carnivore Code”- Interview with Paul Saladino, MD, Is autoimmune disease REVERSIBLE? With Terry Wahls, MD, Carnivore Diet: Crazy delicious, or just plain crazy? Ep47 – Paul Saladino Interview (Gundry transcript), How to slow down aging! A conversation with David Sinclair PhD, and Carnivore vs. Vegans! A friendly debate with Cyrus and Robby from Mastering Diabetes. The last video involves two fruitarians. That is a benefit in listening to Dr. Saladino; he isn’t dogmatic nor is he trapped in an echo chamber.

He was recently on a mainstream show, The Doctors, during which he was attacked and not allowed to talk but he handled it far better than most. Here is the original video and some responses to it — one by Saladino and another by the two sisters who also were guests on the show, along with videos made by others: Is It Healthy to Eat Only Meat?, Dr. Saladino on DoctorsTV… but it’s actually watchable, My RESPONSE to THE DOCTORS!, WE WERE ON THE DOCTORS TV SHOW, Carnivore vs the Doctors and vegan fan mail, Paul Saladino vs “The Doctors” Review – VERY strong language throughout…, Carnivore advocate is ambushed on The Doctors TV show, and Carnivore Advocate Goes on ‘The Doctors’ TV Show REACTION!.

It was mainstream authority defending the status quo, at a time when nutrition studies is in the middle of a replication crisis (Felice Jacka Defends Boundaries of Allowable Dietary Thought). On the positive side, when they attack you they are forced to acknowledge you. They only acknowledge opponents when the tactic of silencing has failed. This mainstream show made many Americans aware of the carnivore diet who had never heard of it before.

* * *

I’ve previously discussed much of this kind of info and related topics. It can be found in the following posts, some of which bring in Dr. Saladino’s view:

The Agricultural Mind
Fiber or Not: Short-Chain Fatty Acids and the Microbiome
High vs Low Protein
Gundry’s Plant Paradox and Saladino’s Carnivory
Multiple Sclerosis and Carnivore Diet
Dietary Risk Factors for Heart Disease and Cancer
Hubris of Nutritionism
Sailors’ Rations, a High-Carb Diet
Are ‘vegetarians’ or ‘carnivores’ healthier?
Like water fasts, meat fasts are good for health.
Eat Beef and Bacon!
Vegetarianism is an Animal-Based Diet
Ancient Greek View on Olive Oil as Part of the Healthy Mediterranean Diet
Blue Zones Dietary Myth

Bonus video from another worthy expert: Georgia Ede: Brainwashed — The Mainstreaming of Nutritional Mythology.

Why Is Average Body Temperature Lowering?

Researchers at Stanford University, according to analysis of data going back to the 1800s, found that average body temperature has decreased (Myroslava Protsiv et al, Decreasing human body temperature in the United States since the Industrial Revolution). Other data supports the present lower norm (J.S. Hausmann et al, Using Smartphone Crowdsourcing to Redefine Normal and Febrile Temperatures in Adults: Results from the Feverprints Study).

They considered that increased health and so decreased inflammation could be the cause, but it’s not clear that inflammation overall has decreased. The modern industrial diet of sugar and seed oils is highly inflammatory. Inflammation has been linked to epidemic of diseases of civilization: obesity, diabetes, heart disease, arthritis, depression, schizophrenia, and much else. In some ways, inflammation is worse than it has ever been. That is why, as a society we’ve become obsessed with anti-inflammatories, from aspirin to turmeric.

The authors of the paper, however, offer other data that contradicts their preferred hypothesis: “However, a small study of healthy volunteers from Pakistan—a country with a continued high incidence of tuberculosis and other chronic infections—confirms temperatures more closely approximating the values reported by Wunderlich”. Since these were healthy volunteers, they should not have had higher inflammation from infections, parasites, etc. So, why were their body temperatures higher than is seen among modern Westerners?

It also has been suggested that there are other potential contributing factors. Ambient temperatures are highly controlled and so the body has to do less work in maintaining an even body temperature. Also, people are less physically active than they once were. The more interesting explanation is that the microbiome has been altered, specifically reduced in the number and variety of heat-producing microbes (Nita Jain, A Microbial-Based Explanation for Cooling Human Body Temperatures).

I might see a clue in the Pakistan data. That population is presumably more likely to be following their traditional diet. If so, this would mean they have been less Westernized in their eating habits, which would translate as fewer refined starchy carbs and sugar, along with fewer seed oils high in omega-6 fatty acids. Their diets might in general be more restricted: fewer calories, smaller portions, less snacking, and longer periods between meals. Plus, as this would be an Islamic population, fasting is part of their religious tradition.

This might point to more time spent in and near ketosis. It might be noted that ketosis is also anti-inflammatory. So why the higher body temperature? Well, there is the microbiome issue. A population on a traditional diet combined with less antibiotic usage would likely still be supporting a larger microbiome. By the way, ketosis is one of the factors that supports a different kind of microbiome, related to its use as treatment for epilspsy (Rachael Rettner, How the Keto Diet Helps Prevent Seizures: Gut Bacteria May Be Key). And ketosis raises the basil metabolic rate which in turn raises temperature. Even though fasting lowers body temperature in the short term, if it was part of an overall ketogenic diet it would help promote on average higher body temperatures.

This is indicated by the research on other animals: “An increased resistance to cold assessed by the rate of fall in body tem-perature in the animals as well as human beings on a high-fat diet has been reported by LEBLANC (1957) and MITCHELL et al. (1946), respectively. LEBLANC (1957) suggested that the large amount of fat accumulated in animals fed a high-fat diet could not explain, either as a source of energy reserves or as an insulator, the superiority of high-fat diet in a cold environment, postulating some changes induced by a high-fat diet in the organism that permits higher sustained rate of heat production in the cold.” (Akihiro Kuroshima, Effects of Cold Adaptation and High-Fat Diet On Cold Resistance and Metabolic REsponses To Acute Exposure In Rats).

And: “Rats on a corn oil diet convert less T4 to active T3 than rats on a lard diet. Rats on a safflower oil diet have a more greatly reduced metabolic response to T3 than rats on a beef fat diet. Rats on a high-PUFA diet have brown fat that’s less responsive to thyroid hormone. Remember, brown fat is the type that generates heat to keep us warm. Rats on a long-term diet high in soybean oil have terrible body temperature regulation, which thyroid function in large part controls” (Mark Sisson, Is Keto Bad For Your Thyroid?). A 1946 study found that a high-fat diet had less of a drop in body temperature in response to cold (H.H. Mitchell, The tolerance of man to cold as affected by dietary modification; carbohydrate versus fat and the effect of the frequency of meals).

Specifically about ketosis, in mice it increases energy expenditure and causes brown fat to produce more heat (Shireesh Srivastava, A Ketogenic Diet Increases Brown Adipose Tissue Mitochondrial Proteins and UCP1 Levels in Mice). Other studies confirm this and some show an increase of brown fat. Brown fat is what keeps us warm. Babies have a lot of it and, in the past, it was thought adults lost it, but it turns out that we maintain brown fat throughout our lives. It’s just that diets have different affects on it.

Bikman points out the relationship between insulin and ketones — when one is high the other is low. Insulin tells the body to slow down metabolism and store energy, that is to say produce fat and to shut down the activity of brown fat. Ketones do the opposite, not only activating brown fat but causing white fat to act more like brown fat. This is what causes the metabolic advantage of the keto diet, in losing excess body fat and maintaining lower weight, as it increases the burning of 200-300 calories per day (metabolizing 10 lbs of body fat a year). By the way, cold exposure and exercise also activate brown fat, which goes back to general lifestyle factors that go hand in hand with diet.

Some people attest to feeling warmer in winter while in ketosis (Ketogenic Forums, Ketosis, IF, brown fat, and being warmer in cool weather), although others claim to not handle cold well which might simply be an issue of how quickly people become fully fat-adapted. A lifetime of a high-carb diet changes the body. But other than permanently damaged biological functioning, the body should be able to eventually shift into more effective ketosis and hence thermogenesis.

