Saturday, December 31, 2016

"Widespread Praise for The Case Against Sugar"

I cut added sugar 30 years ago. Well worth it...

Link via Gary Taubes

Tuesday, December 27, 2016

"THIS IS SAD: ‘Star Wars’ Actress Carrie Fisher Dies at 60 After Suffering Heart Attack…."

Indeed...

Link via Instapundit

"THEY TOLD ME IF WE ELECTED DONALD TRUMP THERE’D BE BOOK BURNINGS AT AMERICAN UNIVERSITIES. AND THEY…"

Horrible.

Link via Instapundit

Thursday, December 1, 2016

"How Paleo Could Revolutionize Medicine"

Pity he doesn't mention Lieberman's "The Story of the Human Body", which is about exactly this topic.

Link via The Paleo Diet – Robb Wolf on Paleolithic nutrition, intermittent fasting, and fitness

Sunday, November 13, 2016

Thoughts on Spreadbury's "Cellular Carbohydrate" Hypothesis



Thanks to Jamie Scott and Melchior Meijer (PolderPaleo) for an interesting discussion about this hypothesis. This embedded tweet should get to you to the entire discussion, if you're interested.


Ian Spreadbury published this paper in 2012 [PDF]:

"Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity"

It's an interesting read, and well-reasoned. At first I skimmed it, but then went back and reread thoroughly.  Spreadbury addresses many of my initial criticisms himself in the paper, so I won't go back and reiterate them. Read the whole thing, it's interesting.

My criticism of it is therefore only two-fold, although the first point is the key one.

First, the basic hypothesis is that "cellular" carbohydrates, that is, starches that are bound up in plant cell walls, are more healthy than "acellular" carbohydrates. An example of an acellular carbohydrate would be wheat flour or refined sugar, and a cellular carbohydrate would be a carrot, raw or cooked.

Plant starches are bound inside of cells, and these cells have largely indigestible (by humans) walls made of cellulose and pectin, basically. Fiber, in other words. In order to access the glucose in the starches for food, we must break down the cell walls.

We can do this in two ways: grinding with our teeth or with some machinery, like a mill; or cooking.

Spreadbury states:

"Tubers, fruits, or functional plant parts such as leaves and stems store their carbohydrates in organelles as part of fiber-walled living cells. These are thought to remain largely intact during cooking, which instead mostly breaks cell-to-cell adhesion."

He provides two links to back this up, one of which looks at carrots, the other at something which has nothing to do with cooking (footnotes 92 and 93 in his paper).

First, a little background. There's a simple way to measure whether the carbohydrates in a food are cellular or acellular.  It's the glycemic index (GI).

GI measures how quickly glucose from food enters the bloodstream.  Since we can't access the glucose inside a cell wall very well, the GI of a food measures how acellular it is: cellular carbohydrates will have a low GI, as our digestive system struggles with the fiber and is unable to access the glucose within.  Acellular carbohydrates will have a high GI, as the cell wall won't impede digestion.

This is demonstrated in the following study, which compares raw and cooked potatoes to raw and cooked carrots:

"The Effect of Cooking upon the Blood Glucose Response to Ingested Carrots and Potatoes"

I'll save you the numbers, here's the summary: raw potatoes and carrots have a similar effect on blood glucose: low.  The glucose is therefore cellular, and generally not available to us or our gut microbiome (I presume they were chewing the potatoes and carrots, so there is some availability). Cooked carrots have little change in GI: cooking may soften the walls, but doesn't break them down enough to allow our digestive tract to easily access the glucose.

Cooked potatoes, on the other hand, have almost the same GI as pure glucose: the cell walls are almost entirely broken down.  This holds in a similar fashion for every tuber I looked at except for carrots.  

Since Spreadbury discusses the Kitivans, I looked at some of their favorite tubers, like taro: same effect.  Cell walls are almost entirely broken down: they're high GI.

Spreadbury's hypothesis is that the high availability of acellular carbohydrates affects the gut microbiome, not blood sugar. But since our gut bacteria have a first shot at high GI foods, any effect on our blood sugar must also represent availability to our gut microbiome. Since clearly these tubers are no longer acellular after cooking, as reflected by the high GI, there must be some other explanation.

Some of these tubers have a higher GI than a hamburger bun, for instance, which is surely an acellular carbohydrate.

So he got that fact wrong.  

Cooked tubers like a potato or what the Kitivans eat are clearly acellular carbohydrates, just as acellular as a hamburger bun.  If you want acellular cooked tubers, you'd best stick to carrots, which are not on the Kitivan menu.

I agree with Spreadbury that low-GI foods are better for you than high-GI foods.  But if the Kitivans aren't obese and leptin resistant (and don't have any other symptoms of the metabolic syndrome commonly blamed on carbohydrates) a high-GI, high-carb, acellular diet cannot be the cause.

Second, Spreadbury notes that these tubers are basically composed of three ingredients: water, fiber, and carbohydrates.  This is correct, so let's examine this avenue as a "weak" version of Spreadbury's theory.  Spreadbury alludes to this here:

"This cellular storage appears to mandate a maximum density of around 23% non-fibrous carbohydrate by mass, the bulk of the cellular weight being made up of water. The acellular carbohydrates of flour,94 sugar and processed plant-starch products are considerably more dense."

Perhaps it's the density?  The fact that the carbohydrates are consumed with fiber and water?  The problem here is that this reading of the hypothesis is not novel.

It was first proposed by Dr. Denis Burkitt in 1966.  Burkitt's "fiber hypothesis" is the reason so many people are today advised to eat fiber.  Since Spreadbury does not mention Burkitt in his paper, I assume he's unaware of him.

Burkitt, like Spreadbury, was quite clear that his was a hypothesis, but Burkitt's was tested extensively over the years.  While people are still writing papers on it, and still recommending it, as far as I'm aware every solid test of fiber on disease has been negative, or such a small effect that it couldn't be said to be causal.  No disease that Burkitt noted has ever been cured by adding back fiber in any form to the diet.  Spreadbury even notes this:

"The proposed importance of the cellularity and low carbohydrate density of fruit and vegetables in maintaining an evolutionarily appropriate microbiota might explain the failure of supplementary fiber, vitamins, or antioxidants to replicate the health effects of a diet of fruit and vegetables when taken with a Western diet."

I came to Burkitt after being afflicted by diverticulosis, which is one of the diseases he attributes to the replacement of fiber-containing "natural" carbohydrates with refined carbohydrates, those in which the fiber has been removed.

Burkitt's theory is a better theory than Spreadbury's, as Spreadbury's relies on a misunderstanding of what cooking does to the cell walls in tubers.  Neither really had an explanation for a mechanism, but you don't need to know the mechanism for a treatment to be effective, so that's fine.

Based on Burkitt's fiber hypothesis, doctors recommended a high-fiber diet to people like me with diverticulosis for decades.  I'll focus on diverticulosis, since Burkitt did, and since I know it well.

As Burkitt explains in an article contained in Western Diseases, their Emergence and Prevention:

"The occurrence of diverticular disease is believed to depend on a long period of exposure to low fibre diets..."

