Category Archives: Fish

Saturated fat, cholesterol, and carbohydrates

“You catch more flies with honey…”

^^^good policy in general, but especially for debating in the realm of nutritional sciences.

 

A short while back, Nina Teicholz discussed low carb ketogenic diets and plant-based diets with John Mackey.  Although I disagree with the dichotomy (keto vs. plant-based), it’s well-worth a watch:

 

 

Three topics that could not be avoided in such a discussion: saturated fat, cholesterol, and carbohydrates.

 

 

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Carbs: Low vs. Lower

 

 

This was met with much backlash from the low carb cavalry, because, well, if low is good then lower must be better

I’m not anti-keto; but I’m not anti-science.  FACT.  

 

“…some people are not genetically equipped to thrive in prolonged nutritional ketosis.” –Peter Attia

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Vegetable oil fatty acids are not essential. 

They are conditionally essential at best, only if docosahexaenoic acid (DHA) is lacking.  We can’t synthesize omega 3 fatty acids, and indeed they do prevent/cure certain manifestations of “essential fatty acid (EFA) deficiency” (Weise et al., 1958), but DHA can do all that and more.  Not that I recommend this, but a diet completely devoid of 18-carbon vege oil fatty acids will not produce EFA deficiency in the presence of DHA. (“vege,” rhymes with “wedge”)

Essential fatty acid metabolism

 

The “parent essential oils” are linoleic acid (LA) and alpha-linolenic acid (ALA).  The others, which I think are more important and the truly “essential” ones are eicosapentaenoic acid (EPA), arachidonic acid (AA), but mostly just DHA.

The first manifestation of EFA deficiency is dermatitis (Prottey et al., 1975).  Some people say LA is necessary to prevent this, but it would be better phrased as “LA prevents dermatitis;” not “LA is necessary to prevent dermatitis.”  All of the evidence suggesting LA is essential is in the context of DHA deficiency.

Technically, we can convert a bit of ALA to DHA, estrogen helps, testosterone doesn’t (women have better conversion rates)… and I’d speculate that the reverse is probably easier (DHA –> ALA).

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Evolution stole this dude’s circadian rhythm

I got a laugh out of this one; not for the actual content, but because of how the authors worded their findings.  They sure love their fishies.

We have two very closely related fish, both Mexican tetra, Astyanax mexicanus, one with eyes who lives on the surface, and another who’s blind and lives in dark caves (“Pachon”).  It’s thought that they were the same species one day; divergent evolution.

 

note: eyeless

note: eyeless

The blind ones are circadian arrhythmic (Moran et al., 2014).  Surface-dwellers are more active during the day than night (blue line, left figure below), and their free-running circadian clock maintains this in the absence of photic input (blue line, right figure).  The blind ones, on the other hand, exhibit no circadian rhythm in the light or dark (orange lines):

 

Circadian rhythm metabolism

 

Cave-dwellers are circadian arrhythmic.  This is both in their natural photoperiod (ie, darkness) and in light-dark conditions (which is technically an environmental mismatch, but since they’re eyeless, it doesn’t really matter).

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Paleo Plants and Carnivory

From what I gather, it’s been difficult to pinpoint the role of plants in the diet of our ancestors for a variety of reasons.  For example, evidence of plants on cooking tools and dental remains is suggestive but doesn’t disprove the possibility that said evidence came from preparing the plants for some other purpose (eg, tools, weapons, or medicine), or that the stomach contents of an herbivore was ingested (which gets partial credit).

That said, after reviewing a few studies on the topic (see below), it’s safe to say that plants were eaten, probably frequently, and the types & quantities varied seasonally & geographically.  Collectively, the data suggest we aren’t carnivores.

…you had to have something to hold you over until the next fish fell prey to your deadly hunting spear…  

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Fish, dark chocolate, and red wine.

Fish oil fatty acids: EPA & DHA.