In humans, there is an evolutionary explanation for this. And humans indeed are unique in being able to more easily enter and remain in ketosis. But think about when ketosis most often happened in the past and you’ll understand why it seems to be inefficient in wasting energy as heat, what is a slight metabolic advantage if you’re trying to lose weight. For most of human existence, carb restriction was forced upon the species during the coldest season when starchy plants don’t grow. That is key.

It was an advantage to not only be able to survive off of one’s own body fa but to simultaneously create extra heat, especially during enforced fasting when food supplies were low as fasting would tend to drop body temperature — an argument made by the insulin researcher Benjamin Bikman (see 9/9/17 interview with Mike Mutzel on High Intensity Health at 20:34 mark, Insulin, Brown Fat & Ketones w/ Benjamin Bikman, PhD; & see Human Adaptability and Health). Ketosis is a compensatory function for survival during the harshest time of the year, winter.

Maybe modern Westerners have lower body temperature for the same reason they are plagued with diseases of civilization, specifically those having to do with metabolic syndrome and insulin resistance. If we didn’t take so many drugs and other substances to manage inflammation, maybe our body temperature would be higher. But it’s possible the lack of ketosis by itself might be enough to significantly keep it at a reduced level. And if not ketosis, something else about the diet and metabolism likely are involved.

* * *

What is the relevance? Does it matter that average body temperature has changed? As I pointed out above, it could indicate how the entirety of physiological functioning has been altered. A major component has to do with the metabolism which relates to diet, gut health, and microbiome. About the latter, Nita Jain wrote that,

“A 2010 report observed that 36.7° C may be the ideal temperature to ward off fungal infection whilst maintaining metabolism. In other words, high body temperatures represent optimization in the tradeoff between metabolic expenditure and resistance to infectious diseases. Our reduced exposure to potentially pathogenic fungi in developed countries may therefore be another possible factor driving changes in human physiology” (A Microbial-Based Explanation for Cooling Human Body Temperatures).

That would be significant indeed. And it would be far from limited to fungal infections: “In general, a ketogenic diet is useful for treating bacterial and viral infections, because bacteria and viruses don’t have mitochondria, so a ketogenic diet starves them of their favorite fuel source, glucose” (Paleo Leap, Infections and Chronic Disorders). Ketosis, in being anti-inflammatory, has been used to treat gout and autoimmune disorders, along with mood disorders that often include brain inflammation.

The inflammatory pathway, of course, is closely linked to the immune system. Reducing inflammation is part of complex processes in the body. Opposite of the keto diet, a high-carb diet produces inflammatory markers that suppress the immune system and so compromises prevention of and healing from infections. Indeed, obese and diabetic patients are hospitalized more often and get worse symptoms of influenza infections (flu).

But it’s not merely the reduction of inflammation. As an energy source, ketones are preferred over glucose by immune cells that fight infections, although maybe some bacteria can use ketones. It’s a similar pattern with cancer, in which ketosis can help prevent some cancers from growing in the early stages, but the danger is once established particular kinds of cancers can adapt to using ketones. So, it isn’t as simple as ketosis curing everything, even if it is a overall effective preventative measure in maintaining immunological health and general health.

What interests us most here are infections. Let’s look further at the flu. One study gave mice an influenza infection (Emily L. Goldberg et al, Ketogenic diet activates protective γδ T cell responses against influenza virus infection; Abby Olena, Keto Diet Protects Mice from Flu). The mice were on different diets. All of those on standard chow died, but half survived on the keto diet. To determine causes, other mice were put on a diet high in both fat and carbs while others were given exogenous ketones, but these mice also died. It wasn’t only the fat or the ketones in the keto diet. Something about fat metabolism seems to have been key, that is to say not only fat and not only the ketones but something about how fat is turned into ketones during ketosis, although some speculate that protein restriction might have been important.

The researchers were able to pinpoint the mechanisms for fighting off the infection. Turning fat into ketones allows the gamma delta subset of T cells in the lungs to be activated in response to influenza. This was unexpected as they haven’t been a focus in previous research. These T cells increase mucus production in epithelial cells in the lungs. This creates a protective barrier that traps the virus and allows it to be coughed up. At the same time, the keto diet blocks the production of inflammasones, multiunit protein complexes activated by the immune system. This reduces the inflammation that can harm the lungs. This relates to the T cell stimulation.

From an anecdotal perspective, here is an interesting account: “I have been undergoing a metabolic reset to begin the year. I have been low carb/keto on and off for the last 4.5 years and hop in and out of ketosis for short periods of time when it benefits me or when my body is telling me I need to. Right now, I decided to spend the first 6 weeks of 2018 in ketosis. I check my numbers every morning and have consistently been between 1.2 and 2.2 mmol/L. I contracted a virus two days ago (it was not influenza but I caught something) and my ketone levels shot through the roof. Yesterday morning I was at 5.2 (first morning of being sick) and this morning I was at 5.8 (although now I am in a fasted state as I have decided to fast through this virus.)” (bluesy2, Keto Levels with Virus/Flu).

Maybe that is a normal response for someone in ketosis. The mouse study suggests there is something about the process itself in producing ketones that is involved in the T cell stimulation. The ketones also might have a benefit for other reasons, but the process of fat oxidation or something related to it might be the actual trigger. In this case, the ketone levels are an indicator of what is going on, that the immune system is fully engaged. The important point, though, is this only happens in a ketogenic state and it has much to do with basil metabolic rate and body temperature regulation.

* * *

98.6 Degrees Fahrenheit Isn’t the Average Anymore
by Jo Craven McGinty

Nearly 150 years ago, a German physician analyzed a million temperatures from 25,000 patients and concluded that normal human-body temperature is 98.6 degrees Fahrenheit.

That standard has been published in numerous medical texts and helped generations of parents judge the gravity of a child’s illness.

But at least two dozen modern studies have concluded the number is too high.

The findings have prompted speculation that the pioneering analysis published in 1869 by Carl Reinhold August Wunderlich was flawed.

Or was it?

In a new study, researchers from Stanford University argue that Wunderlich’s number was correct at the time but is no longer accurate because the human body has changed.

Today, they say, the average normal human-body temperature is closer to 97.5 degrees Fahrenheit.

“That would be a huge drop for a population,” said Philip Mackowiak, emeritus professor of medicine at the University of Maryland School of Medicine and editor of the book “Fever: Basic Mechanisms and Management.”

Body temperature is a crude proxy for metabolic rate, and if it has fallen, it could offer a clue about other physiological changes that have occurred over time.

“People are taller, fatter and live longer, and we don’t really understand why all those things have happened,” said Julie Parsonnet, who specializes in infectious diseases at Stanford and is senior author of the paper. “Temperature is linked to all those things. The question is which is driving the others.” […]

Overall, temperatures of the Civil War veterans were higher than measurements taken in the 1970s, and, in turn, those measurements were higher than those collected in the 2000s.

“Two things impressed me,” Dr. Parsonnet said. “The magnitude of the change and that temperature has continued to decline at the same rate.” […]

“Wunderlich did a brilliant job,” Dr. Parsonnet said, “but people who walked into his office had tuberculosis, they had dysentery, they had bone infections that had festered their entire lives, they were exposed to infectious diseases we’ve never seen.”

For his study, he did try to measure the temperatures of healthy people, she said, but even so, life expectancy at the time was 38 years, and chronic infections such as gum disease and syphilis afflicted large portions of the population. Dr. Parsonnet suspects inflammation caused by those and other persistent maladies explains the temperature documented by Wunderlich and that a population-level change in inflammation is the most plausible explanation for a decrease in temperature.

Decreasing human body temperature in the United States since the Industrial Revolution
by Myroslava Protsiv, Catherine Ley, Joanna Lankester, Trevor Hastie, Julie Parsonnet

Annotations

Jean-Francois Toussaint
Feb 15

This substantive and continuing shift in body temperature—a marker for metabolic rate—provides a framework for understanding changes in human health and longevity over 157 years.

Very interesting paper. Well done. However, a hypothesis still remains to be tested. The decline of the infectious burden well corresponds to the decrease of the body temperatures between the XIXth and XXth century cohorts (UAVCW vs NHANES), but it does not explain the further and much more important reduction between the XXth and XXIth century studies (NHANES vs STRIDE); see Figure 1 (distributions gap) and Figure 1 / Supp 1 (curve gap), where the impact seems to be twice as large between 1971 and 2007 than between 1860 and 1971.