In 2012, the same year Spreadbury's paper was published, someone finally got around to testing Burkitt's fiber hypothesis as it relates to diverticulosis.  It was published in the journal Gastroenterology:


"The complications of diverticulosis cause considerable morbidity in the United States; health care expenditures for this disorder are estimated to be $2.5 billion per year. Many physicians and patients believe that a high-fiber diet and frequent bowel movements prevent the development of diverticulosis. Evidence for these associations is poor. We sought to determine whether low-fiber or high-fat diets, diets that include large quantities of red meat, constipation, or physical inactivity increase risk for asymptomatic diverticulosis."

Their findings?
  
"A high-fiber diet and increased frequency of bowel movements are associated with greater, rather than lower, prevalence of diverticulosis. Hypotheses regarding risk factors for asymptomatic diverticulosis should be reconsidered."

Burkitt himself should have figured this out, as the Maasai warriors in Africa, where he practiced, ate a low-fiber diet for decades, and didn't suffer any of the ill-effects that he describes.

But the important thing to note is that the Africans Burkitt encountered had a "high-fiber diet and increased frequency of bowel movements", but did not get diverticulosis.  So something else must be causative.

Spreadbury's article is a very interesting one, and he contains many observations with which I agree. I will also note that replacing the Standard American Diet with almost anything else is an improvement, a view with which I suspect Spreadbury would agree.  But I see no convincing evidence that this is because the replacement diet contains fiber, cellular or otherwise.  In fact, a diet comprised wholly of cellular foods has been shown to be very insufficient, given the human digestive tract.

Unfortunately his central thesis depends on a misunderstanding of the effects of cooking on cellular structures in food, and even, as he himself notes, the weak explanation of his theory has never been shown to work.

After first finding Burkitt's book six or so years ago, I've continued to study the matter of what causes what he terms Western Diseases.  There are better explanations, which better fit the universe of facts we have, and for which we have at least some understanding of the mechanisms.

That's one of the missions of this blog, after all.

P.S.  Here are Spreadbury's two comments on this topic.  First, to the twitter discussion:


.@TuckerGoodrich @PolderPaleo - Response from Dr Ian Spreadbury on our previous Twitter thread re: cellular vs acelluar CHO
It's true we don't know enough about what different forms of cooking are doing to cellular or subcellular structure. There were a few papers I cited in 2012, which indicated cells were breaking off their neighbours, but were staying mostly intact. Cellularity is only one theoretical difference of life-derived minimally processed foods though, whatever is going on in poi after a long period of cooking likely doesn't make a difference to health, as that's how I believe a lot of the Kitavan root veg was being prepared. Exactly where on the slippery slope / grey area of cooking and more advanced processing things start becoming a problem is something that needs a lot more study. I don't feel too worried about whether it's whole cells knocking around, or complex molecular chaperoning, the patterns of microbial gene activation by a complex substrate, or just a reduced density of the rapidly usable stuff - at the end of the day it's nutrient broth versus life, the role of the food - bacterial - neuroimmune - metabolic interaction still seems a decent explanation however the details shake out.

I'm thinking much more about the parallels with periodontal disease these days - bacterial infiltration into cells and all sorts starting to be unraveled. This is so much more complex than LPS, and the periodontal chaps are still trying to work out what's going on in as accessible an area as the mouth.

Second,  to this post.  The second has an Easter egg in it that refutes one of my presumptions above. See if you can pick it out. ;)

.@TuckerGoodrich @PolderPaleo A speedy reply from Ian Spreadbury to Tucker's post.
He's right that we just don't know the factors that are making the difference, but it's something of a side argument. I take a stab at proposing some mechanisms by which bacteria might behave differently in the presence of 'real food'. However, it's ultimately Cooper's microbiota profiling from dental tartar and the broader dental archaeology that strongly suggest that somehow a flour / sugar interaction is what is going on, at least in the mouth. ‎How it works is going to be interesting for sure, but I'm not basing the argument on those micro-mechanisms. ‎Our mouth's microbial friends are somehow changed by modern foods, and a similar change is what I'm arguing then drives the health problems one swallow away in the gut.‎

This is why Cleave ducked the argument , he was a smarter man than I ;)

'"there is no need to discuss here the biological mechanisms involved in this resistance; what matters is that such resistance is not present in inert foods".

Friday, November 4, 2016

Putting the Icing on the Cake: Zach Bitter and Phil Maffetone

So what happens when a top endurance runner (two American records and a World) who's Paleo and runs in Minimalist shoes, takes up the Maffetone Method?

He gets faster, quickly.  Although starting at a 6:15 MAF pace doesn't hurt!

A great podcast at Endurance Planet.


From the looks of it, he's getting the hang of trail running, too.

Wednesday, November 2, 2016

"Indistinguishable From Magic?"

Sounds like this might be a factor in biological systems...

Link via In the Pipeline

Wednesday, October 12, 2016

Saturday, October 8, 2016

"R.I.P., Brock Yates. “Yates told you that the speed limits were bad, and then he broke them in publ…"



Link via Instapundit

"Facing a Silent Liver Disease Epidemic" or Willful Blindness?

This article, from Chemical & Engineering News via Scientific American, is a rather perfect example of much of what's wrong with what passes for science and journalism, and scientific journalism.

They're discussing non-alcoholic fatty liver disease (NAFLD), and they mention diet as a fix, but only in the following fashion:

"Right now, a doctor can only recommend lifestyle changes—better diet, more exercise, less alcohol—to stop or reverse damage to the liver, which has an amazing ability to regenerate healthy cells. Unfortunately, studies have shown again and again that people are unable to stick to a healthier regime, and liver specialists would like to be able to offer treatments."

And:

"Some involved are convinced that—barring a significant change in diet and exercise to prevent fat from continuing to accumulate in the liver—people will need to be treated chronically, much like with a diabetes drug. Intercept’s Pruzanski says the treatment approach will likely come down to how effective drugs are at sustainably reversing the course of the disease."

That's it, those are the two mentions of "diet".

My first problem with this article is that there is no mention of this study:

"Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease--A pilot study."

Building on work done by the US National Institute of Health, this Polish team found this result:

"Following the six-month dietary intervention, hepatic steatosis resolved completely in all patients."
That came out a year before the current news article.  

So here's the problem: we have an article about an incurable, widespread disease, with a bunch of purported experts in the field interviewed, and the only study to show a 100% cure rate of this condition isn't even mentioned.  100% cure rates in any field are virtually unheard of, and never in pharmacology.  

If "science" was working the way we all think it should, this paper and work inspired by it would be the entire basis of the article.  But no, all we get is crickets, and the dismissal of dietary therapy because people are "unable to stick" to it.

Well, so this gets down to a simple analysis of odds.  Let's assume the Polish study is a valid result.

On the other hand, we have a pharmaceutical industry that has a success rate of pretty close to zero for targeting a disease and developing a therapy with a 100% cure rate, as this post makes clear.  

