Fats and Health

[moda0306]

Report:

Had a big glass of coconut milk today with only a little food to go with it.  No indigestion.

A big leap from pouring it in my coffee to ease my stomach into it.


Thanks, Benko.

[MachineGhost]

#19 seems best.  #15 is good for junkin' low glycemic.

23 Studies on Low-Carb and Low-Fat Diets – Time to Retire The Fad
http://authoritynutrition.com/23-studie ... fat-diets/

[MachineGhost]

[quote=http://medicalxpress.com/news/2015-04-s ... heart.html]Olive oil is universally considered a much healthier alternative to meat fat. Plant-derived oils (such as olive oil, canola oil, and vegetable oil) largely consist of unsaturated fatty acids, whereas animal fat is richer in the saturated ones. After a typical meal, carbohydrates are the primary source of energy production by the heart. Under fasting conditions, however, free fatty acids become the major energy producer. Saturated fat in a diet is known to be detrimental to heart health, but its impact on the cardiac muscle has been studied only recently.

Interestingly, while saturated fatty acids are toxic to cells, unsaturated fatty acids are not only harmless but also provide protection against the damage done by saturated fatty acids. Studies conducted on many cell lines have indicated that saturated fatty acids can cause cell death involving the "endoplasmic reticulum stress (ER stress)", a cellular process known to be involved in the development of many diseases. A new paper, "Saturated fatty acids induce endoplasmic reticulum stress in primary cardiomyocytes", just published in open access in Endoplasmic Reticulum Stress in Diseases by De Gruyter Open shows that there are striking differences in the accumulation of saturated and unsaturated fatty acids in cardiac muscle cells, and that saturated fatty acids induce the death of these cells through the ER stress. In stalking contrast, unsaturated fatty acids protect the same cells from such damage.

A research group from the Montreal Heart Institute in Canada, led by Dr. Nicolas Bousette, evaluated the impact of palmitate and oleate on cellular fatty acid absorption, triglyceride synthesis, intracellular lipid distribution, ER stress, and cell death in primary cardiomyocytes. This is the first time that such phenomena were observed in cells directly derived from the heart, validating a critical role for saturated fatty acids in the development of heart diseases. Given a primary role for lipid metabolism in the development of type II diabetes, the current finding might suggest a probable role for saturated fatty acids in the development of heart conditions among diabetic patients. The current results and future research in this direction might improve our understanding on the possible connection between intracardiomyocyte lipid accumulation and the development of diabetic cardiomyopathy.[/quote]

[moda0306]

I'm interested to know what pro-sat-fat paleo folks around here think of this.

[Benko]

1.  If you pull the paper in question:

"Saturated fatty acids induce endoplasmic reticulum stress in primary cardiomyocytes"
http://www.degruyter.com/view/j/ersc.20 ... 4.pdf  [full paper]

the conclusion is:

Conclusion: Palmitate causes ER stress and apoptotic cell death in primary cardiomyocytes and this is associated
with apparent differences in BODIPY staining compared to oleate treated cardiomyocytes. Importantly, the
lipotoxic effects of palmitate are abolished with the co-administration of oleate

i.e. palmitate [most common fatty acid (saturated) found in animals] stresses and results in cell deaith of heart cells, but this can be prevented by taking oleate  at the same time.

Oleate:  found in olive oil, pecan oil, canola oil,[4] peanut oil, macadamia oil,  sunflower oil (the latter in the high oleic variant), grape seed oil, sea buckthorn oil, and sesame oil,[2] and 14% of poppyseed oil.[7] It is abundantly present in many animal fats, constituting 37 to 56% of chicken and turkey fat[8] and 44 to 47% of lard.

So many animal fats contain "good fats" which counteract the fats that are implied to be bad here.  In addition:

2. "mouse and rat neonatal cardiomyocytes"

Study was performed on newborn mouse and rat ISOLATED HEARTS.  Organs taken out of the body and studied are not always representative of their behavior as part of a system. And human bodies don't always behave the same as mice and rat bodies.

Bottom line is nothing to be worried about.  Well unless you are one of the uncommon blood profiles for which sat fats are actually bad (forget details.  See heart scan blog forum). 

[Mark Leavy]

I'm interested to know what pro-sat-fat paleo folks around here think of this.

I'm not paleo (too many plants) but I am a big fan of getting most of my energy from saturated fat, alcohol and a wide variety of animal parts.

I generally look at the mechanism the human body uses to store excess energy for future use.  It stores it as saturated fat.