Besides regulating the ambient room temperature (through winter heating in the early XXth century and summer air conditioning in the late XXth and early XXIth century), another hypothesis was not discussed here ie the significant decline in daily physical activity, one of the primary drivers of physiological heat production.

Regular physical activity alters core temperature even hours after exercising; 5h of moderate intensity exercise (60% VO2max) also increase the resting heart rate and metabolic rate during the following hours and night with a sympathetic nervous system activated until the next morning (Mischler, 2003) and higher body temperatures measured among the most active individuals (Aoyagi, 2018).

As in most developed countries, the North American people – who worked hard in agriculture or industry during the XIXth century – lost their active daily habits. We are now spending hours, motionless in front of our screens, and most of our adolescents follow this unsettling trend (Twenge, 2019); such an effect on temperature and energy regulation should also be considered as it may have an important impact on the potential progresses of their life expectancy and life duration.

Jean-François Toussaint Université de Paris, Head IRMES

Mischler I, et al. Prolonged Daytime Exercise Repeated Over 4 Days Increases Sleeping Heart Rate and Metabolic Rate. Can J Appl Physiol. Aug 2003; 28 (4): 616-29 DOI: 10.1139/h03-047

Aoyagi Y, et al. Objectively measured habitual physical activity and sleep-related phenomena in 1645 people aged 1–91 years: The Nakanojo Community Study. Prev Med Rep. 2018; 11: 180-6 DOI: 10.1016/j.pmedr.2018.06.013

Twenge JM, et al. Trends in U.S. Adolescents’ media use, 1976–2016: The rise of digital media, the decline of TV, and the (near) demise of print. Psychol Pop Media Cult, 2019; 8(4): 329-45. DOI: 10.1037/ppm0000203

Nita Jain
(edited Feb 15) Feb 14

Although there are many factors that influence resting metabolic rate, change in the population-level of inflammation seems the most plausible explanation for the observed decrease in temperature over time.

Reduced body temperature measurements may also be the result of loss of microbial diversity and rampant antibiotic use in the Western world. Indeed, the authors mention that a small study of healthy volunteers from Pakistan reported higher mean body temperatures than those encountered in developed countries where exposure to antimicrobial products is greater.

Rosenberg et al. reported that heat provision is an under-appreciated contribution of microbiota to hosts. Previous reports have estimated bacterial specific rates of heat production at around 168 mW/gram. From these findings, we can extrapolate that an estimated 70% of human body heat production in a resting state is the result of gut bacterial metabolism.

Consistent with this idea are reports that antibiotic treatment of rabbits and rodents lowers body temperature. Germ-free mice and piglets similarly displayed decreased body temperatures compared to conventionally raised animals and did not produce a fever in response to an infectious stimulus.

Although heat production by symbiotic microbes appears to be a general phenomenon observed in both plants and animals, its significance in humans has hardly been studied. Nonetheless, the concomitant loss of diversity and heat contribution of the gut microbiota may have far-reaching implications for host metabolic health.

A Microbial-Based Explanation for Cooling Human Body Temperatures
by Nita Jain

I would like to propose that our reduced body temperature measurements may be the result of loss of microbial diversity and rampant antibiotic use in the Western world. Indeed, a small study of healthy volunteers from Pakistan reported higher mean body temperatures than those encountered in developed countries where exposure to antimicrobial products is greater.

Heat provision is an under-appreciated contribution of microbiota to hosts. Microbes produce heat as a byproduct when breaking down dietary substrates and creating cell materials. Previous reports have estimated bacterial specific rates of heat production at around 168 mW/gram. From these findings, we can extrapolate that an estimated 70% of human body heat production in a resting state is the result of gut bacterial metabolism.

Consistent with this idea are reports that antibiotic treatment of rabbits and rodents lowers body temperature. Germ-free mice and piglets similarly displayed decreased body temperatures compared to conventionally raised animals and did not produce a fever in response to an infectious stimulus. The relationship also appears to be bi-directional, as host tolerance to cold has been shown to drive changes in the gut microbiomes of blue tilapia.

Heat production in goats was found to decrease by about 50% after emptying the rumen to values similar to what would be expected during a fasting state. These observations suggest that during fasting, microbial fermentation is responsible for half of the animal’s heat production while host metabolism accounts for the other half. The warming effect of microbes has also been reported in plants. Yeast populations residing in floral nectar release heat when breaking down sugar, increasing nectar temperature and modifying the internal flower microenvironment.

What is Moderate-Carb in a High-Carb Society?

If we were eating what the government actually funded in agricultural supports, we’d be having a giant corn fritter, deep fried in soybean oil. And it’s like, that’s not exactly what we should be eating.
~ Mark Hyman

A couple years back (2018), researchers did an analysis of long-term data on intake of carbohydrates, plant foods, and animal foods: Sara B Seidelmann, et al, Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis). The data, however, turns out to be more complicated than how it was reported in the mainstream news and in other ways over-simplified.

This was an epidemiological study of 15,000 people done with notoriously unreliable self-reports called Food Frequency Questionnaires based on the subjects’ memory of years of eating habits. The basic conclusion was that a diet moderate in carbs is the healthiest. That reminds me of the “controlled carbs” that used to be advocated to ‘manage’ diabetes that, in fact, worsened diabetes over time (American Diabetes Association Changes Its TuneAmerican Diabetes Association Changes Its Tune) — what was being managed was slow decline leading to early death. Why is it the ruling elite and its defenders, whether talking about diet or politics, always trying to portray extreme positions as ‘moderate’?

Let’s dig into the study. Although the subjects were seen six times over a 25 year period, the questionnaire was given only twice with the first visit in the late 1980s and with the third visit in the mid 1990s — two brief and inaccurate snapshots with the apparent assumption that dietary habits didn’t change from the mid 1990s to 2017. As was asked of the subjects, do you recall your exact dietary breakdown for the the past year? In my personal observations, many people can’t recall what they ate last week or sometimes even what they had the day before — the human memory is short and faulty (the reason nutritionists will have patients keep daily food diaries).

There was definitely something off about the data. When the claimed total caloric intake is added up it would’ve meant starvation rations for many of the subjects, which is to say they were severely underestimating parts of their diet, most likely the parts of their diet that are the unhealthiest (snacks, fast food, etc). Shockingly, they didn’t even assess or rather didn’t include carbohydrate intake for all those periods for they later on extrapolated from the earlier data with no explanation for this apparent data manipulation.

To further problemitize the results, those who developed metabolic health conditions (diabetes, stroke, heart disease) in the duration, likely caused by carbohydrate consumption, were excluded from the study, as were those who died — it was expected and one might surmise it was intentionally designed to find no link between dietary carbs and health outcomes. That is to say the study was next to worthless (John Ioannidis, The Challenge of Reforming Nutritional Epidemiologic Research). Over 80% of the hypotheses of nutritional epidemiology are later proved wrong in clinical trials (S. Stanley Young & Alan Karr, Deming, data and observational studies).

Besides, the researchers defined low-carb as anything below 40% and very high-carb as anything above 70%, though the study itself was mainly looking at percentages in between these. This study wasn’t about the keto diet (5% carbs of total energy intake, typically 20-50 grams per day) or even generally low-carb diets (below 25%) and moderate-carb diets (25-33% or maybe slightly higher). Instead, the researchers compared diets that were varying degrees of high-carb (37-61%, about 144 grams and higher). It’s true that one might argue that, compared to the general population, a ‘moderate’-carb diet could be anything below the average high-carb levels of the standard American diet (50-60%), the high levels the researchers considered ‘moderate’ as in being ‘normal’. But with this logic, the higher the average carb intake goes the higher ‘moderate’ also becomes, a not very meaningful definition for health purposes.

