Thursday, May 7, 2020

Is There More To Obesity Than N-6 PUFA?

Peter at Hyperlipid has a series of posts [1, 2, 3] looking at the Surwit diet, an obesogenic rodent diet from Research Diets (D12330). [4]
"There is more to obesity than [n-6] PUFA (gasp)." [1]
Not so fast!

I was of course curious to see what Surwit et al were up to here. They have a very fat-agnostic view of diet: fat is fat. He changes the formulation of his high-fat, high sucrose (HH) diet from F1850 [5] to D12330 in 1992, but still uses the old studies as references for the new ones, despite switching from lard to hydrogenated coconut oil plus soybean oil.

Fat is fat. Or is it?
"...we used mice and precisely defined isocaloric diets to compare the metabolic effects of saturated fat from coconut oil, unsaturated fats from soybean oil and fructose. To our knowledge, this is the first study not only to compare the effects of these three dietary factors in mice, but also to perform genome-wide expression profiling and metabolomics analysis of livers from animals fed a soybean-oil enriched diet." [6]
"Four isocaloric diets with 4.87 kcal/gm (5.56 kcal total) (Table 1) were formulated in conjunction with Research Diets, Inc. (New Brunswick, NJ). The diets are based on the Surwit diet..."
1.2 kcal% (control) vs 2.2 kcal% vs 10 kcal% from n-6 linoleic acid (LA).

The title says it all: [6]
"Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver"
She was subsequently hired to show that low-LA GMO soybean oil (Plenish) is less obesogenic than regular soybean oil. [7] Which she did. [8]

Neat bit:
"One of these genes, Pdk4, which was upregulated in SO-HFD livers, is known to inhibit the pyruvate dehydrogenase complex that links the TCA cycle with glucose and fatty acid metabolism. Repression of the pyruvate dehydrogenase complex shifts the balance towards gluconeogenesis which could result in hyperglycemia [76]. Consistent with our findings are reports that PDK4 expression is increased in diabetics [122] and that Pdk4-/- mice are resistant to HFD-induced hepatic steatosis and are more glucose tolerant [123,124]. Thus Pdk4 upregulation may be a contributing factor to both lipid accumulation in the liver and the development of diabetes and glucose ntolerance in SO-HFD mice." [6]
That could be a problem...

Lots more interesting findings. Pity Surwit didn't have a more nuanced view of fat.

There's definitely more to obesity than just n-6 fats. But they do seem to play a central role.

(I was looking for some sort of explanation as to why Surwit had switched from F1850 to D12330, and changed the fat used but still added soybean oil. Couldn't find it; Research Diets just mentions that he called them up and specified what became D12330 aka D12331.)

This was originally posted as a comment at [1], there may be responses there.

P.S. Peter replied:
"Ha! These people are so superficial. PDK4 is upregulated in the liver of diabetics because that's how gene expression tries to protect you from the ministrations of the PUFAphiles. PDH complex probably down regulates because normal soybean oil is supplying a sh!tload of low FDAH2:NADH linoleic acid which means the supply of acetyl-CoA will be in excess of the cell's needs and getting more from pyruvate is not needed. So the liver uses PDK4 to avoid even more of a disaster than the cardiologists are pushing for... 
"Just looking down at the ETC level. 

Dobromylskyj P. Surwit diet and derivatives. Hyperlipid. Published April 30, 2020. Accessed May 7, 2020.

Dobromylskyj P. Surwit diet and derivatives (2) It’s the insulin. Hyperlipid. Published May 2, 2020. Accessed May 7, 2020.

Dobromylskyj P. Surwit diet and derivatives (3) 5LJ5 vs D12330: Chow vs Surwit. Hyperlipid. Published May 4, 2020. Accessed May 7, 2020.

D12331 Formula - OpenSource Diets. Research Diets, Inc. Accessed May 7, 2020.

Mouse Diet, High Fat, Fat Calories (60%), Paste. Bio-Serv. Accessed May 7, 2020.