I also look at any diet that is a "weight loss" diet.  That diet is high in saturated (human) fat.

I'm a simple man.

[Benko]

I'm interested to know what pro-sat-fat paleo folks around here think of this.

I'm not paleo (too many plants) but I am a big fan of getting most of my energy from saturated fat, alcohol and a wide variety of animal parts.

I generally look at the mechanism the human body uses to store excess energy for future use.  It stores it as saturated fat.

I also look at any diet that is a "weight loss" diet.  That diet is high in saturated (human) fat.

I'm a simple man.

Mark,

Very helpful way of looking at things.

Would you care to say more about: "(too many plants)"?  Unless you mean the nightshade thing which perhaps is an issue for some, but not many others.

Thanks.

[Mark Leavy]

Would you care to say more about: "(too many plants)"?  Unless you mean the nightshade thing which perhaps is an issue for some, but not many others.

In all honesty, I think Paleo is a pretty reasonable way to eat.  No complaints from me.

My personal preference is to not eat (too many) plants for energy.  I love coffee and spices and tomatoes and pickles - but just for the flavor or the bite or the drug or the poison.  Plants with zero (or almost zero) calories (like lettuce or tomatoes or berries) are a no-op.  If you like them, eat them.  Not good or bad.

In general, I will eat plants with calories if they have been fermented in some fashion (i.e. the bacteria or yeast has converted the carbohydrates into animals and animal piss).

Also, there are some fatty plants that have a decent fat profile - some even better than animal fats.  Coconuts, Cacao, Macadamia Nuts, Olives (maybe...), Avocados (maybe...), Palm Oil.  In general, plants that have had to produce fats in hot weather.  It seems that evolution has driven fat development to produce the largest chains it can for the temperature (and still stay viscous).  Mammals and tropical plants have long chain (saturated) fats.  As the average body (or climate) temperature goes up - so does the proportion of saturated fat.

The truth, though, is that I prefer animal fats.  I'll definitely eat some guacamole or drink a "pain killer" loaded with coconut milk - but it is hard to beat brisket or bacon.

Okay - that is enough of a thread derailment.  Standard disclaimer - don't take advice from random internet posters

[dragoncar]

It's been 7 pages, did you guys agree on anything yet?  Saturated fat bad?

[Benko]

It's been 7 pages, did you guys agree on anything yet?  Saturated fat bad?

Yes (most or best I can tell, almost all here agree).

Nope.

[MachineGhost]

I generally look at the mechanism the human body uses to store excess energy for future use.  It stores it as saturated fat.

Really?  All that blubbering spillover folds of fat on Ghostbusters-style Stay Puft obese people is saturated fat?

[Mark Leavy]

Really?  All that blubbering spillover folds of fat on Ghostbusters-style Stay Puft obese people is saturated fat?

At 98.6 degrees its not as hard as the lard in the refrigerator case, but pork lard is nearly identical in composition to human lard.

[l82start]

Really?  All that blubbering spillover folds of fat on Ghostbusters-style Stay Puft obese people is saturated fat?

At 98.6 degrees its not as hard as the lard in the refrigerator case, but pork lard is nearly identical in composition to human lard.

i don't think it matters one bit what human fat is made of or the nature of its composition.. it matters what triggers its growth, the best explanation i have heard recently (i will do my best to recreate it) is that if you had to go out in the wild almost anywhere on the planet and collect/hunt food for your survival for a few weeks, and you counted the source of the calories you acquired and ate, they would end up being approximately 70 - 75% fat and around 20% protein, the few remaining percentage would be carbs. if the percentage of carbs goes up it is sign that there is an abundance and that your body should use that abundance to store those extra calories (from carbs) as fat (to see you through future famine)..  this is the food reality that humanity evolved with for millions of years , having flour sugar and easy fast carbs in abundance for the last 100 or 1000 years hasn't changed how our body reacts to them.

(eat fat you burn fat ....  eat carbs you store the extra as fat - to burn as fat later)

[MachineGhost]

(eat fat you burn fat ....  eat carbs you store the extra as fat - to burn as fat later)

I'm skeptical.  At the homeostasis point of carbs (30% of calories), athletic performance starts to be impacted and gets very dramatic into anemia-like conditions when in the extreme of ketosis (0% carbs).  I have a hard time visualizing our ancestors doing steady-state exercise from chasing wooly mammoths for miles on end on such a low carb diet as you suggest.  I think both the diet composition and our image of what our ancestors did for exercise is probably somewhat wrong.