Based on bad data and confounded factors for this high-carb population, the researchers speculated that diets below 37% carbs would show even worse health outcomes, but they didn’t actually have any data about low-carb diets. To put this in perspective, traditional hunter-gatherer diets tend to be closer to the ketogenic level of carb intake with, on average, 20% at the lower range and 40% at the highest extreme, and that is particularly ketogenic with a feast-and-fast pattern. Some hunter-gatherers, from Inuit to Masai, go long periods with few if any carbs, well within ketosis, and they don’t show signs of artherosclerosis, diabetes, etc.

The study simply looked at correlations without controlling for confounders: “The low carb group at the beginning had more smokers (33% vs 22%), more former smokers (35% vs 29%), more diabetics (415 vs 316), twice the native Americans, fewer habitual exercisers (474 vs 614) ” (Richard Morris, Facebook). And alcohol intake, one of the single most important factors for health and lifespan, was not adjusted for at all. Taken together, that is what is referred to as the unhealthy user bias, whereas the mid-range group in this study were affected by the healthy user bias. Was this a study of diet or a study of lifestyle and demographic populations?

On top of that, neither was data collected on specific eating patterns in terms of portion sizes, caloric intake, regularity of meals, and fasting. Also, the details of types of foods eaten weren’t entirely determined either, such as whole vs processed, organic vs non-organic, pasture-raised vs factory-farmed — and junk foods like pizza and energy bars weren’t included at all in the questionnaire; while whole categories of foods were conflated  with meat being lumped together with cakes and baked goods, as separate from fruits and vegetables. A grass-finished steak or wild-caught salmon with greens from your garden was treated as nutritionally the same as a fast food hamburger and fries.

Some other things should be clarified. This study wasn’t original research but was data mining older data sets from the research of others. Also, keep in mind that it was published in the Lancet Public Health, not in the Lancet journal itself. The authors and funders paid $5,000 for it to be published there and it was never peer-reviewed. Another point is that the authors of the paper speak of ‘substitutions’: “…mortality increased when carbohydrates were exchanged for animal-derived fat or protein and mortality decreased when the substitutions were plant-based.” This is simply false. No subjects in this study replaced any foods for another. This an imagined scenario, a hypothesis that wasn’t tested. By the way, don’t these scientists know that carbohydrates come from plants? I thought that was basic scientific knowledge.

To posit that too few carbs is dangerous, the authors suggest that, “Long-term effects of a low carbohydrate diet with typically low plant and increased animal protein and fat consumption have been hypothesised to stimulate inflammatory pathways, biological ageing, and oxidative stress.” This is outright bizarre. We don’t need to speculate. In much research, it already has been shown that sugar, a carbohydrate, is inflammatory. What happens when sugar and other carbs are reduced far enough? The result is ketosis. And what is the affect of ketosis? It is an anti-inflammatory state, not to mention promoting healing through increased autophagy. How do these scientists not know basic science in the field they are supposedly experts in? Or were they purposefully cherrypicking what fit their preconceived conclusion?

Here is the funny part. Robb Wolf points out (see video below) that in the same issue of the same journal on the same publishing date, there was a second article that gives a very different perspective (Andrew Mente & Salim Yusuf, Evolving evidence about diet and health). The other study concluded a low-carb diet based on meat and animal fats particularly lowered lifespan which probably simply demonstrated the unhealthy user effect (these people were heavier, smoked more, etc), but this other article looked at other data and came to very different conclusions,

“More recently, studies using standardised questionnaires, careful documentation of outcomes with common definitions, and contemporary statistical approaches to minimise confounding have generated a substantial body of evidence that challenges the conventional thinking that fats are harmful. Also, some populations (such as the US population) changed their diets from one relatively high in fats to one with increased carbohydrate intake. This change paralleled the increased incidence of obesity and diabetes. So the focus of nutrition research has recently shifted to the potential harms of carbohydrates. Indeed, higher carbohydrate intake can have more adverse effects on key atherogenic lipoproteins (eg, increase the apolipoprotein B-to-apolipoprotein A1 ratio) than can any natural fats. Additionally, in short-term trials, extreme carbohydrate restriction led to greater short-term weight loss and lower glucose concentrations compared with diets with higher amounts of carbohydrate. Robust data from observational studies support a harmful effect of refined, high glycaemic load carbohydrates on mortality.”

Then, in direct response to the other study, the authors warned that, “The Findings of the meta-analysis should be interpreted with caution, given that so-called group thinking can lead to biases in what is published from observational studies, and the use of analytical approaches to produce findings that fit in with current thinking.” So which Lancet article should we believe? Why did the media obsess over the one while ignoring the other?

And what about the peer-reviewed PURE study that was published the previous year (2018) in the Lancet journal itself? The PURE study was much larger and better designed. Although also observational and correlative, it was the best study of its kind ever done. The researchers found that carbohydrates were linked to a shorter lifespan and saturated fat to a longer lifespan, and yet it didn’t the same kind of mainstream media attention. I wonder why.

The study can tell us nothing about low-carb diets, even if low-carb diets had been included in the study. Yet the mainstream media and health experts heralded it as proof that a low-carb diet was dangerous and a moderate-carb diet was the best. Is this willful ignorance or intentional deception? The flaws in the study were so obvious, but it confirmed the biases of conventional dietary dogma and so was promoted without question.

On the positive side, the more often this kind of bullshit gets put before the public and torn apart as deceptive rhetoric the more aware the public becomes about what is actually being debated. But sadly, this will give nutrition studies an even worse reputation than it already has. And it could discredit science in the eyes of many and could bleed over into a general mistrust of scientific experts, authority figures, and public intellectuals (e.g., helping to promote a cynical attitude of climate change denialism). This is why it’s so important that we get the science right and not use pseudo-science as an ideological platform.

* * *

Will a Low-Carb Diet Shorten Your Life?
by Chris Kresser

I hope you’ll recognize many of the shortcomings of the study, because you’ve seen them before:

  • Using observational data to draw conclusions about causality
  • Relying on inaccurate food frequency questionnaires (FFQs)
  • Failing to adjust for confounding factors
  • Focusing exclusively on diet quantity and ignoring quality
  • Meta-analyzing data from multiple sources

Unfortunately, this study has already been widely misinterpreted by the mainstream media, and that will continue because:

  1. Most media outlets don’t have science journalists on staff anymore
  2. Even so-called “science journalists” today seem to lack basic scientific literacy

In light of the Aug 16th, 2018 Lancet study on carbohydrate intake and mortality, where do you see the food and diet industry heading? (Quora)
Answered by Chris Notal

A study where the conclusion was decided before the data.

They mentioned multiple problems in their analysis, but then ignored this in their introduction and conclusion.

The different cohorts: the cohort with the lowest consumption of carbs also had more smokers, more fat people, more males, they exercised less, and were more likely to be diabetic; each of these categories independently of each other more likely to result in an earlier death. Also, recognize that for the past several decades we have been told that if you want to be healthy, you eat high carb and low fat. So even if that was false, you have people with generally healthier habits period who will live longer than those who do their own thing and rebel against healthy eating knowledge of the time. For example, suppose low carb was actually found to be healthier than high carb: it wouldn’t be sufficient to offset the healthy living habits of those who had been consuming high carb.
Also, look at the age groups. The starting ages were 46–64. And it covered the next 30 years. Which meant they were studying how many people live into their 90’s. Who’s more likely to live into their 90’s, a smoker or non-smoker? Someone who is overweight or not? Males or females? Those who exercise or those who don’t? The problem is that each variable they used in the study along with high carb, on their own supports living longer than the opposite.

Carbs, Good for You? Fat Chance!
By Nina Teicholz

A widely reported study last month purported to show that carbohydrates are essential to longevity and that low-carb diets are “linked to early death,” as a USA Today headline put it. The study, published in the Lancet Public Health journal, is the nutrition elite’s response to the challenge coming from a fast-growing body of evidence demonstrating the health benefits of low-carb eating…

The Lancet authors, in recommending a “moderate” diet of 50% to 60% carbohydrates, essentially endorse the government’s nutrition guidelines. Because this diet has been promoted by the U.S. government for nearly 40 years, it has been tested rigorously in NIH-funded clinical trials involving more than 50,000 people. The results of those trials show clearly that a diet of “moderate” carbohydrate consumption neither fights disease nor reduces mortality.