Deol P, Evans JR, Dhahbi J, et al. Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver. PLoS One. 2015;10(7):e0132672-e0132672. doi:10.1371/journal.pone.0132672

GM soybean oil causes less obesity and insulin resistance but is harmful to liver function: Mouse study compares Plenish to conventional soybean, coconut, and olive oils. ScienceDaily. Accessed May 7, 2020.

Deol P, Fahrmann J, Yang J, et al. Omega-6 and omega-3 oxylipins are implicated in soybean oil-induced obesity in mice. Scientific Reports. 2017;7(1):1-13. doi:10.1038/s41598-017-12624-9

Sunday, April 5, 2020

COVID-19: Is Italy — and Mass Quarantine — "Flattening the Curve" or Riding the Trend?

March 16:
To take the COVID-19 pandemic "seriously", must we institute a mandatory shut down, AKA a mass quarantine?

This question prompted me, as always, to ask: has this been tested?

March 16:
Without going through the entire history of epidemics and measures designed to stop them, it can be said that clearly quarantine is one tool to stop the spread of disease.

Nevertheless, as observed in the Journal of School Health in 1951 [1]:
"Anderson and Arnstein in "Communicable Disease Control," 1948, in discussing poliomyelitis, say: "School closure, as well as closure of moving picture theaters, Sunday schools, and other similar groups, is frequently attempted in response to popular demand that 'something be done.' Although tried repeatedly, it is of no proved value, never altering the usual curve of the epidemic: nor has the disease been more prevalent or persistent in those communities with the courage to resist those demands.""
Mass Quarantine and Polio [1]
Now no one would suggest that polio is not a serious disease. While many forget the annual polio epidemics that once terrified Americans, there are few diseases in history that were more serious.

Additionally, since polio was an annual disease, much like influenza, they had a pretty good data set of interventions that worked.

Quarantining the sick to prevent them from spreading the disease was the practice. Quarantining everyone to prevent disease spread through the population was not.

In the case of COVID-19, this is the difference between the intervention pursued in South Korea [2], where the infected and their contacts were tracked:
"“South Korea is a democratic republic, we feel a lockdown is not a reasonable choice,” says Kim Woo-Joo, an infectious disease specialist at Korea University."
And Italy, where the whole country was locked down on March 9. (The Italian lockdown started in the region of Lombardy where the worst infection emerged, on February 21 [3] and spread to all of Lombardy on March 7 [4] then the entire country on the 9th.)

So as Italy developed into the one of the worst COVID-19 outbreaks in the world, I was curious to see if there was any evidence that the severe measures they took had a discernible effect.

For starters, I was curious about the claims of exponential growth. The influential Imperial College (IC) report (whence the phrase "flatten the curve") stated:
"Infection was assumed to be seeded in each country at an exponentially growing rate (with a doubling time of 5 days)..." [5]
This allowed IC to predict that 81% of Americans (220 million) would be infected 90 days out. There are some other problems with these assumptions, but first let's look at that one.

Exponential Growth

Is the spread of this virus exponential?

Exponential means a given initial value, and a constant rate of increase. In order to get to their projected infection prevalence of 220 million Americans, the IC people must have used a "seed", an assumed value of infected people, and then a rate of increase each day of around 15%.

In looking at the Italian data [6], it quickly becomes apparent that the initial spread of COVID-19 in Italy was remarkably fast, far faster than that predicted by the IC in their worst-case analysis. I created two exponential curves, one to match the actual cases on March 9, when the lockdown occurred, and one to match cases on March 27, when I started looking into this.

In this chart, March 9 is indicated in the X axis labels, and you can see there's an inflection in the cases recorded on the date the lockdown was implemented (red arrow). The exponential growth rate for the March 9 curve was 39.72%, and 28.24% for the March 27 curve. (I didn't bother graphing the IC grown projection, as it was almost a flat line at the bottom of the graph.  But what's also immediately apparent is that the curve of the actual cases is not exponential, as the rate of increase appears to be steadily declining (the line crosses both of the exponential curves). Growth is higher early on, but steadily declines.