And that near-zero chance of curing a disease comes after years of research, by which point everyone currently suffering from the disease is likely to be dead.

I know where I'd bet, given those two options.  The Polish study doesn't require perfect adherence to that diet, as I follow their approach a whole lot more diligently than the people in that study did, and yet they all benefited.

So your odds of treating this disease are almost infinitely higher on the dietary therapy, than the near-zero chance of a pharmaceutical treatment with the same level of efficacy.

We do know that despite the gloomy assessment of the efficacy of diet in the news story that people will, in fact, change their actions based on health claims.  We all switched to the diet that induces fatty liver disease because of the health claims, now recognized as erroneous.  

Most people stopped smoking after the health implications became clear.  Education was far more successful than any anti-smoking drug.

So this article is being written in complete ignorance, apparently, of the only approach that one should logically advocate: the one with a 100% cure rate and immediate availability.

That's a pretty damning indictment of the whole enterprise, in my opinion.

What's even more damning is that what's also not mentioned is that there is a pharmaceutical candidate that has shown benefits for NAFLD, using the same approach as the dietary one above, albeit with a far lower efficacy:

"Pentoxifylline decreases oxidized lipid products in nonalcoholic steatohepatitis: New evidence on the potential therapeutic mechanism"

But you wouldn't know about this from that piece, which has the unique characteristic of entirely missing all the useful information going on in this field of study.

Tuesday, October 4, 2016

Thursday, September 29, 2016

Kilian Journet Cancelled Everest Attempt

Just saw this.

Bummer, but smart.  Everest will be there next year, and with a fatality rate that varies from 33% to 10%, that mountain is not to be trifled with.

Tuesday, September 27, 2016

"15 facts about running"

More like 8 facts. Which is pretty good by running-advice standards!

Link via Google Alert - daniel lieberman

Sunday, September 25, 2016

Thoughts on "Is the High-Fat, Low-Carb Ketogenic Diet Right for You?"


Interesting article, and a decent overview of the topic:

"In May, I sat down with a former Special Forces medic (who asked not to be named) who served multiple combat tours. He said that at the most elite levels of the U.S. military, people aren’t waiting for research to confirm the benefits of a keto diet. “I’d say more than a third of the guys are doing it, for the endurance and also for the cognition,” he said. As research by D’Agostino and others indicates, the anti-­inflammatory benefits of ketone bodies on the brain may add a measure of injury protection. In fact, the medic told me that he used the keto diet to supplement his own TBI treatment at Walter Reed hospital."

However, it does contain the usual journalistic silliness:

"Even if it’s the right path to follow, low-carb eating in a high-carb world is tricky. Outside Online’s editor, Scott Rosenfield—a long-distance mountain biker—tried the diet earlier this year, leaning heavily on canned sardines and staying under 50 grams of carbs per day. He liked the results. “One day I did a 100-mile solo ride on my fat-tire bike,” he said. “I felt like Superman.” 
"The sustained power was one thing; sustaining the diet was another. “It got monotonous,” Rosenfield said. Another problem was ordering “weird” food at restaurants and having to explain the diet to bewildered friends and service staff. Predictably, eating sardines became a chore. He fell off."

I'm a big fan of sardines, but I surely don't eat them every day.  The missing part of this article is the dangers of too much polyunsaturated fats, either omega-3, like in sardines, or omega-6, like in seed oils.

My mainstay while travelling is a cheeseburger and bacon with no bun or fries.  Generally restaurants are happy to offer extra pickles or a side salad in exchange.  Just skip the salad dressing, which is usually high in omega-6 fats.  There's not much of a trick to it.

I also question the "too much protein is bad" commentary.  We're uniquely adapted to both ketosis (we have higher body fat than any other primate) and a high-protein diet. So I doubt that they're in conflict.  A significant component of protein is leucine, a branched-chain amino acid, which is metabolized to ketones, not glucose.  So it's possible that the reduction in serum ketone levels after protein consumption is due to leucine metabolism, which takes place inside the cells, and is not visible via serum tests.

But overall an interesting article, especially to those not overly-familiar with the topic.

Via Mark's Daily Apple.

Tuesday, August 9, 2016

"Understand the Brain? Let’s Try Donkey Kong First."

Absolutely brilliant approach. "Here we take a simulated classical microprocessor as a model organism, and use our ability to perform arbitrary experiments on it to see if popular data analysis methods from neuroscience can elucidate the way it processes information. We show that the approaches reveal interesting structure in the data but do not meaningfully describe the hierarchy of information processing in the processor. This suggests that current approaches in neuroscience may fall short of producing meaningful models of the brain."

Link via In the Pipeline

"The Sad State of Human Dietary Research"



Link via In the Pipeline

Thursday, July 28, 2016

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

I think we're pretty close to putting this whole thing to bed.  Two of the three Hardrock 100 winners are low-carb athletes, and the third, while high-carb, trains fasted for hours on end and can do prodigious feats on stored fat along.  (I haven't done a post yet on any of them!).

Now this.

"Especially the carbs, he's got such a sweet tooth. But he's found now that if he does cut back on carbs the weight does come down a lot easier than it did in the past. And cutting out foods like breakfast cereals and a lot of the wheat products and bread but still eating enough food — the right food — that he is able to not feel hungry during the day. If you look at his build from the 2011 Vuelta compared to now, he's still lean but his muscles look a lot more defined. So now he has found a way of doing it ..."
That's his girlfriend and nutrition advisor.

Here's the athlete:

"In the Vuelta that year (2011), I think my muscles were probably lighter. I was gangly. You wouldn't look at me and say, 'That's someone who's strong.' Whereas now, my diet is a lot more protein based. I've cut back on carbs completely but I'm not losing muscle."

Yeah, that is how it works.

"I think hard about the quality of the food I'm eating – organic fruit, vegetables and meat wherever possible. It's a common misconception that because we're training five or six hours a day that we can eat what we want and burn it off. It really is a case of watching every little thing you put in your mouth and how it's going to benefit you. Your body really does respond to tweaks then."

Paul Jaminet would approve of this:

"I try to go very light in terms of diet. In the mornings I limit myself to just the one bowl of porridge, and normally a two-egg omelette, with no hint of extras on the side. No second helpings, no picking, nothing. If there is a big stage ahead that day I'll try a three-egg omelette, but warily, and I'll mix a small amount of white rice into the porridge ..."

So he's not no-carb, but he's pretty explicitly low-carb.

The incomprehension of this feat in the press is simply priceless.  I found this article, "This is what you have to eat to compete in the Tour de France", which states:

"09:00 Breakfast 
"Riders have their breakfast around three hours before the race — carbohydrate-rich foods like bread, muesli, cereal, fruit, coffee, smoothies, orange juice and even noodles help top up glycogen stores. 
"“One thing all riders avoid is eating heavy food,” says Judith Haudum, sports nutritionist to the BMC Racing team
"“They have to resist the enticing pastries from the hotel breakfast bar because this type of food isn’t fully digested in time for the start, making riders’ stomachs feel uncomfortably heavy.” 
10:30 Pre-race snack 
"Transfers from hotels to stage starts can be long, offering an opportunity to top up carbohydrate and calories — typically, rice cakes with honey, raisin bread or a sports bar are consumed with fluid."