Deflating Another Dietary Dogma
By Dan Murphy

Just the linking of “carbohydrate intake” and “mortality” tells you all you need to know about the authors’ conclusions, and Teicholz pulls no punches in challenging their findings, calling them “the nutrition elite’s response to the challenge coming from a fast-growing body of evidence demonstrating the health benefits of low-carb eating.”

By way of background, Teicholz noted that for decades USDA’s Dietary Guidelines for Americans have directed people to increase their consumption of carbohydrates and avoid eating fats. “Despite following this advice for nearly four decades, Americans are sicker and fatter than ever,” she wrote. “Such a record of failure should have discredited the nutrition establishment.”

Amen, sister.

Teicholz went on to explain that even though the study’s authors relied on data from the Atherosclerosis Risk in Communities (ARIC) project, which since 1987 has observed 15,000 middle-aged people in four U.S. communities, their apparently “robust dataset” is something of an illusion.

Why? Because the ARIC relied on suspect food questionnaires. Specifically, the ARIC researches used a form listing only 66 food items. That might seem like a lot, but such questionnaires typically include as many as 200 items to ensure that respondents’ recalls are accurate.

“Popular foods such as pizza and energy bars were left out [of the ARIC form],” Teicholz wrote, “with undercounting of calories the inevitable result. ARIC calculated that participants ate only 1,500 calories a day — starvation rations for most.”

Low carbs and mortality
by John Schoonbee

An article on carbohydrate intake and mortality appeared in The Lancet Public Health last week. It is titled “Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis”. In the summary of the article, the word “association” occurs 6 times. The words “cause”, “causes” or “causal” are not used at all (except as part of “all-cause mortality”).

Yet the headlines in various news outlets are as follows:

BBC : “Low-carb diets could shorten life, study suggests”

The Guardian : “Both low- and high-carb diets can raise risk of early death, study finds”

New Scientist : “Eating a low-carb diet may shorten your life – unless you go vegan too”

All 3 imply active causality. Time Magazine is more circumspect and perhaps implies more of the association noted in the article : “Eating This Many Carbs Is Linked to a Longer Life”. These headline grabbing tactics are part of what makes nutritional science so frustratingly hard. A headline could perhaps have read : “An association with mortality has been found with extreme intakes of carbohydrates but no causality has been shown”

To better understand what an association in this context means, it is perhaps good to use 2 examples. One a bit silly, but proves the point, the other more nuanced, and in fact a very good illustration of the difference between causality and association.

Hospitals cause people to die. Imagine someone saying being in hospital shortens your life span, or increases your mortality. Imagine telling a child going for a tonsillectomy this! Of course people who are admitted to hospital have a higher mortality risk than those (well people) not admitted because they are generally sicker. This is an association, but it’s not causal. Being in a hospital does not cause death, but is associated with increased death (of course doctor-caused iatrogenic deaths and multidrug resistant hospital bugs alters this conversation).

A closer example which more parallels the the Lancet Public Health article, is when considering mortality among young smokers, men particularly. Young men who smoke have a higher mortality risk, mostly related to accidental death. Does this mean smoking causes increased deaths in young men? Clearly the answer is NO. But smoking is certainly associated with an increased death rate in young men. Why? Because these young men who smoke have far higher risk taking profiles and personalities, leading to more risk taking behavior including higher risk driving styles. Using a product that has severe health warnings and awful pictures, with impunity, clearly indicates a certain attitude towards risk. They are dying more because of their risk taking behavior which is associated with a likelihood of smoking. But it’s not the smoking of cigarettes that is killing them when they are young. (When they are older, the cancer and heart disease is of course caused by the cigarette smoking, but at an earlier age, that is not the case.)

The guidelines for “healthy” eating since the late 1970’s (which were not evidence based) have stipulated a certain proportion carbohydrate intake. Guidelines have typically also biased plants as being healthier than animal sources of protein and fat. In this context then, “healthy eating” is understood to be consuming 50-55% of carbohydrates, and having less animal products, and more plants, as general rules. It means those who then choose to ignore these guidelines – hence eat far higher amounts of animal fat and protein – would conceivably be those that are snubbing generally accepted “good health” advice (whether evidence based or not) and who probably do not care as much about their health. Their lifestyles would not unreasonably therefore be expected to be unhealthier in general.

The Lancet Public Health article shows that in the quintile of their study participants having the least amount of carbohydrate intake, they significantly

  • are more likely to be male
  • smoke more
  • exercise less
  • have higher bmi’s and
  • are more likely to be diabetic.

“Those eating the least carbohydrates smoked more, exercised less, were more overweight, and were more likely to be diabetic”

This seems to confirm an unhealthy user bias. Interestingly the authors also note that “the animal-based low carbohydrate dietary score was associated with lower average intake of both fruit and vegetables“. Ignoring conventional wisdom around the health of fruit and vegetables reaffirms the data and conclusion that the low carb intake group lack a certain healthy mindset.

Low, moderate or high carbohydrate?
by Zoe Harcombe

In 1977 the Senator McGovern committee issued some dietary goals for Americans (Ref 1). The first goal was “Increase carbohydrate consumption to account for 55 to 60 percent of the energy (caloric) intake.” This recommendation did not come from any evidence related to carbohydrate. It was the inevitable consequence of setting a dietary fat guideline of 30% with protein being fairly constant at 15%.

Call me suspicious, but when a paper published 40 years later, in August 2018, concluded that the optimal intake of carbohydrate is 50-55%, I smelled a rat. The study, published in The Lancet Public Health (Ref 2), also directly contradicted the PURE study, which was published in The Lancet, in August 2017 (Ref 3). No wonder people are confused. […]

I wondered what kind of person would be consuming a low carbohydrate diet in the late 1980s/early 1990s (when the 2 questionnaires in a 25 year study were done). The characteristics table in the paper tells us exactly what kind of person was in the lowest carbohydrate group. They were far more likely to be: male; diabetic; and current smokers; and far less likely to be in the highest exercise category. The ARIC study would adjust for these characteristics, but, as I often say, you can’t adjust for a whole type of person.

The groups have been subjectively chosen – not even the carb ranges are even. Most covered a 10% range (e.g. 40-50%), but the range chosen for the ‘optimal’ group (50-55%) was just 5% wide. This placed as many as 6,097 people in one group and as few as 315 in another.

This is the single biggest issue behind the headlines.

The subjective group divisions introduced what I call “the small comparator group issue.” This came up in the recent whole grains review (Ref 6). I’ll repeat the explanation here, and build on it, as it’s crucial to understanding this paper.

If 20 children go skiing – 2 of them with autism – and 2 children die in an avalanche – 1 with autism and 1 without – the death rate for the non-autistic children is 1 in 18 (5.5%) and the death rate for the autistic children is 1 in 2 (50%). Can you see how bad (or good?) you can make things look with a small comparator group?

From subjective grouping to life expectancy headlines

For the media headlines “Low carb diets could shorten life, study suggests” (Ref 5), the researchers applied a statistical technique (called Kaplan-Meier estimates) to the ARIC data. This is entirely a statistical exercise – we don’t know when people will die. We just know how many have died so far.

This exercise resulted in the claim “we estimated that a 50-year-old participant with intake of less than 30% of energy from carbohydrate would have a projected life expectancy of 29·1 years, compared with 33·1 years for a participant who consumed 50–55% of energy from carbohydrate…  Similarly, we estimated that a 50-year-old participant with high carbohydrate intake (>65% of energy from carbohydrate) would have a projected life expectancy of 32·0 years, compared with 33·1 years for a participant who consumed 50–55% of energy from carbohydrate.”

Do you see how both of these claims have used the small comparator group extremes (<30% and >65%) to make the reference group look better?

Back to the children skiing… If we were to use the data we have so far (50% of autistic children died and 5.5% of non-autistic children died) and to extrapolate this out to predict survival, life expectancy for the autistic children would look catastrophic. This is exactly what has happened with the small groups – <30% carb and >65% carb – in this study.

The data have been manipulated.