To drill down on what was actually happening, I next graphed the percentage increase in actual cases.

The orange line again represents the actual number of cases, showing the actual percentage change for each date. The green line again marks the 39.72% exponential growth curve, and the blue line the 28.24% curve. (Since exponential growth is a constant percentage rate of growth, those lines are flat.)

This chart makes it very apparent that the initial increase was explosive, with a 425% increase on one day—from 4 cases to 21. But that sort of increase isn't sustainable. The next day was 276%, then 99%, then 46%.  These early increases are likely artifacts of discovering new cases, so don't represent an actual growth rate, however the spread of the virus was certainly real.

The fascinating thing about looking at the actual data is the things you learn. We already see how fast the initial rate of growth is, but we also see that it's clearly not exponential, it's a steadily declining growth rate.

We also see that the initial rate of increase was worse than the worst-case scenario in the IC paper, in the short term.

Yet, despite implementing draconian lockdown measures, there's no evidence of an inflection point in the curve of the epidemic in Italy. In the initial chart there was what looked like an inflection point on March 9, the day of the full lockdown, but in this view of the data it's clear that was just a tick down in the declining growth rate, which increased back to trend line the following day.

So the next thing to look at is the trends in the data.

"Flattening the Curve"

This chart shows the same as the above, with the increase to 425% truncated out. I think it's an outlier, and not worth considering in looking at the data. When I first did this analysis, I truncated all the data prior to 2/24, but got similar results (with much higher R2), so here I leave it in.

The green line is a logarithmic trend line, the red a 10-day moving average. I picked the 10-day moving average because the median incubation period for COVID-19 is 5 days, with 5 days expected for serious symptoms to occur.

So we see that after an initial explosive growth in cases, the growth rate rapidly declines, and the trends for growth also rapidly decline. The increase on 3/29 is 6%, the increase on 3/31 (not shown) is 4%. The IC expectation for the worst-case was 15% at this point. There's no apparent change in the trend after the nation-wide lockdown of March 9.

So what's clear is that the predictions of exponential growth of 15% per day absent draconian measures was grossly wrong. Actual growth in cases was far higher. There is no clear effect of the implementation of draconian lockdown measures in the curve of growth, as predicted in 1948 [1]:

Riding the Trend
"Although tried repeatedly, it is of no proved value, never altering the usual curve of the epidemic..." [1]
When I started this analysis, I expected to see that the lockdown would have had some effect, what I was surprised to see was the high growth rate initially and the lack of any apparent effect at all.

Unfortunately, given the nature of this epidemic and the lack of testing for it (which is typical of epidemics), cases might be the wrong measure to look at. Cases are dependent on testing, and it's possible that cases are being missed, due to mild effects, in fact it's pretty much guaranteed that mild cases are under-counted.

So I also looked at deaths.

But the curves are almost the same same. Which implies that we may be missing the mild cases, but the cases being tracked do have a close relationship to the death rate. What we do see now though, is that it appears that the deaths track pretty closely to the exponential line (40.6% p/d) up until the lockdown was implemented. This is of course likely why the lockdown was implemented.

If we zoom in to see the details of the growth rate:

Again, an explosive early increase, delayed behind the increase in cases. The date rate increase tracked with the two exponential lines until around the time of the lockdown.

So I also ran the trendlines:

Here the inflection point is closer to the lockdown date, but it still seems to precede it by a few days.

If the nationwide lockdown had caused the downturn in the increases in the deaths, we would expect that we would see an inflection point after the lockdown, not before it.

The concordance between these death and cases lines suggest that the rate of infection shown by the actual cases data is a pretty good indication of some level of serious infection, although we are probably missing a lot of mild and asymptomatic cases. There's also an indication that deaths in Italy may be over-counted, but if so it at least seems to be a consistent over-counting. [7] Unfortunately, due to lack of data from widespread testing and inconsistencies between how statistics are counted in different countries, it's hard to estimate a non-serious infection rate.