No mention of Chris Froome, who won the race last year and again this year. We saw what he's eating above.  Is a three-egg omelete "heavy"?

Breakfast of champions
Here's his breakfast on a recovery day:

"The carbohydrates in the avocado (which contains about 320 calories) provide him with a source of quick energy, while the hefty amount of protein and fat in the eggs (70 calories each), avocado, and fish (100 calories for 3 ounces) helps fuel muscles and slow the breakdown of food in the body. 
"That helps steady energy levels and stave off hunger pangs. Plus, since the eggs are poached and the fish is smoked, they have no added fats or oils.
"As an added energy boost, Froome has a sachet of cherry-juice concentrate, 2 tablespoons of which would give him about 18 grams of carbohydrates and about 70 calories."
"Carbohydrates in the avocado"!?!  An avocado contains 17 grams of carbs, and a lot of that is fiber, which enters the bloodstream as fat, not glucose.  I'd be surprised if there are more than a few grams of digestible carbs in an avocado.  So that puts him at 20-30 grams of carbs for breakfast, a far, far cry from what's "required"!

I can't tell you how many times I've heard that a low-carb athlete could never win the Tour. "Once is an accident. Twice is coincidence. Three times is an enemy action."  The enemy in this case is coming to obliterate the carbs-are-needed-for-performance baloney we've been sold for decades.

The other thing I always hear is that low-carb doesn't improve performance.  It pretty clearly improved Chris Froome's performance!

"After Chris Froome cut back on carbs for more protein, he lost 20 pounds, started winning the Tour de France, and became a millionaire"


Your results may vary.

Via the excellent Diet Doctor.

Wednesday, July 27, 2016

"America's First Double Hand Transplant Recipient Wishes He Could Have Limbs Removed"

This is pretty horrible:
"Mr Kepner, from Augusta, Georgia, had lost his hands in 1999 due to sepsis, which begun as a throat infection and spread. 
"He used prosthetics, and was able to drive and have a job. 
"He says his functionality has reduced from around 75 per cent to zero since the double hand transplant, and his wife Valerie has resigned from her job to look after him full time. 
"“From day one I have never been able to use my hands,” he said. “I can do absolutely nothing. I sit in my chair all day and wear my TV out.""

Surgeons get away with murder.  If a medical device or pharmaceutical company was performing experiments like this on human subjects, they'd throw them in prison.

Kempner's at least taking responsibility for his own decision:

"“That’s the chance you take,” he said. “And that’s the chance I took.”"

Sadly, they can't even remove the hands and give back the 75% of his life that he had before.

Tuesday, July 26, 2016

"Appalachian Trail Record Attempt #3….here we go again"

Good luck! (I like the support from the Jureks. Is ultra running the last redoubt of sportsmanship?)

Link via Karl "Speedgoat" Meltzer – World Class Endurance Runner

Sunday, July 24, 2016

Varicose Veins and Linoleic Acid

I've really come to think that my little dietary odyssey is coming to it's close.  This is just getting too easy.

So this morning I went for a run with a fellow who had surgery for really bad varicose veins.  He disclosed this in a conversation where I suggested that he was training too hard (he said his zone 2 HR was 140-160, based on a max HR of 220: the old, debunked formula).  Needless to say, he was struggling.  I used to follow the same approach, so I know what it feels like.

I suggested he'd benefit from reading Maffetone's work, and he said he'd knew of Maffetone, but was following his doctor's advice.  He seemed very dismissive.

Oh Lord, please help all those who follow their doctor's advice.  No one else can.

So I got curious about causation of varicose veins.  They're highly correlated with generic cardio-vascular disease, after all, and might well share the same cause, as the symptoms are superficially similar.

It's become overwhelmingly clear to me that oxidative linoleic acid metabolites (OxLAMs), which are produced in the body in the mitochondria, and are often highly toxic, are the likely cause.

"HODEs are stable oxidation products of linoleic acid (LA; C18:2, omega-6). LA is the most abundant fatty acid in atherosclerotic plaques, being seven times more abundant than arachidonic acid (AA). Oxidized lipids accumulate at sites of tissue injury, including atherosclerotic plaque. It was recognized more than 50 years ago that oxidized fatty acids accumulated in low-density lipoprotein (LDL) with age, particularly in individuals susceptible to atherosclerosis []. HODEs were 20 times more abundant in the LDL of patients with atherosclerosis compared with controls []. The structure of 9-HODE and 13-HODE, are shown in Figure 1, along with LA and the omega-3 fatty acid α-linolenic acid (ALA; C18:3, omega-3). Although the structures of these fatty acids differ only subtly, there is accumulating evidence that HODEs have distinct biological properties. Accumulation of HODEs in human atherosclerotic lesions was described nearly two decades ago [], when they were shown to be components of both the cholesterol ester and phospholipid fractions. LA accounts for 40–45% of the polyunsaturated fatty acid (PUFA) in plaque, and 30% of PUFAs in plaque are oxidized. HODEs are the most abundant oxidation products in plaque, and they are present in all advanced lesions, although the quantity varies from patient to patient []."

I've not found a randomly-controlled study just yet, (although this one comes close):

"The Lyon diet-heart study was one of the most successful intervention trials of all time. The experimental group increased their intake of fish, poultry, root vegetables, green vegetables, bread and fruit, while decreasing intake of red meat and dairy fat. A key difference between this study and other intervention trials is that participants were encouraged to eat a margarine rich in omega-3 ALA. In sum, participants decreased their total PUFA intake, decreased omega-6 intake and increased intake of ALA and long-chain omega-3s. After an average of 27 months, total mortality was 70% lower in the intervention group than in the control group eating the typical diet!"

Linoleic acid (LA) is the primary polyunsaturated omega-6 fat in the Modern American Diet. OxLAMs are produced in the body from excess LA in the diet, can be reduced by a reduction of LA from the diet, and such reduction appears to have (in one small study) a 100% success rate in reducing at least one major aspect of the Metabolic Syndrome, the primary health scourge of our time.

Took a while, a couple of hours, but here we are:

"Generation of reactive oxygen species by a sufficient, insufficient and varicose vein wall
(Full-text PDF, backup link here.)

I'll snip a few relevant points:

"Despite numerous theories, the etiology and pathogenesis of primary varicose veins remain unclear. The etiology of chronic venous diseases (CVDs) known as chronic venous insufficiency (CVI) is related to leukocyte trapping. Leukocyte trapping involves trapping of white cells in vessel walls followed by their activation and translocation outside the vessel. Release of reactive oxygen species (ROS) from trapped white cells has been documented. Superoxide dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as malonyldialdehyde (MDA). The aim of this study was to determine the involvement of free radicals in the etiology of venous changes."

Well there we go.  MDA, along with 4-HNE and acrolein (and a whole host of others) are OxLAMs. I will object to their statement that OxLAMs are generated by ROS, as it's clear that they're generated independently.