When Bad Science Can Harm You
by Angela Stanton

“Statistical Analysis

We did a time varying sensitivity analysis: between baseline ARIC Visit 1 and Visit 3, carbohydrate intake was calculated on the basis of responses from the baseline FFQ. From Visit 3 onwards, the cumulative average of carbohydrate intake was calculated on the basis of the mean of baseline and Visit 3 FFQ responses…”

WOW, hold on now. They collected carbohydrate information from the first and third visit and then they estimated the rest based on these two visits? Do they mean by this that

  1. The data for years 2,4,5, and 6 didn’t match what they wanted to see?
  2. The data for years 2,4,5, and 6 didn’t exist?

What kind of a trick might this hide? Not the kind of statistics I would like to consider as VALID STATISTICAL ANALYSIS.

“…WWhen Bad Science Can Harm You
Angela A Stanton, Ph.D. Angela A Stanton, to reduce potential confounding from changes in diet that could arise from the diagnosis of these diseases… The expected residual years of survival were estimated…”

Oh wow! So those who ate a lot of carbohydrates and developed diabetes, stroke, heart disease during the study were excluded? This does not reduce confounding changes but actually increases them. That is because the very thing they are studying is how carbohydrates influence health and longevity, that is no diabetes, no strokes, and no heart disease. By excluding those that actually ended up with them completely changes the outcome to the points the authors are trying to make rather than reflect the reality.

Also, if they presume a change in diet for these participants, why not for the rest? Do you detect any problems here? I do! […]

There are 3 types of studies on nutrition:

  1. Bad
  2. Good
  3. Meaningless–meaning it repeats something that was already repeated hundreds of times

This study falls into Bad and Meaningless nutrition studies. It is actually not really science–these researchers simply cracked the same database that others already have and manipulated the data to fit their hypothesis.

I have commented all through the quotes from the study of what was shocking to read and see. What is even more amazing is the last 2 sentences, a quote, in the press release by Jennifer Cockerell, Press Association Health Correspondent:

Dr Ian Johnson, emeritus fellow at the Quadram Institute Bioscience in Norwich, said: ‘The national dietary guidelines for the UK, which are based on the findings of the Scientific Advisory Committee on Nutrition, recommend that carbohydrates should account for 50% of total dietary energy intake. In fact, this figure is close to the average carbohydrate consumption by the UK population observed in dietary surveys. It is gratifying to see from the new study that this level of carbohydrate intake seems to be optimal for longevity.‘”

It is not gratifying but horrible to see that the UK, one of the most diseased countries on the planet today, plagued by type 2 diabetes, obesity, and heart disease, should consider its current general carbohydrate consumption levels to be ideal and finds support in this study for what they are currently doing.

I suppose that if type 2 diabetes, obesity, and other metabolic diseases is what the country wants (and why wouldn’t it want that? Guess who profits from sick people?), then indeed, a 50% carbohydrate diet is ideal.

Latest Low-Carb Study: All Politics, No ScienceLatest Low-Carb Study: All Politics, No Science
by Georgia Ede

Where’s the Evidence?

Ludicrous Methods. The most important thing to understand is that this study was an “epidemiological” study, which should not be confused with a scientific experiment. This type of study does not test diets on people; instead, it generates guesses (hypotheses) about nutrition based on surveys called Food Frequency Questionnaires (FFQs). Below is an excerpt from the FFQ that was modified for use in this study. How well do you think you could answer questions like these?

Provided by Lancet Public Health
Source: Provided by Lancet Public Health

How is anyone supposed to recall what was eaten as many as 12 months prior? Most people can’t remember what they ate three days ago. Note that “I don’t know” or “I can’t remember” or “I gave up dairy in August” are not options; you are forced to enter a specific value. Some questions even require that you do math to convert the number of servings of fruit you consumed seasonally into an annual average—absurd. These inaccurate guesses become the “data” that form the foundation of the entire study. Foods are not weighed, measured, or recorded in any way.

The entire FFQ used contained only 66 questions, yet the typical modern diet contains thousands of individual ingredients. It would be nearly impossible to design a questionnaire capable of capturing that kind of complexity, and even more difficult to mathematically analyze the risks and benefits of each ingredient in any meaningful way. This methodology has been deemed fatally flawed by a number of respected scientists, including Stanford Professor John Ioannidis in this 2018 critique published by JAMA.

Missing Data. Between 1987 and 2017, researchers met with subjects enrolled in the study a total of six times, yet the FFQ was administered only twice: at the first visit in the late 1980s and at the third visit in the mid-1990s. Yes, you read that correctly. Did the researchers assume that everyone in the study continued eating exactly the same way from the mid-1990s to 2017? Popular new products and trends surely affected how some of them ate (Splenda, kale chips, or cupcakes, anyone?) and drank (think Frappucinos, juice boxes, and smoothies). Why was no effort made to evaluate intake during the final 20-plus years of the study? Even if the FFQ method were a reliable means of gathering data, the suggestion that what individuals reported eating in the mid-1990s would be directly responsible for their deaths more than two decades later is hard to swallow.

There are other serious flaws to cover below, but the two already listed above are reasons enough to discredit this study. People can debate how to interpret the data until the low-carb cows come home, but I would argue that there is no real data in this study to begin with. The two sets of “data” are literally guesses about certain aspects of people’s diets gathered on only two occasions. Do these researchers expect us to believe they accurately represent participants’ eating patterns over the course of 30 years? This is such a preposterous proposition that one could argue not only that the data are inaccurate, but that they are likely wildly so.

Learn why we think you should QUESTION the results of the recent Lancet study which suggests that a low carb diet is bad for your health.
by Tony Hampton

1) Just last year, the Lancet published a more reliable study with over 120,000 participates entitled Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. This study involved participates actually visiting a doctors office where various biomarkers were tracked. Here is the link to this study: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32252-3/abstract In this study, high carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. This is consistent with Dr. Hope and my recommendation to consume a lower carb high-fat diet.

2) Unlike the PURE study, the new Lancet study containing only 15,428 participates entitled Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis used food frequency questionnaires (FFQ) containing 66 questions asking participates what they ate previously. This is not as reliable as a randomized control trial where participants are divided by category into separate groups to compare interventions and are fed specific diets. Using FFQ is simply not reliable. Can you remember what you ate last week or over the last year? FFQ also are unreliable because participates tend to downplay their bad eating habits and describe what they think the researchers want to hear. FFQ are simply inherently inaccurate compared to randomized control trails and allow participates to self-declare themselves as eating low carb in this study.

3) Of the groups participating in the new Lancet study, the lower carb group’s participates were the least healthy of the study participates with higher rates of smokers (over 70% smoked or previously smoked), diabetics, overweight, and those who exercised less. This was not true of the other group’s participates.

4) The so-called low carb group at less than 40% carbs is not really a low carb diet. The participates in this group consuming 35-40% carbs are consuming nearly 200 carbs per day. Many of our patients on a low carb diet are consuming less than 50 carbs per day. So are the participates in this study really on a low carb diet? We would suggest they are not.

5) Declaration of interests: When Dr. Hope and I learned to review research studies, the first question we were taught to ask was: who funded the study. If you click on the study link above and go to the bottom of the study, you will see under the declaration of interest section that there were some personal fees from two pharmaceuticals (Novartis and Zogenix). Pharmaceuticals provide needed resources to fund much-needed research. The big message here, however, is full disclosure. Just as I discussed at the beginning of this post, Dr. Hope and I are somewhat biased towards a low carb high-fat diet. We felt you needed to be aware of this as you read this post. You also need to know who funded the Lancet study we are discussing. You decide how to use that information.

6) The Lancet study is an observational study. Observational studies only show an association, not causation. Association is weak science and should always be questioned.

7) The moderate carb diet in this study was associated with the lowest mortality. In this study, participates ate a diet with 50-55% carbs. This mirrors the current USDA diet which has been recommended over the last 40 plus years. During this timeline, Americans followed the USDA recommendations and reduced saturated fat while increasing carbs in their diets. This led to the onset of the obesity epidemic. Let us not go back to recommendations which have not worked.

8) Media sensationalism and bias. I know it’s frustrating to keep hearing mixed messages and dramatic headlines but this is how the media gets your attention, so don’t be convinced by headlines. If you are still reading at this point in the post, you won’t be sidetracked by dramatic press releases.