I have read that the failure of the lockdown in Italy to prevent Italy from becoming a worst-case scenario is due to the nature of the Italians, who have a reputation for enjoying life without the highest regard for regulation. Whatever the truth of that view may be, I don't think it explains this phenomenon.

A few quotes:
"Residents of Lombardy describe deserted streets and panic after seven virus deaths.... “It’s a surreal situation,” Enrico Bianchi, who owns a veterinary pharmacist, told the Guardian. “People are locked in their houses for fear of going out. It is really strange to go around the town, the few people around are wearing masks.” [1]
From February 24. From March 20 [8]:
"Italian authorities have pressed charges against more than 40,000 people for violating the lockdown, according to figures from the interior ministry."
And the gem:
"Giuseppe Conte, the prime minister, had said the beneficial effects of the lockdown would be felt two weeks from its start as the coronavirus is thought to carry an incubation period of two to 14 days."
That would be March 23rd:

There doesn't seem to be much of a change in the data at that point. His prediction doesn't seem to have born fruit.

But perhaps the most interesting evidence for the compliance of the Italians with the lockdown is this new service from Google [9] which tracks compliance of their users with the lockdown orders, using data they collect from their Android cell-phone operating system.

Italian compliance is far higher than what is happening in the U.S. right now, where workplace reduction numbers are in the order of 38% (in the area where I live).

Italians are clearly obeying the lockdown, and in large numbers, and non-compliance is being dealt with. I'm not aware of a single person that has been arrested in the U.S. for non-compliance.

Life has ground to a halt in Italy, apparently.

"However, the work at hand does provide some cause for limited optimism, suggesting that, even at today’s rapid pace, if a city acts quickly it can buy time even when the pandemic appears at its gates."
That is from a review [10] of two papers analyzing the Influenza Pandemic of 1918. [11, 12] What those papers make clear is that while lockdowns can be effective in containing a quarantine, they are most effective when implemented before a community is infected. This should surprise no one, as even people living in medieval times knew that the best barrier to plague was to live within a walled city. [13] But as a Japanese study looking at influenza in schools noted, looking at the results of their model:
"[Reactive] School closure has a remarkable impact on decreasing the number of infected students at the peak, but it does not substantially decrease the total number of infected students."
Even the peak closure decrease of 24% was in the model, the actual observed data was higher. Reactive closure means closure after the school has been exposed to the pathogen, it's in the community, and while communication from one student to another in school may be blocked, there are other routes of transmission. So whatever benefit reactive closures offered, it was small, and short-lived, as once closures were ended, influenza came right back, infecting most of those students in missed in the first (or second) pass.

So mass quarantine seems to be effective if you are living in a walled city in Spain or in a simulation. As we can see from the Italian case, it seems to be quite ineffective in real life, even in a situation where serious police enforcement is in place to ensure compliance.

It appears to be clear from the Italian data that the claimed success of the lockdowns is simply a matter of the natural course of the epidemic. Comparing Italy to the rest of the world, as the Financial Times does [14] reveals that the gradually-decreasing curve of growth of infections in Italy is typical of the epidemic in other countries:

From Financial Times' COVID-19 Tracking Site
With the notable exception of South Korea, where lockdowns have not been used.

It seems apparent that if you are actually looking to "flatten the curve", then lockdowns are not the most effective means of doing it.

It also seems apparently that the apocalyptic growth estimates used by the Imperial College and others were both too hysterical as to later growth trajectories and also not severe enough to recapitulate the actual course of the epidemic and the ability of authorities to proactively implement mitigation strategies, based on the Italian experience.

Should polio close schools? Journal of School Health. 1951;21(7):249-252. doi:10.1111/j.1746-1561.1951.tb01445.x

How Italy, South Korea differ in tackling coronavirus outbreak | News | Al Jazeera. Accessed March 16, 2020.

