Another Study Challenges The Benefits Of Fasting

Another study that challenges the benefits of intermittent fasting:

Intermittent Fasting Reduces Body Fat But Exacerbates Hepatic Insulin Resistance In Young Rats Regardless Of High Protein And Fat Diets, The Journal of Nutritional Biochemistry, February 2017

Intermittent fasting (IMF) is a relatively new dietary approach to weight management, although the efficacy and adverse effects have not been full elucidated and the optimal diets for IMF are unknown.

We tested the hypothesis that a one-meal-per-day intermittent fasting with high fat (HF) or protein (HP) diets can modify energy, lipid, and glucose metabolism in normal young male Sprague–Dawley rats with diet-induced obesity or overweight.

The rats that fasted had higher serum glucose during an oral glucose tolerance test. They also had higher insulin levels. Both of these point to insulin resistance. They found as much. (HOMA-IR is a test for insulin resistance.):

HOMA-IR revealed significantly impaired attenuated insulin sensitivity in the IMF groups.

In conclusion, IMF especially with HF increased insulin resistance, possibly by attenuating hepatic insulin signaling, and lowered glycogen phosphorylase expression despite decreased fat mass in young male rats. These results suggest that caution may be warranted when recommending intermittent fasting, especially one-meal-per-day fasting, for people with compromised glucose metabolism.

In this diagram, when rats were allowed to eat ad libitum, when they wanted, their glucose gradually declined after a meal. When they were on a fasting diet, their glucose stayed elevated.

Insulin resistance accompanies type 2 diabetes, the hallmark of which is high blood glucose. Where does the glucose come from when you’re fasting? Hormones break down glucose stored in liver and muscles and release it to the bloodstream. When those stores are depleted, say, during an extended fast or a low-carb diet, the body breaks down muscle for energy – which would exacerbate sarcopenia (age-related muscle loss).

Study: The Animals Around Us Are Getting Fat Too And It’s Not Because They Watch Too Much TV.

This study looked at animals – over 20,000 animals, 8 species, living with humans or not. It found that, over the last few decades, the animals were getting fatter. The authors say the odds of this happening by chance are 1 in 10 million.

Canaries In The Coal Mine: A Cross-Species Analysis Of The Plurality Of Obesity Epidemics, Proceedings: Biological Sciences, June 2011

A dramatic rise in obesity has occurred among humans within the last several decades. Little is known about whether similar increases in obesity have occurred in animals inhabiting human-influenced environments. We examined samples collectively consisting of over 20 000 animals from 24 populations (12 divided separately into males and females) of animals representing eight species living with or around humans in industrialized societies. In all populations, the estimated coefficient for the trend of body weight over time was positive (i.e. increasing).

The probability of all trends being in the same direction by chance is 1.2 × 10−7.

Surprisingly, we find that over the past several decades, average mid-life body weights have risen among primates and rodents living in research colonies, as well as among feral rodents and domestic dogs and cats. The consistency of these findings among animals living in varying environments, suggests the intriguing possibility that the aetiology of increasing body weight may involve several as-of-yet unidentified and/or poorly understood factors (e.g. viral pathogens, epigenetic factors).

Even when they didn’t eat too much, even when they didn’t exercise too little. Just like us. They got fat:

Our findings reveal that large and sustained population increases in body weights can occur in mammalian populations, just as they have occurred among human populations, even in the absence of those factors that are typically conceived of as the primary determinants of the human obesity epidemic via their influence on diet (e.g. access to vending machines) and physical activity (e.g. less physical education classes in schools).

Even when they were fed as part of lab experiments; even when they were let out to pasture; even when, in the case of humans, they weren’t old enough to feed themselves:

  • “Obesity … is a growing problem for dogs and cats … (and 2007) saw a 19% increase in claims related to obesity.”
  • “Others reported that 19% of horses in a large cohort were obese, even among largely pasture-fed animals.”
  • “An increase in body weights was observed among rats used in carcinogenicity studies in France between 1979 and 1991, despite similar husbandry conditions.”
  • “It is also noteworthy that the obesity epidemic has also occurred among children of six months of age and under, an age group for which explanations involving food marketing, less physical education is schools, and more labour-saving devices seem questionable.”

You know what I think it is? Of course you do because I’ve been saying it for years. It’s chemicals in the environment, notably endocrine disruptors which are known to be obesogenic. These authors think so too:

One set of putative contributors to the human obesity epidemic is the collection of endocrine-disrupting chemicals (endocrine-disruptors), widely present in the environment.