I’ve read that EPA tends to show slightly better results in outcomes related to mood, whereas DHA tends to be slightly better for cognition.  Not mutually exclusive; probably a lot of overlap.  This meta-analysis by Martins showed EPA fared better than DHA for depressive symptoms (2009); another one here, stressing the high %EPA relative to %DHA necessary for improvements (Sublette et al., 2011).  Whereas the reverse is true for certain cognitive outcomes in this study by Sinn and colleagues (2012).  Very few studies test EPA vs. DHA directly, and their effects on metabolism are relatively similar.  They’re the ball bearings of fatty acids.epa dpa dha

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Non-sequiter nutrition V. The neglected fats

update: I learned a new trick.  If you haven’t been receiving the regular updates to which you subscribed, it’s probably due to spam filters.  Cure: find the update in your spam folder and reply to it.  You don’t have to write anything, but the mere act of replying somehow tells your spam filter that the email wasn’t spam.  It works for gmail, fwiw.

I [still] predict public approval of dietary fat will come along at a snail’s pace, and it won’t be a pan-approval of dietary fat at all.  Instead, it will be selective approval of individual fatty acids.  First, it was the medium chain fatty acids found in MCTs and coconut oil.  Then, it was the fish oil fatty acids eicosapentaenoic and docosahexaenoic acids (EPA and DHA, respectively).  Then, palmitoleic acid.  Corn and soybean oil, on the other hand, are being appropriately recognized as bad.  The utter hatred and fear of saturated fats is starting to wane, and we might even see a transition back to lard before I die (circa 2113).  But today’s post is on another topic: trans fats, oxidized fish oils, and dairy fat.

What happens when dietary fat is abused?

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Mediterranean Diet Fail – Nutrition Disinformation, Part I.

Do not get your hopes up, do not pass GO!  do not collect $200.  The Mediterranean Diet.  Fail.

Primary Prevention of Cardiovascular Disease with a Mediterranean Diet (Estruch et al., 2013)

This is one of the biggest diet studies we’ve seen in a while, and no doubt it was a very good one.  It very effectively put the Mediterranean Diet to the test.

I felt compelled to write about this study out of fear for the nutrition disinformation that it would likely inspire.  The Mediterranean Diet is associated with all good things, happiness, red wine and olive oil; whereas the Atkins Diet is associated with artery clogging bacon-wrapped hot dogs and a fat guy who died of a heart attack.  Nutrition disinformation.

If you ran a diet study with 3 intervention groups for 5 years, and by the end of the study everybody (in all 3 groups) was on more prescription medications, would you conclude any of the diets were “healthy?”  If so, then we should work on your definition of “healthy.”

Study details: big study, lasted roughly 5 years, and the diet intervention was pristine.  Mediterranean diet plus extra virgin olive oil (EVOO) vs. Mediterranean diet plus nuts vs. low fat control.  They even used biomarkers to confirm olive oil and nut intake (hydroxytyrosol and linoleate, respectively).  Compliance was good.

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what is our proper “natural” diet?

Figuring out how best to eat, physiological insulin resistance, and an homage to pioneering nutrition research.

Insulin resistance, as we know it today, is associated with poor nutrition, obesity, and the metabolic syndrome.  But it’s FAR more interesting than that.  Indeed, it could even save your life.  At the time when the pioneering studies discussed below were occurring, the researchers had no idea insulin resistance was going to become one of the most important health maladies over the course of the following century.  Furthermore, these somewhat-primitive studies also shed some light, possibly, on how we should be eating.  hint: it might all come down to physiological insulin resistance.

The reduced sensitivity to insulin of rats and mice fed on a carbohydrate-free, excess fat diet (Bainbridge 1925, Journal of Physiology)

Rats were fed either a normal starch-based diet (low fat), or a high butter diet (low carb) for one month, then fasted overnight and injected with a whopping dose of insulin (4 U/kg).  First, take a guess, what do you think happened and why.  Then, click on the table below.

To make a long story short, all the starch-fed rats died while all the butter-fed rats lived.