Palermo AGLT in. Italians struggle with “surreal” lockdown as coronavirus cases rise. The Guardian. Published February 24, 2020. Accessed March 30, 2020.

Northern Italy quarantines 16 million people. BBC News. Published March 8, 2020. Accessed March 30, 2020.

Ferguson NM, Laydon D, Nedjati-Gilani G, et al. Impact of Non-Pharmaceutical Interventions (NPIs) to Reduce COVID- 19 Mortality and Healthcare Demand. London: Imperial College; 2020:20.

Italy Coronavirus: 105,792 Cases and 12,428 Deaths - Worldometer. Accessed April 1, 2020.

Global Covid-19 Case Fatality Rates. CEBM. Accessed April 3, 2020.

Why Italy’s coronavirus death toll continues to spike despite lockdown – and what the UK can learn. The Independent. Published March 20, 2020. Accessed March 30, 2020.

COVID-19 Community Mobility Report. Accessed April 3, 2020.

Morse SS. Pandemic influenza: Studying the lessons of history. PNAS. 2007;104(18):7313-7314. doi:10.1073/pnas.0702659104

Markel H, Lipman HB, Navarro JA, et al. Nonpharmaceutical Interventions Implemented by US Cities During the 1918-1919 Influenza Pandemic. JAMA. 2007;298(6):644-654. doi:10.1001/jama.298.6.644

Public health interventions and epidemic intensity during the 1918 influenza pandemic | PNAS. Accessed April 3, 2020.

CNN. The hilltop fortress town that cut itself off from the world — and coronavirus. CNN. Accessed April 4, 2020.

Smith A, Blood D, Tilford C, et al. Coronavirus tracked: the latest figures as the pandemic spreads. Published February 8, 2020. Accessed April 3, 2020.

Monday, January 20, 2020

Mark Sisson Wants Me On Joe Rogan's Podcast

I was running in the woods on Sunday, and I got an email.

From an old colleague, who congratulated me on what Mark Sisson had said.

"Umm, what?"

Sunday with Sisson
Sisson's weekly "Sunday with Sisson" newsletter had gone out. I can't find an archive on his site, but here's a newsletter archive site (don't click on links there, they won't work correctly):
I've got an action item for you all.
If you happen to use Twitter, hop on and retweet my tweet asking Joe Rogan to have Tucker Goodrich on the podcast (or send him one of your own). Tucker has been banging the seed oil drum for many years now, and if we could get one of the strongest anti-seed oil voices onto the most popular and influential podcast in the world, the collective health of the podcast-listening community would skyrocket. Seed oils are one of those health topics that requires some time and detail. Sugar's easy to explain. Grains are too. You can hit those in a single elevator ride and get the point across. But seed oil? To really understand the predicament requires at least a 5- to 10-minute conversation.
Joe's podcasts last up to 3 or 4 hours. They are extremely long form. You can really get into the weeds, and the weeds is sometimes where you need to go.
Here's the tweet:
WOW. Thanks, Mark!

The Joe Rogan Experience is the biggest podcast in the world.

This would be an amazing honor, and a fantastic way to get what I think is the most important health message out to the world. He's had lots of great diet topics and debates, including Stephan Guyenet, Chris Kresser, Gary Taubes, and of course Mark Sisson:

Wednesday, January 8, 2020

How Mitochondrial Defects Can Cause Various Seemingly Unrelated Diseases

"A Mitochondrial Etiology of Common Complex Diseases" [1]

An hour-long discussion of how mitochondrial dysfunction can result in various chronic diseases, and how the assumption that an anatomical division of disease is a driving assumption for how medicine is organized, and how that may block correct description and diagnosis of disease.

The speaker is Douglas C. Wallace, Ph.D.; Director, Center for Mitochondrial and Epigenomic Medicine (CMEM); Professor, Department of Pathology & Laboratory Medicine, The Children's Hospital of Philadelphia.

He does an especially good job of describing how malfunction in a single organelle can cause various diseases in various seemingly unrelated organs.