If you sit around on your butt like most do, you don't need more than 30%.  But if you're a competitive athlete, your performance will certainly suffer if you don't ingest enough carbs to refuel your muscles glycogen stores.  This isn't ideology or opinion, its empirical fact.

[l82start]

doesn't protein get turned into glycogen? and Gluconeogenesis take place at a Stable Rate? (i am far from the in depth geek-out  level you are at so you may have to dumb down the answer)

i suspect that the in Inuit (Eskimo) population surviving, hunting, and traveling in the arctic, eating probably the most extreme fat/protein based diet of any humans might put doubts about it being an inherently anemic.


i just ran across this conclusion of a study on the topic of ketogenic diet and exersise

It can be concluded that long-term, high fat diets may be favorable for aerobic endurance athletes, during the preparatory season, when a high volume and low to moderate intensity of training loads predominate in the training process. High volume training on a ketogenic diet increases fat metabolism during exercise, reduces body mass and fat content and decreases post exercise muscle damage. Low carbohydrate ketogenic diets decrease the ability to perform high intensity work, due to decreased glycogen muscle stores and the lower activity of glycolytic enzymes, which is evidenced by a lower LA concentration and a maximal work load during the last 15 min of the high intensity stage of the exercise protocol

it would seem to be saying that for endurance its beneficial. and for high intensity exercise it decreases ones ability, this  would seem to me to suggest it works well for paleo survival needs/output and not so well for competitive athletics...

[MachineGhost]

doesn't protein get turned into glycogen? and Gluconeogenesis take place at a Stable Rate? (i am far from the in depth geek-out  level you are at so you may have to dumb down the answer)

Yes, but it's a horribly inefficient process with tons of steps and can't possibly work "on demand" for starving muscles.

I guess the critical question is if these low carber natives or ancestors had a limit on their endurance?  You can't possibly do any more physical effort when your muscles are depleted of glycogen.  You turn into a anemic Raggedy Ann doll and collapse.

Then again, competitive endurance athletics is pretty unnatural to begin with and causes a tremendous amount of free radical damage to the heart, etc..

[MachineGhost]

This is a very interesting study.  It claims that more cholesterol equates to more muscle hypertrophy, not protein or calories.

[quote=http://biomedgerontology.oxfordjournals ... /1164.long]It is well accepted that proper nutrition, especially adequate protein, is important to maximize lean mass gains with RET (5,6,13,15,16). When protein consumption was standardized, we observed a strong direct association of dietary cholesterol to the magnitude of lean mass gains that was consistent with the association of serum cholesterol to lean mass gains. This finding was supported by a significant association of dietary cholesterol and change in strength. Moreover, statin users also had greater lean mass gains, independent of dietary and serum cholesterol. This intervention was also associated with significant reductions in systolic and diastolic blood pressure that were not influenced by dietary cholesterol levels.

The results of this study were unexpected given the well-established effects of cholesterol on health and effects of statins on skeletal muscle. It is important to note that a vast majority of these studies do not account for the interaction of these factors with exercise. Nonetheless, we sought alternate explanations for these associations. For example, a sedentary population may have the greatest potential for muscle mass gains, may be more obese, and may consume more cholesterol. However, this is not likely to have affected our results because we selected a population with low physical activity, and obesity was not associated with either dietary cholesterol consumption or muscle gain. The association of cholesterol with other foods, particularly protein, may have also confounded our results. However, we extensively examined protein and found no association with muscle responses. We speculated that this result was due to postexercise protein supplementation (18). It is still possible that a micronutrient such as creatine (not analyzed by our software and known to enhance muscle responses) caused greater muscle mass gains and is also associated to dietary cholesterol (e.g., meat sources). This would not explain the association of blood cholesterol to muscle gain. The well-known limitations of dietary records and their tendency to underestimate intake may be attenuated by the collection of 36 records in 12 weeks. Similar studies typically collect three records at the beginning and at the end of training. This tendency to underestimate dietary intake may be more common in obese individuals; therefore, our failure to identify an association of obesity with muscle gain may have been affected by reporting differences. Even though these results were unexpected, there exists supporting evidence in the literature that cholesterol and statins affect muscle response to RET.