On a high-fat zero-carb diet, plasma insulin levels are low.  Insulin is low because there no carbs (i.e., it’s supposed to be low).  Under conditions of low insulin, unrestrained adipose tissue lipolysis leads to a mass exodus of fatty acids from adipose tissue.  These fatty acids accumulate in skeletal muscle and liver rendering these tissues insulin resistant.  But this doesn’t matter, because insulin sensitivity is unnecessary when there aren’t any carbs around.  So if that rogue research scientist who’s always trying to jab you with a syringe filled with insulin actually succeeds, you won’t die.  The high-fat diet prevents insulin-induced hypoglycemic death.  This is physiological and absolutely critical insulin resistance.

To determine if this was specific to dairy (butter) or a general effect of a high fat zero carb diet, Bainbridge repeated the experiments with lard.  Lo-and-behold, lard-fed rats were just as fine as those dining on butter.  

To be sure, these studies exhibited a high degree of animal cruelty… but their simplicity is laudable.  And Bainbridge’s findings are not an isolated case.

Studies on the metabolism of animals on a carbohydrate-free diet.  Variations in the sensitivity towards insulin of different species of animals on carbohydrate-free diets (Hynd and Rotter, 1931)

Instead of starch, lard, and butter, Hynd and Rotter used milk and bread, cheese, and casein.  And their findings were essentially identical to Bainbridge’s: mice, rats, or rabbits fed carbohydrate-free diets were insulin resistant and protected against insulin-induced tragedies.

The interesting finding was in kittens, who sadly maintained insulin sensitivity when fed fish (high protein) or cream (high fat).

You’re probably thinking: why would I say any state of heightened insulin sensitivity is “sad?”  WELL, I say “sad” because we’re talking about physiological insulin resistance; a condition when resistance to the hypoglycemic effect of insulin is essential, and lack thereof is incompatible with survival.  To be clear: 1) kittens remain insulin sensitive on high fat and protein diets; and 2) this is OK because there aren’t any rogue research scientists running around trying to jab them with insulin.  While I can’t say for sure, this might have something to do with what kittens are supposed to eat, i.e., their natural diet.  High protein and fat diets won’t make them insulin resistant because unlike rodents, that is their normal diet.  (real mice eat fruits and seeds; laboratory mice eat pelleted rodent chow; cartoon mice eat cheese.)   Lard causes ectopic lipid deposition in insulin sensitive tissues in rodents because they aren’t accustomed to it.  Mice are optimized to eat a high carb diet.  Kittens eat protein and fat, usually in the form of mice.  But when given bread, kittens develop insulin resistance.  There is no bread in mice.

While we shouldn’t base our diet around the possibility of turning a corner and being jabbed with a syringe filled with insulin, perhaps we are simply more similar to kittens.  Hypercaloric diets loaded with sugar, excess carbohydrates, and empty calories cause [pathological] insulin resistance (which could theoretically save your life if a rogue research scientist jabbed you with insulin), whereas the opposite is true for diets high in fat and protein.  This is repeatedly demonstrated in diet intervention studies, most recently in the notorious Ebbeling study (Missing: 300 kilocalories).  When people were assigned to the very low carbohydrate diet, insulin sensitivity was significantly higher than when they were on low fat diets:Soapbox rant: I’m not saying low carb is what we are supposed to eat.  Nor am I saying it is the optimal diet.  IMHO any diet which excludes processed junk food and empty calories is “healthy.”  The Paleo diet isn’t healthy because some nutritionista says it’s what we are supposed to eat; Paleo is healthy for the same reason as Atkins, Zone, South Beach, and a million others: no junk food.

Maybe the diet we’re supposed to eat has nothing to do with the healthiest diet.  Maybe not.  But it probably isn’t bad for you.  just sayin’

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LPL, insulin, and diet, Op. 62

There are many ways to address the etiology of obesity and insulin resistance (or insulin resistance and obesity).  For example, you can follow a group of healthy people for a long time and compare those who become insulin resistant with those who don’t; alternatively, you can study a population who is predisposed to insulin resistance (e.g., offspring of type II diabetics)… regarding the latter, although it’s kind of grim, apparently healthy children of obese or diabetic parents are often in an intermediate state of insulin resistance.  It’s impossible to exclude a genetic component, but I believe environmental influences are dominant: the poor diet and lifestyle of obese parents is just as likely as obesogenic DNA to be passed on to their children.