Some useful quotes below the video:

"Our hypothesis (that we've been testing for the last 45 years) is that bioenergetic dysfunction lies at the nexus of the genetic and environmental "causes"; and that the "common-complex" diseases are bioenergetic diseases, and not anatomical diseases." 7:07.
"Now each cell has hundreds of thousands of these mitochondrial DNAs, and they're constantly replicating inside your cells right now. And if you doubt that they're active and vital in there, talking to each other; tonight when it's very very quiet and your spouse is not snoring if you just concentrate you'll feel them wiggling in there." 16:49 
Discussing cells with different mitochondrial genotypes from mutation and division:
"Some with good mitochondrial DNAs and high energy, some with bad mitochondrial DNAs and low energy, and if it's below the minimum energy for that tissue, then you will get a phenotype. The equivalent of a biological, a metropolitan brownout. So if there was a line voltage decline in LA, all the electrical systems wouldn't fail at one time. The first thing that would go would be the fluorescent light bulbs, then certain elevators, then certain electrical motors, but the incandescent light bulbs would just get dimmer and dimmer.  
"Well the same is true for your body. Different parts of your body rely on energy to different extents, so as the energy declines, you're going to get organ-specific symptoms of a systemic defect." 17:35 
Noting the wild variation in expression between mitochondrial defects:
"If you inherit that from your mother you're fine until midlife, and then you'll lose your hearing (sensory-neural hearing loss). But if you get treated by aminoglycoside antibiotics, you'll go deaf within a week. OK? Mutation in the tRNA leucine gene, another protein synthesis mutation at 3243; at 30 % mutant will give you diabetes, 50% mutant give your neuromuscular disease, 100% mutant and you are dead." 18:55 
He goes on with many more examples.
"So we have a quantitative genetics with totally different clinical phenotypes." 20:15 
Tissue-specific Symptomatology
"So why would there be tissue-specific symptomatology? Well because different tissues rely on mitochondrial energy for different extents [sic]... [Examples] ...So in fact when you think energetically, much of anatomy is about energetics, not anatomy." 21:12
"The take-home lesson"
"If the, in fact, the cells are sick, they cannot undergo apoptosis, then the mitochondria are released into the bloodstream, and they are perfectly good bacteria, and you're going to get inflammation. And that's why we believe all of these diseases have an inflammatory component." 23:54

He doesn't discuss my favorite topic, the impact of omega-6 fats on mitochondria and therefore health, but it fits nicely with his hypothesis. For instance, the part of mitochondria that causes the immune reaction and inflammation he describes is cardiolipin released with oxidized linoleic acid into the blood stream. [2]

Do watch the whole thing!

1. A Mitochondrial Etiology of Common Complex Diseases. UCLA CTSI; 2017. Accessed December 20, 2019.

2. Tuominen Anu, Miller Yury I., Hansen Lotte F., Kesäniemi Y. Antero, Witztum Joseph L., Hörkkö Sohvi. A Natural Antibody to Oxidized Cardiolipin Binds to Oxidized Low-Density Lipoprotein, Apoptotic Cells, and Atherosclerotic Lesions. Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26(9):2096-2102. doi:10.1161/01.ATV.0000233333.07991.4a

Sunday, October 20, 2019

The Paleo Canteen Podcast: Tucker Goodrich — Goodbye Mr. Wholewheat

A new podcast interview, with Ally Houston.

This is the first of two episodes, the next one with Ken Strain and me should drop next week.

 Resources for topics discussed are below. (Yes, the format kind of stinks, but that's what happens when you do html formatting in Microsoft Excel via formulas.)

Timestamp format is Hour:Minutes:Seconds

If you find anything egregious as far as typos go, let me know in the comments.


P.S. Timestamps adjusted: -26 seconds. It will match the podcast now.