Cholesterol is an essential component of biological membranes. It increases membrane viscosity, which increases the exposure of membrane proteins to extracellular fluids (19). Cholesterol is also essential to the formation of lipid rafts, which function as platforms for the assembly of components of signaling pathways through protein sorting and construction of signaling complexes (20). Cholesterol depletion can induce protein missorting and reduced signal transduction (21,22). Lipid rafts have been implicated as essential for signaling through nitric oxide synthase, protein kinase C-alpha (PKC-?), G-protein ? subunits, insulin receptor, insulin-like growth factor-1 (IGF-1) receptor, tumor necrosis factor-alpha (TNF-?), nuclear factor-kappa B (NF-?B), phosphoinositide kinase-3 (PI3K), protein kinase C (PKC), epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), interleukin-6 (IL-6), extracellular signal-regulated kinase 2 (ERK2), AKT1, and steroid hormone receptor (21–24). These signaling pathways have been identified as contributors to skeletal muscle adaptation to exercise training (23,24). Thus, one possible explanation for greater skeletal muscle hypertrophy in persons with higher dietary and serum cholesterol is improved cellular signaling as a result of greater membrane cholesterol and signaling assembly through lipid rafts.

Cholesterol may also play a role as an essential building block to repair microtears that occur in the skeletal muscle membrane with RET. However, a readily available supply of circulating cholesterol suggests that this may not be the major mechanism of cholesterol-induced muscle hypertrophy. Immediate reductions in serum cholesterol (within 2 hours, lasting up to 72 hours) following exercise causing muscle injury have been suggested to be part of the process to repair the membrane damage (25,26). These microtears are also associated with an acute immune/inflammatory response that is widely believed to play an important role in skeletal muscle hypertrophy through local production of cytokines and anabolic factors to repair damaged tissue (27).

We observed greater hypertrophy in participants using certain statins. This result was unexpected considering that several studies have reported adverse effects of statins on skeletal muscle (9,27). However, statins increase the susceptibility of skeletal muscle to membrane injury in response to an acute exercise challenge (28), which may potentiate hypertrophy if the magnitude of this injury and inflammatory response is directly related to the magnitude of hypertrophy through inflammation-related growth factors. Conversely, a decrease in the synthesis of cholesterol intermediates by statins results in a suppression of isoprenoid derivatives essential for prenylation of Ras and Rho GTPases (29). Reduced function of these GTPases has been shown to decrease myocyte proliferation in cell culture, as they are essential for skeletal muscle differentiation and regulate MyoD and myogenin expression (29). The conflicting observations may be explained by differences in in vivo and in vitro experimental protocols and unique complexity of an exercise intervention.

Recently, it has been proposed that statin-induced reduction in the cholesterol synthesis metabolite isopentenyl-pyrophosphate may explain statin myopathy (30). Isopentenylation of selenocysteine-transfer RNA (sec-tRNA) is required for its role in the expression of selenoproteins (31). Selenoprotein N has been linked to myogenesis and myoregeneration, and a genetic mutation in the Selenoprotein N1 (SEPN1) gene results in several forms of congenital juvenile myopathy with similar features to statin-induced myopathy (32). It is interesting that transgenic mice have been developed that reduces selenoproteins through the expression of a dominant mutant form of sec-tRNA. In response to synergistic ablation, a model of exercise overload, these transgenic mice increased muscle mass ?50% more than their wild-type controls (33). Prior to the synergistic ablation, the AKT and p70s6k phosphorylation states were altered and the increased hypertrophy was blocked by the AKT/mammalian target of rapamycin (mTOR) inhibitor rapamycin. Thus statin inhibition of isopentenyl-pyrophosphate and selenoproteins may explain our observed promotion of hypertrophy with statin use.

The direct association between dietary cholesterol and changes in strength further supports the potential anabolic role of cholesterol. Moreover, the significant indirect association of HDL cholesterol with absolute strength both before and after training highlights the potential role of subfractions in the physiology of this response. Whereas the LDL subfraction delivers cholesterol to tissues and is strongly associated with muscle gain, the HDL subfraction delivers cholesterol away from tissues to be metabolized. Previous studies on cholesterol and muscle characteristics are quite limited; however, Kohl and colleagues (34) reported a strong inverse association, consistent with our findings, between HDL and 1 RM strength for chest and leg press (same as in the present report) in 5460 men.