STUDY: Do Low Carb Diets Increase Mortality?
by Siim Land

Here’s my debunking:

  • The “low carb group” wasn’t actually low carb and had a carb intake of 37% of total calories…It’s much rather moderate carb
  • “Low carb participants” were more sedentary, current smokers, diabetics, and didn’t exercise
  • The study was conducted over the course of 25 years with follow-ups every few years
  • No real indication of what the people actually ate in what amounts and at what macronutrient ratios
  • The same applies to the increased mortality rates in high carb intake – no indication of food quality of carb content
  • Correlation does not equal causation
  • Animal proteins and fats contributed more to mortality than plant-based foods, which again doesn’t take into account food quality and quantities
  • It’s true that too much of anything is bad and you don’t want to eat too many carbs, too much fat, too much meat, or too much protein…

Is Keto Bad For You? Addressing Keto ClickBait
by Chelsea Malone

Where Did the Study Go Wrong?

  1. This was not a controlled study. Other factors that influence lifespan like physical activity, stress levels, and smoking habits were recorded, but not adjusted for. The “low-carb” group also consisted of the highest amount of smokers and the lowest amount of total physical activity conducted.
  2. The data collection process left plenty of room for errors. In order to collect the data on total carbohydrate consumption, participants were given a questionnaire (FFQ) where they indicated how often they ate specific foods on a list over the past several years. Most individuals would not be able to accurately recall total food consumption over such a long period of time and were likely filled with errors.
  3. Consuming under 44% of total daily calories from carbohydrates was considered low carb. To put this into perspective, if the average person consumes 2,000 calories a day, that is 220 grams of carbohydrates. This is nowhere near low-carb or keto territory.
  4. This study is purely correlational, and correlation does not equal causation. Think of it like this: If a new study was published showing individuals who wear purple socks were more likely to get into a car crash than individuals wearing red socks, would you assume that purple socks cause car accidents? You probably wouldn’t and the same principle applies to this study.

#Fakenews Headlines – Low Carb Diets aren’t Dangerous!
by Belinda Fettke

Not only was the data cherry-picked from a Food Frequency Questionnaire that lumped ‘meat in with the cakes and baked goods’ category while dairy, fruit, and vegetables were all kept as separate entities (implying that meat is a discretionary and unhealthy food??), they also excluded anyone who became metabolically unwell over the 25 year period since the study began (but not from baseline). […]

Dr Aseem Malhotra took it to another level in his interview on BBC World News.

Here are a couple of Key Points he outlined on Facebook:

1. Reviewing ALL the up to date evidence the suggestion that low carb diets shorten lifespan from this fatally flawed association study is COMPLETELY AND TOTALLY FALSE. To say that they do is a MISCARRIAGE OF SCIENCE!

2. The most effective approach for managing type 2 diabetes is cutting sugar and starch. A systematic review of randomised trials … reveals its best for blood glucose and cardiovascular risk factors in short AND long term. […]

The take-away message is please don’t believe everything that is written about the latest study to come out of Harvard T.H Chan School of Public Health. The authors/funders of this paper; Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis paid $5,000 to be published in the Lancet Public Health (not to be confused with the official parent publication – The Lancet). While it went past an editorial committee it has not yet been peer reviewed.

Low-carb or high carb diet: What I want you to know about the ‘healthiest diet’, as an NHS Doctor
by Dr Aseem Malhotra

1418: Jimmy Moore Rant On Anti-Keto Lancet Study
from The Livin’ La Vida Low-Carb Show

Antipsychotics: Effects and Experience

Many people now know how antidepressants are overprescribed. Studies have shown that most taking them receive no benefit at all. Besides that, there are many negative side effects, including suicidality. But what few are aware of is how widely prescribed also are antipsychotics. They aren’t only used for severe cases such as schizophrenia. Often, they are given for treatment of conditions that have nothing to do with psychosis. Depression and personality disorders are other examples. Worse still, it is regularly given to children in foster care to make them more manageable.

That was the case with me, in treating my depression. Along with the antidepressant Paxil, I was put on the antipsychotic Risperdal. I don’t recall being given an explanation at the time and I wasn’t in the mindset back then to interrogate the doctors. Antipsychotics are powerful tranquilizers that shut down the mind and increase sleep. Basically, it’s an attempt to solve the problem by making the individual utterly useless to the world, entirely disconnected, calmed into mindlessness and numbness. That is a rather extreme strategy. Rather than seeking healing, it treats the person suffering as the problem to be solved.

For those on them, they can find themselves sleeping all the time, have a hard time concentrating, and many of them unable to work. It can make them inert and immobile, often gaining weight in the process. But if you try to get off of them, there can be serious withdrawl symptoms. The problems is that prescribers rarely tell patients about the side effects or the long term consequences to antipsychotic use, as seen with what some experience as permanent impairment of mental ability. This is partly because drug companies have suppressed the information on the negatives and promoted them as a miracle drug.

Be highly cautious with any psychiatric medications, including antidepressants but especially antipsychotics. These are potent chemicals only to be used in the most desperate of cases, not to be used so cavalierly as they are now. As with diet, always question a healthcare professional recommending any kind of psychiatric medications for you or a loved one. And most important, research these drugs in immense detail before taking them. Know what you’re dealing with and learn of the experiences of others.

Here is an interesting anecdote. Ketogenic diets have been used to medically treat diverse neurocognitive disorders, originally epileptic seizures, but they are also used to treat weight loss. There was an older lady, maybe in her 70s. She had been diagnosed with schizophrenia since she was a teenager. The long-term use of antipsychotics had caused her to become overweight.

She went to Dr. Eric Westman who trained under Dr. Robert Atkins. She was put on the keto diet and did lose weight but she was surprised to find here schizophrenic symptoms also reduce, to such an extent she was able to stop taking the antipsychotics. So, how many doctors recommend a ketogenic diet before prescribing dangerous drugs? The answer is next to zero. There simply is no incentive for doctors to do so within our present medical system and many incentives to continue with the overprescription of drugs.

No doctor ever suggested to me that I try the keto diet or anything similar, despite the fact that none of the prescribed drugs helped. Yet I too had the odd experience of going on the keto diet to lose weight only to find that I had also lost decades of depression in the process. The depressive funks, irritability and brooding simply disappeared. That is great news for the patient but a bad business model. Drug companies can’t make any profit from diets. And doctors that step out of line with non-standard practices open themselves up to liability and punishment by medical boards, sometimes having their license removed.

So, psychiatric medications continue to be handed out like candy. The young generation right now is on more prescribed drugs than ever before. They are guinea pigs for the drug companies. Who is going to be held accountable when this mass experiment on the public inevitably goes horribly wrong when we discover the long-term consequences on the developing brains and bodies of children and young adults?

* * *

Largest Survey of Antipsychotic Experiences Reveals Negative Results
By Ayurdhi Dhar, PhD

While studies have attributed cognitive decline and stunted recovery to antipsychotic use, less attention has been paid to patients’ first-person experiences on these drugs. In one case where a psychiatrist tried the drugs and documented his experience, he wrote:

“I can’t believe I have patients walking around on 800mg of this stuff. There’s no way in good conscience I could dose this BID (sic) unless a patient consented to 20 hours of sleep a day. I’m sure there’s a niche market for this med though. There has to be a patient population that doesn’t want to feel emotions, work, have sex, take care of their homes, read, drive, go do things, and want to drop their IQ by 100 points.”

Other adverse effects of antipsychotics include poor heart health, brain atrophy, and increased mortality. Only recently have researchers started exploring patient experiences on antipsychotic medication. There is some evidence to suggest that some service users believe that they undermine recovery. However, these first-person reports do not play a significant part in how these drugs are evaluated. […]

Read and Sacia found that only 14.3% reported that their experience on antipsychotics was purely positive, 27.9% of the participants had mixed experiences, and the majority of participants (57.7%) only reported negative results.

Around 22% of participants reported drug effects as more positive than negative on the Overall Antipsychotic Rating scale, with nearly 6% calling their experience “extremely positive.” Most participants had difficulty articulating what was positive about their experience, but around 14 people noted a reduction in symptoms, and 14 others noted it helped them sleep.