"The levels of oxidative stress markers strongly correlated with lesions observed by USG in insufficient and varicose veins. In both a higher concentration of MDA was observed, which is a sign of lipid peroxidation. Antioxidative mechanisms, SOD activity and total antioxidative power expressed as FRAP were inversely proportional to MDA concentration. In insufficient and varicose veins both FRAP and SOD activities were significantly lower than in normal veins. The severity of clinical changes was inversely dependent on the efficiency of scavenging of ROS, which additionally proves the participation of free radicals in pathogenesis of CVDs."

There you have it.

"These results confirm that a patients suffering from chronic venous insufficiency are constantly under oxidative stress. Their TAS is lowered and lipid peroxidation level (measured as MDA concentration) increased.... 
"...Interaction between leukocytes and endothelium (which results in toxic metabolites e.g., MDA; Rojas & Phillips, 1999) is promoted by slow venous flow (Danielsson et al., 2003). Mahmound et al. (2002) found strong lipid peroxidation (increased MDA concentration) around insufficient venous valves (compared to normal noninflamed vessels). This phenomenon was also confirmed in our research. Also Tryankina et al. (2003) drew attention to decreased amount of plasma antioxidants and increased lipid peroxidation in patients with varicose veins in comparison to healthy individuals. All this shows how strongly oxidative stress can decrease defense mechanisms of patients witch [sic] CVI (Wlaschek et al., 2005)."

This also suggests that the mechanism behind varicose veins is identical to that behind atherosclerosis.

LA isn't directly toxic, but it turns into poison in the body.  Excess LA consumption is to be avoided like the plague.

P.S.  Well, I missed this:

"First, all parameters we researched: antioxidant enzyme activity, TAS and FRAP bring us to a conclusion that the main reason behind CVI is antioxidative system dysfunction."

That's wrong.  It's antioxidative system overload.  Reduce the load, resolve the disease.

"Also simple modification of the patients diet and lifestyle can have beneficial effects."

They're right about that, but they don't specify what to do.  If you're dealing with an overload of oxidative linoleic acid metabolites, and linoleic acid solely enters the body through the diet, the answer should be clear...

Friday, July 22, 2016

Barefoot Running and Working Memory

"The aim of the present study was to compare the potential cognitive benefits of running barefoot compared to shod. Young adults (N = 72, M age = 24.4 years, SD = 5.5) ran both barefoot and shod on a running track while stepping on targets (poker chips) and when not stepping on targets. The main finding was that participants performed better on a working memory test when running barefoot compared to shod, but only when they had to step on targets. These results supported the idea that additional attention is needed when running barefoot to avoid stepping on objects that could potentially injure the foot. Significant increases in participant's heart rate were also found in the barefoot condition. No significant differences were found in participants' speed across conditions. These findings suggested that working memory may be enhanced after at least 16 minutes of barefoot running if the individual has to focus attention on the ground."
Emphasis mine.

The certainly falls under the "No Duh" category of scientific studies!  Anyone who's ever run barefoot can attest to the fact that you pay much closer attention.  The idea that it may have some larger benefit is neat, of course.

And the higher heart rate is likely just a factor of novice barefoot runners.  I've consistently noticed over the years that my HR drops a few beats per minute when I take off the shoes during a run, even if they're minimalist shoes.


Via:

Thursday, July 21, 2016

Primates Prefer Alcohol

And are, apparently, well-adapted to consuming it:

"It’s somewhat “shocking” that the animals preferred beverages with the highest alcohol levels, says Matthew Carrigan of Santa Fe College in Gainesville, Fla., who was not involved in the research. Alcohol is loaded with valuable calories, but “it’s a challenge to use those calories without getting inebriated. … If you are climbing around in the trees, 40 to 50 feet off the ground, perhaps at night and surrounded by predators, would you want to be drunk?”
Probably not a great idea.  

I've always pooh-poohed the idea that moderate alcohol consumption is more healthy, since alcohol is a toxin, after all.  But the dose makes the poison, and everything's toxic in the wrong amount.

If we're well-evolved for it, perhaps it's because there's a benefit.  This study doesn't show that, but it makes me think...

Research links:

Alcohol discrimination and preferences in two species of nectar-feeding primate

Tools to tipple: ethanol ingestion by wild chimpanzees using leaf-sponges

Thursday, July 14, 2016

"Paying Farmers To Go Organic, Even Before The Crops Come In"

The power of the free market.  Corporations respond to their customers' demands.

Reminds me of Yvon Chouinard:

TH: Well, let's talk about politics for a second. I've got a quote here from you that I really like. "A million or ten million dollars a year won't go far toward solving the world's problems; however, if you want to change government, change the corporations, and government will follow. If you want to change corporations, change consumers." 
Are you trying to change the government through consumers? 
YC: Well, I've kind of given up on government, the idea that government is going to solve our problems. If you look at the candidates now, the environment hardly even shows up. But they're all talking about symptoms: Iraq is a symptom, healthcare is a symptom. They're all symptoms of society breaking down. Nobody is really attacking the causes. 
And so I'm trying to change corporations, and I'm trying to change consumers.


He succeeded in his business, and set the model for everyone else to follow.


 

"If You Have Back Pain Do Not Forget About Your Feet"

Great post.

Link via The Paleo Diet – Robb Wolf on Paleolithic nutrition, intermittent fasting, and fitness

Thursday, June 16, 2016

"How running shoes change the muscles in your feet"

“People who walk barefoot tend to have stiffer, stronger feet,” said Daniel Lieberman, a professor in the department of human and evolutionary biology ... They're only measuring two muscles, and other studies have found contradictory results. My own experience was that my feet got dramatically stronger after going minimalist, so much so that they changed shape.

Link via Google Alert - daniel lieberman

Friday, June 10, 2016

"1944 OSS Sabotage Manual"

"Someone noticed that parts of it read like standard modern office procedures."

Link via Schneier on Security

Friday, June 3, 2016

"Understand the Brain? Let’s Try Donkey Kong First."

Absolutely brilliant approach. "Here we take a simulated classical microprocessor as a model organism, and use our ability to perform arbitrary experiments on it to see if popular data analysis methods from neuroscience can elucidate the way it processes information. We show that the approaches reveal interesting structure in the data but do not meaningfully describe the hierarchy of information processing in the processor. This suggests that current approaches in neuroscience may fall short of producing meaningful models of the brain."

Link via In the Pipeline

Saturday, May 21, 2016

Something went crazy...

Don't know why all those posts from Instapundit suddenly showed up here.  They've been removed, except for the ones I meant to publish from earlier in the week.

Friday, May 6, 2016

Numena: The Absurdity of Certainty

A new documentary a friend of mine is working on.  Check out the promo below.  It looks very interesting!

"An Inspiring, Surreal, Cerebral Documentary
"Explore the rise of certainty in the Western worldview with quantum physicist turned reclusive philosopher, Dr. F. David Peat, as he makes a humorous plea for Gentle Action."