0:02:13, comment: "Mr. Whole Wheat", resource: ""Diverticulitis": My Story"

0:07:53, comment: "Somewhat bizzare blogger", resource: "Malocclusion: Disease of Civilization, Part III"

0:08:20, comment: "Weston Price's book", resource: "Nutrition and Physical Degeneration"

0:12:58, comment: "Carbohydrate cravings", resource: "Linoleic Acid, Fat Rats In Labs, and Fat Humans"

0:15:21, comment: "I can't remember the term for not being able to recognize faces", resource: "Prosopagnosia Information Page"

0:15:35, comment: "Later in the attack… Supergirl", resource: "Supergirl (TV series)"

0:21:03, comment: "There's a quote that doctors always use…", resource: "The Plural of Anecdote is Data"

0:22:11, comment: "An RCT of parachutes", resource: "Parachute use to prevent death and major trauma when jumping from aircraft: randomized controlled trial"

0:22:28, comment: "Parachute invented by a scientist", resource: "Louis-Sebastien Lenormand"

0:25:01, comment: "The effect it had on my health", resource: "My Vitamin D Experiment"

0:25:56, comment: "ADHD… Dr. Alessio Fasano", resource: "Neurologic and Psychiatric Manifestations of Celiac Disease and Gluten Sensitivity"

0:31:28, comment: "[Dr.] Tro Kalajian", resource: "Dr. Tro's Medical Weight Loss & Direct Primary Care"

0:36:07, comment: "Dr. [Michael] Eades", resource: "The Blog of Michael R. Eades, M.D."

0:39:45, comment: "Dr. Atkin's Book", resource: "Robert C. Atkins, 72, Creator of Controversial Diet, Dies"

0:49:47, comment: "Lots of babies", resource: "RESULTS OF THE SELF-SELECTION OF DIETS BY YOUNG CHILDREN"

0:53:49, comment: "Inject either THC or 2-AG", resource: "Endocannabinoid levels in rat limbic forebrain and hypothalamus in relation to fasting, feeding and satiation: stimulation of eating by 2‐arachidonoyl glycerol"

0:53:50, comment: "Inject either THC or 2-AG", resource: "Observational analysis of feeding induced by Δ9-THC and anandamide"

0:53:58, comment: "2-AG goes up normally in the body", resource: "The role of fatty acids and their endocannabinoid-like derivatives in the molecular regulation of appetite"

0:54:24, comment: "They preferentially eat sugar", resource: "Cannabinoid influences on palatability: microstructural analysis of sucrose drinking after Δ9-tetrahydrocannabinol, anandamide, 2-arachidonoyl glycerol and SR141716"

0:54:38, comment: "When it hits the stomach, it's triggered by seed oils", resource: "The role of fatty acids and their endocannabinoid-like derivatives in the molecular regulation of appetite"

0:55:06, comment: "There was a human drug… that blocked 2-AG's effect", resource: "Leptin-regulated endocannabinoids are involved in maintaining food intake"

0:57:00, comment: "The increase in seed oils", resource: "Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century"

0:57:22, comment: "How much is actually in people's fat tissues", resource: "Increase in Adipose Tissue Linoleic Acid of US Adults in the Last Half Century"

0:57:56, comment: "There's a couple of studies where they take people on a high carb diet", resource: "Effect of a 6-Month Intervention with Cooking Oils Containing a High Concentration of Monounsaturated Fatty Acids (Olive and Canola Oils) Compared with Control Oil in Male Asian Indians with Nonalcoholic Fatty Liver Disease"

0:57:56, comment: "There's a couple of studies where they take people on a high carb diet", resource: "Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease—A pilot study"

0:58:33, comment: "They're the leanest industrail population on Earth", resource: "Big Government, Small Bellies: What Japan Can Teach Us About Fighting Fat"

0:59:08, comment: "How sticky the starch is", resource: "Yes Virginia, The Paleo Diet Was Low-Carb"

0:59:42, comment: "The rate of periodontal disease", resource: "Periodontal Disease"

1:01:27, comment: "All of the animal populations", resource: "Lab animals and pets face obesity epidemic"