Of those who stated they had adverse effects, 65% reported withdrawal symptoms, and 58% reported suicidality. In total, 316 participants complained about adverse effects from the drugs. These included weight gain, akathisia, emotional numbing, cognitive difficulties, and relationship problems. […]

Similar results were reported in a recent review, which found that while some patients reported a reduction in symptoms on antipsychotics, others stated that they caused sedation, emotional blunting, loss of autonomy, and a sense of resignation. Participants in the current survey also complained of the lingering adverse effects of antipsychotics, long after they had discontinued their use.

Importantly, these negative themes also included negative interactions with prescribers of the medication. Participants reported a lack of information about side-effects and withdrawal effects, lack of support from prescribers, and lack of knowledge around alternatives; some noted that they were misdiagnosed, and the antipsychotics made matters worse.

One participant said: “I was not warned about the permanent/semi-permanent effects of antipsychotics which I got.” Another noted: “Most doctors do not have a clue. They turn their backs on suffering patients, denying the existence of withdrawal damage.”

This is an important finding as previous research has shown that positive relationships with one’s mental health provider are considered essential to recovery by many patients experiencing first-episode psychosis.

Red Flag of Twin Studies

Consider this a public service announcement. The moment someone turns to twin studies as reliable and meaningful evidence, it’s a dead give away about the kind of person they are. And when someone uses this research in the belief they are proving genetic causes, it demonstrates a number of things.

First and foremost, it shows they don’t understand what is heritability. It is about population level factors and can tell us nothing about individuals, much less disentangle genetics from epigenetics and environment. Heritability does not mean genetic inheritance, although even some scientists who know better sometimes talk as if they are the same thing. The fact of the matter is, beyond basic shared traits (e.g., two eyes, instead of one or three), there is little research proving direct genetic causation, typically only seen in a few rare diseases. All that heritability can do is point to the possibility of genetic causes, but all that allows is the articulation of a hypothesis to be tested by actual genetic research which is rarely done.

And second, this gives away the ideological game being played. Either the person ideologically identifies as a eugenicist, racist, etc or has unconsciously assimilated eugenicist, racist, etc ideology without realizing it. In either case, there is next to zero chance that any worthwhile discussion will follow from it. It doesn’t matter what is the individual’s motivations or if they are even aware of them. It’s probably best to just walk away. You don’t need to call them out, much less call them a racist or whatever. You know all that you need to know at that point. Just walk away. And if you don’t walk away, go into the situation with your eyes wide open for you are entering a battlefield of ideological rhetoric.

So, keep this in mind. Twin studies are some of the worst research around, opposite of how they get portrayed by ideologues as being strong evidence. Treat them as you would the low quality epidemiological research in nutrition studies (such as the disproven Seven Countries Study and China Study). They are evidence, at best, to be considered in a larger context of information but not to be taken alone as significant and meaningful. Besides, the twin studies are so poorly designed and so sparse in number that not much can be said about them. If anything, all they are evidence for is how to do science badly. That isn’t to say that, theoretically, twin studies couldn’t be designed well, but as far as I know it hasn’t happened yet. It’s not easy research to do for obvious reasons, as humans are complex creatures part of complex conditions.

For someone to even mention twin studies, other than to criticize them, is a red flag. Scrutinize carefully anything such a person says. Or better yet, when possible, simply ignore them. The problem with weak evidence that is repeated as if true is that it never really is about the evidence in the first place. Twin studies is one of those things that, like dog whistle politics, stands in for something else. It is what I call a symbolic conflation, a distraction tactic to point away from the real issue. Few people talking about twin studies actually care about either twins or science. You aren’t going to convince a believer that their beliefs are false. If anything, they will become even more vehement in their beliefs and you’ll end up frustrated.

* * *

What Genetics Does And Doesn’t Tell Us
Heritability & Inheritance, Genetics & Epigenetics, Etc
Unseen Influences: Race, Gender, and Twins
Weak Evidence, Weak Argument: Race, IQ, Adoption
Identically Different: A Scientist Changes His Mind

Exploding the “Separated-at-Birth” Twin Study Myth
by Jay Joseph, PsyD

“The reader whose knowledge of separated twin studies comes only from the secondary accounts provided by textbooks can have little idea of what, in the eyes of the original investigators, constitutes a pair of ‘separated’ twins”—Evolutionary geneticist Richard Lewontin, neurobiologist Steven Rose, and psychologist Leon Kamin in Not in Our Genes, 19841

“The Myth of the Separated Identical Twins”—Chapter title in sociologist Howard Taylor’s The IQ Game, 19802

Supporters of the nature (genetic) side of the “nature versus nurture” debate often cite studies of “reared-apart” or “separated” MZ twin pairs (identical, monozygotic) in support of their positions.3 In this article I present evidence that, in fact, most studied pairs of this type do not qualify as reared-apart or separated twins.

Other than several single-case and small multiple-case reports that have appeared since the 1920s, there have been only six published “twins reared apart” (TRA) studies. (The IQ TRA study by British psychologist Cyril Burt was discredited in the late 1970s on suspicions of fraud, and is no longer part of the TRA study literature.) The authors of these six studies assessed twin resemblance and calculated correlations for “intelligence” (IQ), “personality,” and other aspects of human behavior. In the first three studies—by Horatio Newman and colleagues in 1937 (United States, 29 MZ pairs), James Shields in 1962 (Great Britain, 44 MZ pairs), and Niels Juel-Nielsen in 1965 (Denmark, 12 MZ pairs)—the authors provided over 500 pages of detailed case-history information for the combined 75 MZ pairs they studied.

The three subsequent TRA studies were published in the 1980s and 1990s, and included Thomas J. Bouchard, Jr. and colleagues’ widely cited “Minnesota Study of Twins Reared Apart” (MISTRA), and studies performed in Sweden and Finland. In the Swedish study, the researchers defined twin pairs as “reared apart” if they had been “separated by the age of 11.”4 In the Finnish study, the average age at separation was 4.3 years, and 12 of the 30 “reared-apart” MZ pairs were separated between the ages of 6 and 10.5 In contrast to the original three studies, the authors of these more recent studies did not provide case-history information for the pairs they investigated. (The MISTRA researchers did publish a few selected case histories, some of which, like the famous “Three Identical Strangers” triplets, had already been publicized in the media.)

The Newman et al. and Shields studies were based on twins who had volunteered to participate after responding to media or researcher appeals to do so in the interest of scientific research. As Leon Kamin and other analysts pointed out long ago, however, TRA studies based on volunteer twins are plagued by similarity biases, in part because twins had to have known of each other’s existence to be able to participate in the study. Like the famous MISTRA “Firefighter Pair,” some twins discovered each other because of their behavioral similarities. The MISTRA researchers arrived at their conclusions in favor of genetics on the basis of a similarity-biased volunteer twin sample. […]

Contrary to the common contemporary claim that twin pairs found in TRA studies were “separated at birth”—which should mean that twins did not know each other or interact with each other between their near-birth separation and the time they were reunited for the study—the information provided by the original researchers shows that few if any MZ pairs fit this description. This is even more obvious in the 1962 Shields study. As seen in the tables below and in the case descriptions:

  • Some pairs were separated well after birth
  • Some pairs grew up nearby to each other and attended school together
  • Most pairs grew up in similar cultural and socioeconomic environments
  • Many pairs were raised by different members of the same family
  • Most pairs had varying degrees of contact while growing up
  • Some pairs had a close relationship as adults
  • Some pairs were reunited and lived together for periods of time

In other words, in addition to sharing a common prenatal environment and many similar postnatal environmental influences (described here), twin pairs found in volunteer-based TRA study samples were not “separated at birth” in the way that most people understand this term. The best way to describe this sample is to say that it consisted of partially reared-apart MZ twin pairs.

The Minnesota researchers have always denied access to independent researchers who wanted to inspect the unpublished MISTRA raw data and case history information, and we can safely assume that the volunteer MISTRA MZ twin pairs were no more “reared apart” than were the MZ pairs