NUMENA: The Absurdity of Certainty from Numena: Absurdity of Certainty on Vimeo.

Wednesday, May 4, 2016

"Medical Errors Now Third Leading Cause of Death in United States"

"Their analysis, published in the BMJ on Tuesday, shows that "medical errors" in hospitals and other health care facilities are incredibly common and may now be the third leading cause of death in the United States -- claiming 251,000 lives every year, more than respiratory disease, accidents, stroke and Alzheimer's. 
"Martin Makary, a professor of surgery at the Johns Hopkins University School of Medicine who led the research, said in an interview that the category includes everything from bad doctors to more systemic issues such as communication breakdowns when patients are handed off from one department to another."

I'll wager that if poor dietary recommendations, like the recommendation to consume seed oils, were included, they'd be number one.

From the study:

"Medical error has been defined as an unintended act (either of omission or commission) or one that does not achieve its intended outcome,3 the failure of a planned action to be completed as intended (an error of execution), the use of a wrong plan to achieve an aim (an error of planning),4 or a deviation from the process of care that may or may not cause harm to the patient.5"

Monday, May 2, 2016

The "Biggest Losers" Seem To Be The Winners

"In fact, most of that season’s 16 contestants have regained much if not all the weight they lost so arduously. Some are even heavier now."

From the article: "Scientists tracked “Biggest Loser” contestants over time. The results, publishing today, may explain why weight loss is so hard."
Doesn't sound very promising.

Saturday, April 23, 2016

A Cardiologist Tries Ketosis

Interesting.

"What is it like in ketoland? Well, for one thing I only need 4 hours of sleep.  Asthma, which has plagued me all my life, is now nonexistent. Wrinkles have melted from my face, like wax from a burning candle. I have boundless energy. The best comparison I can come up with is the transformation Jeff Goldblum underwent in David Cronenberg’s (1986) The Fly. Come to think of it, he was probably also on a LCHF diet. Hopefully, I won’t experience his complete transformation."

I think if you're worry about carbs from cauliflower as he does you don't understand this way of eating well enough, and I for sure don't spoon-feed myself coconut oil.  I did at the very beginning, when I was both low-carb and low-fat for a couple of weeks, since I didn't really understand what I was doing, and had cut out linoleic acid as my primary fat but not replaced it with anything.  Boy, was that spoon-full heavenly at the time!

What was really interesting about that experiment was that my body didn't crave linoleic acid in any way.  It was only the healthier fats that I would fantasize about.

And I never noticed any reduction in sleep requirements, but then people are variable.

Thursday, April 21, 2016

Juicing

Fancy Juice Doesn’t Cleanse the Body of Toxins. “To say that drinking juice detoxifies the body isn’t quite the same as claiming leeches suck out poisons, but it’s fairly close.”


Hey, if you enjoy it, fine.  But be realistic.

Tuesday, April 19, 2016

Interesting Boston Race Results

Didn't watch the race, so I have no idea how the elites did, but I just came across this article with some notable finishers:
Amby Burfoot, 69, 4:17:48, 1968 Boston Marathon winner and Runner’s World writer at large. 
Scott Jurek, 42, 4:09:27, ultrarunner who set the Appalachian Trail thru-hike speed record last year
Daniel Lieberman, 51, 3:34:21, paleoanthropologist at Harvard University whose work helped inspire the barefoot running movement.
Yep, Dan Lieberman beat Scott Jurek, 9 years his junior, in a race.  And you thought he was just smart.

I don't know what he was wearing on his feet!

P.S. See the comments below, Jurek decided at the last minute to run—how does that work, anyway?  I thought Boston was hard to get into!—so it's probably not fair to point out the Lieberman beat him.

However, Arnulfo Quimare, who beat Jurek in the race that was the climax of Born to Run, also ran Boston this year.  Lieberman beat him, too.

Arnulfo Quimare, 33, 3:38:11, the Tarahumara runner who defeated Scott Jurek in the 2006 race that was featured in the book Born to Run

Thursday, April 7, 2016

Native American Running Events at the Boston Marathon

From Dan Lieberman, this morning.  Please spread the word!

Native American Running: Culture, Health, Sport

Harvard University and the Boston Athletic Association are pleased to co-sponsor Native American Running: Culture, Health, Sport on April 15 and 16.  Coinciding with both the 2016 Boston Marathon and with the 80th anniversary of Ellison Myers “Tarzan” Brown, Sr. (Narragansett) winning the Marathon in 1936, this multi-day event will explore the history and importance of Native American running traditions, present efforts to support and encourage running in Native American communities today, and promote the many benefits of running.

The multi-day event kicks off with a conference on Friday, April 15 1:30 – 5:00 at Harvard's Science Center (Room C) featuring talks by native American runners including Olympian Billy Mills (Oglala Lakota), Oren Lyons (Haudenosaunee), Arnulfo Quimare (Tarahumara), Irma Chavez (Tarahumara), Dustin Martin (Navajo), Chris Sockalexis (Penobscot), Mathew Gilbert (Hopi), Alyssa Mt. Pleasant (Tuscorara), Tleena Ives (Port Gamble S’Klallam) and others.  There will also be talks by David Carrasco, Daniel Lieberman, Chris McDougall, and more.

The conference is free, and no registration is required. See the full schedule at https://www.peabody.harvard.edu/native-american-running.

On Saturday April 16 at the Boston Marathon Expo (Hynes Convention Center), Billy Mills will speak at 11:00, and there will be a panel discussion from 12-1:00 featuring Rob De Castella, Irma Chavez, Dan Lieberman, Dustin Martin, Chris McDougall, Arnuflo Quimare and more.
This event is also free and open to the public

If you've never been to an event with Dan Lieberman and Chris McDougall, make it a priority.  They're both very knowledgeable (although Prof. Lieberman takes the cake!), and very entertaining speakers.  Most highly recommended.

Thursday, March 31, 2016

"Remembering Todd Ragsdale"

Just saw this. He died back in January. He held the world record for barefoot running in 24 hours (102 miles). He died the same way Caballo Blanco did: out doing what he loved. RIP.

Link via iRunFar.com

Thursday, March 10, 2016

"The £3.45 ‘Alzheimer’s Drink’ that Stops Brain from Shrinking"

Contains omega-3 fats, choline, among other things.  DHA is an important component of brain mitochondria.

We've Been Eating Processed Food For 3.5 Million Years


"The origins of the genus Homo are murky, but by H. erectus, bigger brains and bodies had evolved that, along with larger foraging ranges, would have increased the daily energetic requirements of hominins1, 2. Yet H. erectus differs from earlier hominins in having relatively smaller teeth, reduced chewing muscles, weaker maximum bite force capabilities, and a relatively smaller gut3, 4, 5. This paradoxical combination of increased energy demands along with decreased masticatory and digestive capacities is hypothesized to have been made possible by adding meat to the diet6, 7, 8, by mechanically processing food using stone tools7, 9, 10, or by cooking11, 12. Cooking, however, was apparently uncommon until 500,000 years ago13, 14, and the effects of carnivory and Palaeolithic processing techniques on mastication are unknown. Here we report experiments that tested how Lower Palaeolithic processing technologies affect chewing force production and efficacy in humans consuming meat and underground storage organs (USOs)....
"...Although cooking has important benefits, it appears that selection for smaller masticatory features in Homo would have been initially made possible by the combination of using stone tools and eating meat."