The results of this study suggest that dietary and serum cholesterol contribute to the skeletal muscle response to resistance exercise, conflicting with recommendations to prevent CVD. The evidence that higher serum cholesterol is associated with greater risk for CVD is clear. However, when confounders of dietary assessment were considered, Kritchevsky and Kritchevsky (35) reported that 1 egg per day (210 mg of cholesterol) was not associated with an elevated risk of coronary events whereas only a small 6% increase in risk was associated with a 200 mg/1000 kcal/d difference. The present study demonstrated a significant reduction in systolic and diastolic blood pressure, and there was not a worsening of serum lipid profile with higher dietary cholesterol. However, the trend toward higher hsCRP suggests at least one cardiovascular risk may be elevated.

Sarcopenia is a prevalent and growing economic burden due to its association with chronic disability and mortality. Exercise interventions are efficacious for prevention and treatment of sarcopenia, although recommendations need to be consistent with other diseases associated with age. The current results clearly suggest and are the first to our knowledge to show that higher dietary and serum cholesterol and statin use are independently associated with greater lean mass responses to RET in this group of generally healthy 60- to 69-year-old men and women. Because cholesterol is negatively associated with cardiovascular health, rigorous efforts to confirm these findings are necessary. Even if results are confirmed, it is necessary to examine changes in cardiovascular risk due to dietary cholesterol consumption (within the context of exercise training) so that reduction in sarcopenia and disability is not at the price of elevated CVD. [/quote]

[Mark Leavy]

This is a very interesting study.  It claims that more cholesterol equates to more muscle hypertrophy, not protein or calories.

That shouldn't be surprising at all.  Eat your egg yolks, dammit!

testosterone significantly improves tissue repair/rebuilding. Nothing works better. Everybody knows this.

What do your testes need for raw material to produce steroids?  Sterols.  Specifically animal based sterols.  Chole sterols.  Not phyto sterols.

[MachineGhost]

Thanks to the legendary Gumby (aka The All Knowing Lord of Wisdom; May He Rest In Peace), our paleo ancestors were NOT low carb:

http://freetheanimal.com/2015/01/paleog ... verup.html

[MachineGhost]

Here are the scarily deranged blood test results from a dogmatic zero carb zealot:

https://web.archive.org/web/20150530231 ... 2015/24818

[Mark Leavy]

Jimmy Moore is a pretty screwed up guy.

A mix of fundamental religion, self-delusion, denial, overeating, junk food, unlimited fat and cream, faux carb free franken foods, 100's of pounds overweight for a decade, then super thin and then overweight again.

The man is a train wreck.  I'm surprised his blood isn't radioactive.

[MachineGhost]

Here's an interesting interview with a researcher about when saturated fats are and are not harmful.  Context matters!

http://www.meandmydiabetes.com/2012/04/ ... t-depends/

[dragoncar]

MG, you've done a ton of research on this.  I've heard that canola oil is maybe the best mainstream oil you're going to find, if you are picking the best of bad choices.  Agree/disagree?

Disagree.  It's refined to death at lofty pizza oven temperatures, has too much oxidized Omega-6 damaged by the refining, may contain toxic erucic acid.  Stick to unrefined, genuine olive oil.

Agree.  But that still leaves what to use for cooking:  I believe you can only use good olive oil at low temp and perhaps medium temps.  Plus there are some things that don't taste good with olive oil taste. 

I would suspect that butter might be good for many people.  I can't use butter (I have food allergy to dairy including butter) so I just use "regular" coconut oil (nutiva)  or the kind without the coconut taste (Jarrow makes some).    Other thoughts  MT?

What do you guys make of these studies showing olive oil is inflammatory, and is not protective against coronary artery disease?

http://www.happyhealthylonglife.com/hap ... l-did.html

Particularly, the monkey study:

http://www.ncbi.nlm.nih.gov/pubmed/7489 ... d_RVDocSum

At this point I'm about to give up and eat anything I want that's not trans-fat.

[MachineGhost]

Ught, please don't listen to Vegan Wackos who cherry pick a decades old study or two to prove their ideology.

EVOO has tons of anti-inflammatory substances.  It's called polyphenols and it prevents LDL oxidization, among other things.  That research will completely overwhelm those Vegan Wacko's studies.

[dragoncar]

Ught, please don't listen to Vegan Wackos who cherry pick a decades old study or two to prove their ideology.

EVOO has tons of anti-inflammatory substances.  It's called polyphenols and it prevents LDL oxidization, among other things.  That research will completely overwhelm those Vegan Wacko's studies.

The study authors are vegans?  More importantly, EVOO is NOT Vegan?  It's quite a stretch to imagine there's some vegan conspiracy against olive oil.