And it’s not going to change anytime soon because makers of these chemicals, like Monsanto and their endocrine-disrupting product Roundup, are having a heyday with the lax regulation  of the current administration. Expect to hear more of the individual-blaming slogans, “Eat less, exercise more!”

Here’s a graph I picked up from the NIH a few years ago. Not that this means anything, but the use of the herbicide Roundup (a potent endocrine disruptor)  took off for agricultural uses in the late 70s. Genetically engineered crops were introduced in the mid-to-late 1990s. GMOs, designed to withstand heavy application of Roundup, were doused with the stuff.

Pesticides aren’t the only sources for endocrine disruptors. BPA in can linings and other plastics and plasticizers are also culprits. Our bodies carry in their tissues a lot more of these chemicals than the bodies of our parents and their parents.

Wary Of This Criticism On Alcohol Study

I saw this tweet from a doctor, Vinay Prasad, where (in a long Twitter thread) he debates the merits of that big Lancet study which said having more than 5-7 drinks a week could be harmful. I follow Dr. Prasad and generally like what he says:

I thought he made some good points (e.g. concordance between epi studies and randomized control trials (RCTs) and, of course, confounding) but I wasn’t dissuaded because:

1. The study withstood peer-review in a prestigious journal. The Lancet has a good reputation, a high impact factor (“the relative importance of a journal within its field; journals with higher impact factors are often deemed to be more important than those with lower ones”)

In the 2014 Journal Citation Reports, The Lancet was ranked second among general medical journals, (with an impact factor of 45), after The New England Journal of Medicine (impact factor of 56).

2. It was a big study (data from nearly 600,000 people). It was international (studies from 19 high-income countries). It had close to 120 co-authors. All of these, to me, improve the credibility of the findings.

3. If the study has problems or is “flawed” (all studies are “flawed”) why not request a formal retraction? Or write a letter to the editor? Or contact the corresponding author with your concerns? I’m not being sarcastic; he seems to have the stock to do this. Why instead go on Twitter and call it “bullshit”? I’m wary of criticisms that degrade into this language.

4. He complains about confounding and publication bias. Good points. But authors of all studies contend with these. There is no pure study. I do like this that he said about confounding:

Confounding, meaning that the people who drink >100g/wk are different than those who drink less, and these differences, not the alcohol drive the outcome.

5. He criticizes epidemiological (epi) studies as a group. But they are useful when, for instance, you can’t ethically perform a trial. Are we to have people consume 10, 20, 30 drinks a week – for years – and compare their disease outcomes to a randomly selected control group that drinks no alcohol? It reminds me of when we gave people syphilis and followed them to record what happened. That was the Tuskegee experiment, one of the last studies of its kind because it was horribly racist and unethical. Ethics is why we don’t conduct a randomly controlled trial on smoking; we’re not going to give people cigarettes to see if they get lung cancer. … Also RCTs have their own problems. They aren’t broadly generalizable, and they too suffer publication and research bias.

6. In the end, he says:

“We may have to make decisions the same way we decide how often to go to the bathroom or movies, i.e. using common sense.”

Common sense. That should be our guide? Forget science? So … How much alcohol should we drink? Use common sense. Never mind that it is subjective and means different things to different people. How many cigarettes should we smoke? How much saturated fat should we eat? How much salt, sugar, coffee, soda pop, trans fat, donuts, burgers, fries, pizza, cookies, bacon, milkshakes? Common sense. (I don’t agree with this.)

There is an element of sexism here in that women who drink alcohol, any amount, increase their risk for breast cancer; men do not.

He didn’t dissuade me about this study. I do not think it is bullshit. There is a biologically plausible mechanism for alcohol’s link to disease. It is an IARC Group 1 carcinogen. It damages tissues. Public health workers should warn consumers about alcohol’s risks and not just tell them to use common sense. Going to the bathroom or the movies will not give you cancer.

When Taking Vitamins Is A Good Idea

Here’s Dr. McDougall on taking vitamins. He’s not a fan.

I’ve posted a lot about the risks of taking too many vitamins. Even the government warns against this. Here’s what they say about calcium:

Getting too much calcium can cause constipation. It might also interfere with the body’s ability to absorb iron and zinc. … In adults, too much calcium (from dietary supplements but not food) might increase the risk of kidney stones. Some studies show that people who consume high amounts of calcium might have increased risks of prostate cancer and heart disease.