Lieberman's previously published research showing that soft food causes deformations of the jaw that's similar to what we see in modern humans who require teeth to be pulled and braces.

Here's some color from the NYT:

"...Other patrons got three courses of meat (goat, in this case). Dr. Zink grilled the meat in the first course, but offered it raw and sliced in the second. In the third course, her volunteers received an uncooked lump of goat flesh. 
"In some of the trials, the volunteers chewed the food until it was ready to swallow and then spat it out. Dr. Zink painstakingly picked apart those food bits and measured their size. 
"“If that was all my dissertation was, I would have quit graduate school,” Dr. Zink said. “It was as lovely as it sounds.”... 
"...As long as 3.5 million years ago, scientists have found, hominins were making stone tools. Cut marks on mammal bones suggest that the tools were used to carve meat from carcasses." 

P.S.  Here's a short (60-Second Science!) interview with Prof. Lieberman.

Tuesday, March 8, 2016

Oxidized Linoleic Acid Metabolites in Obesity

Interesting study:

Oxidized Linoleic Acid Metabolite (HNE)
"...In conclusion, oxidative stress or more precisely the level of oxidative damage to lipids and consequently proteins, as measured by free MDA and by HNE–protein adducts, was significantly increased in obese humans if compared to healthy controls." 
"Measurement of HNE-protein adducts in human plasma and serum by ELISA—Comparison of two primary antibodies"

They were testing a mechanism to measure HNE levels, not obesity per se, but it's an interesting result nevertheless.

Obesity is, of course, correlated with the rest of the metabolic syndrome.

Monday, March 7, 2016

"Statisticians Found One Thing They Can Agree On: It’s Time To Stop Misusing P-Values"

In statistics, one rule did we cherish:
P point oh five we publish, else perish!
Said Val Johnson, “that’s out of date, Our studies don’t replicate
P point oh oh five, then null is rubbish!”

If they actually did this, the medical research field would be out of business...

"Sailors Face More Lenient Body Fat Rules"

"The service branch loosened its body fat restrictions in January and is allowing those who failed their exams three or more times to get one more opportunity to be tested this spring under the more lenient guidelines. The Navy said it has been losing too many talented sailors. Some were resorting to liposuction, diet pills and other measures to save their careers."

The military follows the USDA guidelines, from what I've seen in the past, so this is hardly surprising.  The Modern American Diet has an amazing ability to make people fat.

""It's absurd the percentage of high school teenagers who are considered to be too fat to join the military," Joyner said. "Maybe there are two problems: One, obesity, and the other that the standards are out of date and not relevant.""

They're out of date because everyone has becmoe too fat.

Thursday, March 3, 2016

"Botswana Loses a National Treasure"


via Science on the Run

"...Shortie's experience immersed in the bush allowed him and his age-mates to track wild animals at an advanced level. Their skill of pursuit was so practiced that they almost became the creatures they were following, and were therefore able to make predictions about where the animal was headed, then test those predictions based on evidence presented by fresh tracks. This allowed them to catch up to animals which would otherwise outpace the hunter. Shortie's teachings allowed Louis [Liebenberg] to develop his theory of tracking as the origin of humankind's scientific mind, from which all science and technology, which the global economy thrives on today, were to ultimately follow. Louis' profound thesis is published in his book, "The Art of Tracking, The Origin of Science."...  
"...He was among the last of the great walking Encyclopedias of the Kalahari, and his passing is somewhat like the burning of a library. It signifies the very nearing end of an Age. Young people in the Kalahari villages do not have the same opportunity to immerse themselves in the bush, nor are they very interested in the old ways. We mourn not only that Shortie is no longer with us in the flesh to colour the present, but the impoverished future around the corner for the coming generations. They might have more material wealth and distractions, but they will understand much less than the immediate generation before them.  
"So long dear friend, we are mere students without a Master.  
 "—The indigenous people of Botswana"

Monday, February 29, 2016

"Pipelines"

Sizes of various (hypothetical) pipelines to convey various "fluids". Pretty fascinating.

via xkcd.com

A Direct Line From Dietary Linoleic Acid To Alzheimer's Disease?

Sure looks like it (PDF).

4-hydroxy-2-noneal (4-HNE) is produced in the mitochondria of those with excess amounts of linoleic acid (LA) in their diets.  It turns out it's also important in Alzheimer's and other neuro-degenerative diseases.

"The mitochondrial enzyme ALDH2 exerts an important physiological protection in a variety of tissues, as it degrades highly toxic aldehydes originating from the lipid peroxidation cascade, mainly 4-HNE. Protection afforded by ALDH2 has been observed in conditions in which oxidative stress and the resulting excessive production of 4-HNE causes tissue damage, often evolving toward degenerative processes (Ohsawa et al., 2008; Wey et al., 2012). Thus, ALDH2 appears to be implicated in diverse pathologies such as Alzheimer’s and Parkinson’s diseases and ischemic conditions (Ohsawa et al., 2008; Wey et al., 2012). Here, we examined the role of ALDH2 in the development of endothelial dysfunction produced by the vasculotropic amyloid Ab (Ab1–40), known to be involved in the pathogenesis of the Alzheimer-associated cerebral amyloid angiopathy (CAA) (Donnini et al., 2010)."

So if they increase ALDH2, they decrease 4-HNE, and reduce the damage to the cell.

"The present work identifies a specific detoxifying mechanism, provided by activation of a mitochondrial enzyme, ALDH2, by means of the selective activator Alda-1. The protection of the vascular endothelium from injuries arising from toxic products of lipid peroxidation [4-HNE] afforded by this activator could have implications for a wide range of diseases in which impairment of mitochondrial function and angiogenesis are the underlying pathogenetic mechanism. Our findings, demonstrating that activation of ALDH2 by Alda-1, prevents the injurious effects of Ab on vascular endothelium and preserves angiogenic phenotype and responsiveness, may have applications for other age-related vasculopathies, including those associated with diabetes and vascular dementia."

Their are other ways to reduce "toxic products of lipid peroxidation", that don't require more research.


Friday, February 26, 2016

"The Least Competent and Most Corrupt Law Enforcement Agency Spent $200 Million Per Arrest"

Yikes.

via View from the Wing

"Oxidative Stress and Mitochondrial Dysfunction in Alzheimer's Disease."