1:01:34, comment: "Racoons in Toronto are getting obese", resource: "Enhanced access to anthropogenic food waste is related to hyperglycemia in raccoons (Procyon lotor)"

1:02:03, comment: "Well you know it's pollution", resource: "HOW TINY NAURU BECAME WORLD'S FATTEST NATION"

1:05:16, comment: "French eat more calories", resource: "List of countries by food energy intake"

1:06:04, comment: "Breed's prone to obesity", resource: "A Brief Guide to the Norwegian Elkhound"

1:09:44, comment: "Diabetics are prone to infections", resource: "Infections in Diabetes Mellitus and Hyperglycemia"

1:11:32, comment: "I read Thomas Malthus' book", resource: "An Essay on the Principle of Population"

1:13:18, comment: "Our back molars grew bigger", resource: "The Story of the Human Body, pg 56 kindle edition"

1:13:22, comment: "Chimpanzees can use tools to dig up tubers", resource: "Savanna chimpanzees use tools to harvest the underground storage organs of plants"

1:13:51, comment: "A lot of the big megafauna went extinct", resource: "Global late Quaternary megafauna extinctions linked to humans, not climate change"

1:13:56, comment: "There start appearing shell middens", resource: "Shell middens as archives of past environments, human dispersal and specialized resource management"

1:14:40, comment: "We ran out of butter and animal fats", resource: "Response to Gary Taubes on Omega-6 Fats (Seed Oils) and Obesity"

1:15:33, comment: "The horrible things that corn and soybean agrictulture is doing", resource: "Perspectives On The Vulnerability Of U.S. Agriculture To Soil Erosion: Discussion"

1:16:20, comment: "I have... a couple of fantastic books about the Indians", resource: "Review: "Empire of the Summer Moon""

1:16:20, comment: "I have... a couple of fantastic books about the Indians", resource: "Plenty-coups: Chief of the Crows"

1:16:28, comment: "What did we feed 'em?", resource: "Response to Gary Taubes on Omega-6 Fats (Seed Oils) and Obesity"

1:17:34, comment: "They are all malnourished", resource: "The world health report, Chapter 4: Childhood and maternal undernutrition"

1:18:08, comment: "You retweeted an article recently by an Indian writer", resource: ""Vegetarianism in India neither comes from a love for animals or humans. It only comes from a love of power and hierarchy.""

1:28:40, comment: "The Maffetone Method", resource: "Dr. Phil Maffetone's "Big Book of Endurance Training and Racing" Review"

1:29:45, comment: "The Seven Phases of Heart-Rate Training", resource: "The Seven Phases of Heart-Rate Training"

Monday, April 1, 2019

Follow-up to 'Low-Carb Athletes: Chris Froome, Tour de France Winner 2013, '15, '16.'

Interesting details. He's not keto, or strictly low-carb, but uses it much as Zach Bitter does, tactically.

"Chris Froome has embraced many nutritional strategies during his cycling career, from consuming more Omega-3-rich salmon to repair his muscles, to stoically devouring 400g of energy-boosting rice for breakfast on race days. But one of his most potent weapons is carbohydrate-restricted training – also known as low-carb training, or simply ‘training low.’ 
"“Low-carb training teaches the body to become more efficient at burning fat as a fuel source, as opposed to just using the readily available glycogen (stored energy) in the muscles,” explains Froome... “There are two benefits. One is obviously weight-loss, as it is important to keep lean for the mountains. But the main side is the adaptation in the body to use fat as a fuel source and not depend entirely on glycogen.”... 
"Recreational athletes who copy Froome’s methods can expect to burn more fat and enjoy better stamina. “One of the main adaptations that comes with having more mitochondria in your muscles is that you use more fat for a given (exercise) intensity,” explains Morton. “That is good for endurance because fat is a good fuel source, but it also means when you need to go quicker later on, you should have more carbohydrates left. All of these adaptations happen with standard endurance training anyway, but with carbohydrate-restricted training you get more bang for your buck.”"