The main reason to be concerned with these questions is that there is considerable disagreement about the specific cause of obesity and insulin resistance; i.e., which came first and does one cause the other?  Or do they simply share a common cause (e.g., hyperinsulinemia)?   I currently lean toward the “common cause” hypothesis.  Alternatively, I’d say “it’s complicated”  … insulin resistance is not one isolated phenomenon, but the end result of many interconnected biological processes.  This has important implications for treatment and prevention- if, for example, hyperinsulinemia causes obesity and/or insulin resistance, then reducing insulin levels or preventing insulin spikes should be prioritized.  And mitochondria also seem to be important.

Regulation of mitochondrial biogenesis by lipoprotein lipase in muscle of insulin-resistant offspring of parents with type 2 diabetes (Morino et al., 2012 Diabetes)

The subjects in this study were body weight and age-matched; the only major difference was impaired glucose tolerance and the presence of at least one diabetic parent in the “insulin-resistant offspring” group.  They took muscle biopsies and found, somewhat surprisingly, one of the biggest differences was the content of lipoprotein lipase (LPL).LPL is responsible for hydrolyzing circulating triacylglycerols (from chylomicrons and VLDL) to free fatty acids for tissue uptake.  Thus, this finding suggests muscle from insulin-resistant offspring is not as good at sequestering fatty acids (despite these subjects oftentimes having paradoxically higher intramuscular fat levels).  This corresponded with lower PPAR activity, mitochondria volume, and fatty acid oxidation.  And interestingly, in a set of follow-up cell culture experiments, they found that the fish oil fatty acid EPA (but not DHA) could correct this deficiency.

Ideally, we would like LPL activated in muscle (to take up and oxidize fatty acids) and inhibited in adipose (to prevent fat cells from getting fatter).  Fortunately, there are some relatively easy ways this can be accomplished… exercise selectively activates LPL in muscle and inhibits it in adipose, while insulin does the exact opposite.  So eat salmon, exercise, and avoid insulinogenic sugars and carb-rich foods!

Tissue-specific responses of lipoprotein lipase to dietary macronutrient composition as a predictor of weight gain over 4 years (Ferland et al., 2012 Obesity)

This study was a little more complicated than inferred by the title.  First, they took healthy adults, measured body composition and then assessed adipose vs. skeletal muscle LPL activity in the fasted and fed states after 2 weeks of a high fat or high carb diet.  To make a long story short:In lean subjects (table above), a high carb meal (after 2 weeks of high carb dieting) markedly increased adipose LPL by 153% (top row) (this is bad), and modestly increased it in skeletal muscle (80%, second row).  The high fat meal (after 2 weeks of high fat dieting) caused a smaller increase in adipose LPL (92% vs. 153%) and bigger increase in skeletal muscle LPL (80% vs. 100%) (this is good).  Thus, a high carb diet caused the most detrimental changes in adipose LPL while a high fat diet caused the most beneficial changes in skeletal muscle LPL.

Next, they compared these acute effects with changes in body composition over the course of 4 years and found that the biggest predictor of increased fat mass was the response of adipose LPL to a high carb diet.

The Morino study showed that increased skeletal muscle LPL was positively associated with insulin sensitivity, while the Ferland study showed that a high carb diet increased adipose LPL and this was positively associated with fat mass gain over 4 years.  Skeletal muscle LPL is good, adipose LPL is bad (Rx: EPA [salmon], exercise, and keep insulin levels low).

Dare I say “nutrient partitioning?”  this might be one way to reduce body fat without drastically cutting calories.  Adopt an LPL-modulating diet and lifestyle!  The effect on fat mass not huge, about a pound per year, but that adds up to 10 pounds over the course of a decade… obesity doesn’t happen overnight.

 

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