Sounds familiar:

"Alzheimer's disease (AD) exhibits extensive oxidative stress throughout the body, being detected peripherally as well as associated with the vulnerable regions of the brain affected in disease. Abundant evidence not only demonstrates the full spectrum of oxidative damage to neuronal macromolecules, but also reveals the occurrence of oxidative events early in the course of the disease and prior to the formation of the pathology, which support an important role of oxidative stress in AD. As a disease of abnormal aging, AD demonstrates oxidative damage at levels that significantly surpass that of elderly controls, which suggests the involvement of additional factor(s). Structurally and functionally damaged mitochondria, which are more proficient at producing reactive oxygen species but less so in ATP, are also an early and prominent feature of the disease. Since mitochondria are also vulnerable to oxidative stress, it is likely that a vicious downward spiral involving the interactions between mitochondrial dysfunction and oxidative stress contributes to the initiation and/or amplification of reactive oxygen species that is critical to the pathogenesis of AD.

Emphasis mine.  From my post on how to prevent oxidative damage in your mitochondria:

"It seems that what they're describing here is a mitochondrial death spiral..."

Thursday, February 25, 2016

Osteoarthritis and Omega-6 Fats (Linoleic Acid)

Well...

"...Conclusions: Linoleic acid [LA] has a pro-inflammatory effect on cartilage whereas oleic acid and palmitic acid seem to inhibit cartilage destruction. These results indicate that altered fatty acid levels may influence loss of cartilage structure in OA." 
"Monounsaturated and Saturated, but Not n-6 Polyunsaturated Fatty Acids Decrease Cartilage Destruction under Inflammatory Conditions"

There's another way to read that, of course, if one assumes that high levels of LA are not normal....

This next study is hilarious; yes, if you assume that high levels of LA (which don't exist naturally) are "normal" this would be a mystifying result:

"We report here the finding that normal, young cartilages, in distinction from all other tissues exa- mined, have unusually high levels of n-9 eicosatrienoic (20:3 cis-i5’8”) acid and low levels of n-6 polyunsaturated fatty acids (n-6 PUFA)....
"...The finding of low levels of n-6 PUFA and high levels of unusual n-9 fatty acids, characteristic of EFA deficiency, in normal cartilage is remarkable in view of the fact that normal levels of EFA are present in serum, muscle, liver, kidney, and bone of the same animals (Tables 1-4). To properly understand this finding, it is important to recognize that when tissue from an EFA-deficient animal is transplanted into a nutritionally normal recipient, the EFA-deficient tissue rapidly recovers and regains a normal fatty acid profile within a period of 5 days (19). Thus it seemed implausible that a tissue should exhibit features characteristic of EFA deficiency in an animal with normal levels of EFA in its other tissues. Yet this phenomenon was consistently seen in normal cartilage of all species so far investigated (chicken, calf, human, rabbit, and pig)." 
"Unique fatty acid composition of normal cartilage: discovery of high levels of n-9 eicosatrienoic acid and low levels of n-6 polyunsaturated fatty acids"

If high LA is not normal, but is a result of a novel diet, this study might be alarming.

Especially if we'd been seeing a rise in the incidence of injuries to cartilage....

More to come...

"President of the Australian Diabetes Society Doesn’t Understand Evolution"

It would be funny if it weren't so sad...

via Cliodynamica

Wednesday, February 24, 2016

"NEVER UNDERESTIMATE THE POWER OF SNACKS AND SERENDIPITY:"

"The Amazing True Story of How the Microwave Was Invented by Accident"

Neat.

via Instapundit

"Recovery Addict: How overemphasizing recovery creates dependency"

tl;dr: Tough it out, buttercup.

via Science of Running

What Effect Does Linoleic Acid Have On Mitochondria?


That's really the key question for metabolic syndrome, for as this paper observes:

"The centerpiece of the pathophysiologic mechanism of metabolic syndrome is insulin resistance. Recently, it is becoming evident that mitochondrial dysfunction is closely related to insulin resistance and metabolic syndrome...." 
"Mitochondrial dysfunction and metabolic syndrome—looking for environmental factors"

Diet is, of course, an "environmental factor".  If linoleic acid (LA) really is the cause of mitochondrial dysfunction, then the solution is quite straightforward.

I found this paper (2011):

"Increased mitochondrial matrix directed superoxide production by fatty acid hydroperoxides in skeletal muscle mitochondria"

The "fatty acid hydroperoxides" (FA-OOH) they're discussing* are all from LA, as the paper makes not as clear as they should.  Since they find that dysfunctional mitochondria have lots of LA hydroperoxides, they're looking to see if that's the cause or an effect.

"...Therefore, the purpose of this study was 1) to determine whether FA-OOH’s alter mitochondrial function (rate of ATP production, RCR [respiratory control ratio] and enzymatic activity of respiratory chain complexes) in skeletal muscle mitochondria and 2) to determine the effect of FA-OOH on the topology and sites of superoxide production, using methodologies that can distinguish between superoxide released towards the matrix and towards the intermembrane space...."

Well that sounds right.  How'd they do?

"...We demonstrate for the first time that low micromolar concentrations of FA-OOH decreases the rate of mitochondrial ATP production, RCR and the enzymatic activity of respiratory chain complexes I and III in skeletal muscle mitochondria. Additionally, using methodologies that distinguish between superoxide generation towards the matrix and intermembrane space, we demonstrate that in skeletal muscle mitochondria, FA-OOH (but not FA-OH [fatty acid hydroxide**]) significantly increases the rate of mitochondrial ROS production directed towards the matrix (and not the intermembrane space) with complex I as the major site of ROS production."

So oxidized LA is bad for your mitochondria, increasing oxidation and decreasing energy production. The relevance of this finding is stated in the discussion:

"Previous studies by our group and others have shown that muscle atrophy is associated with an increase in mitochondrial oxidative stress and dysfunction [2, 7, 47, 48]. Our recent study showed that mitochondria isolated from atrophied muscles generate significant levels of lipid hydroperoxides [19]. However, no studies thus far have investigated the role of fatty acid hydroperoxides in the modulation of mitochondrial oxidative stress and dysfunction in skeletal muscle mitochondria."

They also note that this effect is not limited to just skeletal mitochondria:

"Other studies in heart, brain and liver mitochondria also indicate that fatty acids and fatty acid hydroperoxides are important modulators of mitochondrial respiration and ATP production [8, 11, 12, 49, 50]."

"Modulators" isn't the word I'd choose, but the point is the same.

Now based on the results described in yesterday's post, I wonder if the ROS they're finding directed into the matrix are coming from the cardiolipin itself, and not from complex I or III, as cardiolipin lines the matrix.  But that's kind of an academic question.

"In conclusion, we describe an important finding that at low micromolar concentrations, FA-OOH (but not FA-OH) induces skeletal muscle mitochondrial dysfunction."

So oxidized LA metabolites are the cause.

Since we already know that, in humans, reducing LA consumption reduces the mitochondrial production of oxidized LA, and the symptoms thereof, that seems like a pretty safe recommendation.

And you don't need to wait for a drug.


*Why they're discussing "methyl linoleate" is a mystery to me, but whatever.  Perhaps because that's what the suppliers are selling?  Eating biodiesel seems like a bad idea that even a doctor could understand.  As the results they're describing are consistent with other evidence, I'm not going to delve deeper into that mystery.

** Soap?  Really?  Don't eat soap, even if it's OK for your mitochondria.