Taking too much is clearly a problem. But what about taking a little bit? The RDA? I have been on the fence for years about vitamins. While I agree with Dr. McDougall here, his advice assumes being able to eat a healthful diet. Some people don’t. The ideal, of course, is to get our vitamins from food, but we do not live in an ideal world. These are some people I think would benefit from taking vitamin supplements:

    • Smokers – Necessitates higher consumption of at least vitamin C
    • Alcoholics – Necessitates higher consumption of at least the B vitamins
    • People who use drugs, either prescription or illicit – e.g. the common diabetes drug Metformin can lead to a vitamin B12 deficiency
    • Older adults – Polypharmacy, forgetfulness, difficulty getting food, cooking food, eating food
    • Mentally ill – Difficulty getting food, cooking food, eating food
    • People who are sick or disabled – Difficulty getting food, cooking food, eating food
    • Dieters – May not eat enough, may cut out nutritious food groups
    • People with eating disorders – May not eat enough, may cut out nutritious food groups
    • Fussy eaters – May not eat enough, may cut out nutritious food groups
    • People who lack transportation – Seniors who no longer drive, college students, difficulty getting food
    • People with low income – Access, in all permutations of the word

This mental exercise has shown me the futility of making a list like this. Just about everyone falls into a category that has them eating less-than-ideal. It’s probably more the rule that people don’t eat well than that they do.

Advocating taking supplements opens a Pandora’s box! What to take, how much. Contamination issues, safety issues. It’s so much easier to say we should get our vitamins from food.

Pet Neglect

Right?

  • Locking your pet up for hours when you go out. Pet neglect.
  • Putting your pet in a cage. A cage. I mean, a cage. Other than when transporting. Pet neglect.
  • Feeding your pet crap from a bag that says “pet food.” Pet neglect.
  • Surgically removing bones (e.g. declawing*) or beaks or tails or other parts of your pet as a convenience to you or your furniture. Pet neglect. No, this is outright animal abuse. Actually a lot of this is animal abuse.
  • Not taking your pet to the vet who can take care of worms, fleas, and other serious diseases. Pet neglect.
  • Not bathing and grooming your pet. Regularly. Pet neglect.
  • Not giving your pet a chance to engage in its natural behaviors, like mating. Like running (or flying) as fast as it can through an open field with no tether**, as it was designed to do, if it was, say, a dog (or a bird). Pet neglect.
  • If there’s any chance your pet could harm a person (e.g. barking at 1:00 a.m. with neighbors in hearing distance), a person’s property, or another pet, you should train it. If it does cause harm, you should take responsibility for it. If not, pet neglect.
  • Should I even say this one? Having your pet put down if you cannot, or don’t want to care for it. Animal abuse.

* Onychectomy, popularly known as declawing, is an operation to remove an animal’s claws surgically by means of the amputation of all or part of the distal phalanges, or end bones, of the animal’s toes. Although common in North America, declawing is considered an act of animal cruelty in many countries.

**

Sourdough Bread Starter

Years ago I tried making my own starter by setting out a bowl of flour and water and hoping some wild yeast would alight. I never had much luck, so this time I bought a little ball of live starter. Mail order! From Breadtopia. So far so good.

This comment on Amazon sold me on Breadtopia:

The wet dough sourdough product is excellent. Upon feeding and expanding it woke up very quickly and leavened loafs extremely well. Lots of classic sourdough taste and lots of gas production. But as a university microbiologist, I can’t just try out a sourdough starter. I had to take it to the lab and find out what’s in it. I am happy to report that the starter contains precisely what it should: one species of yeast and one species of lactic acid bacteria. It is a complex task to definitively identify them as the authentic Saccharomyces exiguus and Lactobacillus sanfranciscensis, but everything is consistent so far with them being derived from authentic San Francisco sourdough. In particular, as one subcultures them repeatedly, the levels of each stay pretty consistent. This is a hallmark of an authentic sourdough starter pair of microbes. I highly recommend this product.

Personal Choice Is A Myth When The Food Environment Is Toxic

In my mind, “convenient” here refers to access. And access is a whole lot more than, “Do they sell it at my store?” Access refers to being able to afford a food, and being able to prepare it: having the kitchen, appliances and utensils, knowledge, time, ability, transportation, storage. “Access” is a big word. The barriers to access make consumption of a nutritious diet more costly as you move down the socioeconomic ladder.