Calories schmalories, alcohol, and chocolate | The poor, misunderstood calorie

Calories schmalories, alcohol, and chocolate | The poor, misunderstood calorie

In another follow-up to Pirola & Lieber, a similarly designed study where the patients were fed via nasogastric tubes an isocaloric exchange of glucose for ethanol in the context of a hypercaloric diet –> weight loss (Reinus et al., 1989).Reinus
C1-3 = control periods (hypercaloric)
LE & HE = low & high ethanol feedings

Not sure if it was intended to be ‘hypercaloric,’ but, well, they gained weight in the control periods = hypercaloric according to the Laws of Energy Balance.  But they lost weight when some of those calories were alcohol, so the same number of calories were no longer hypercaloric?  Still in agreement with the Laws of Energy Balance, but unfortunately not CICO.  It wasn’t just ‘metabolic ward,’ it was full-on nasogastric metabolic ward.

These were metabolic ward studies.  Give me a hundred other metabolic ward studies showing altered macronutrients don’t affect energy balance.  Thanks.  Here’s another black swan.

*Speculative end note (don’t get caught up on this): if 50% of the calories in Lieber’s diet amounted to 313 grams of carbs, and we can assume 15% protein, then they were ingesting a 35% fat diet and lost 900 grams during 7 days of 50% alcohol feeding = 129 g/d.  Reinus opted for a much lower fat diet, ~12%, and his subjects lost 630 grams during 7 days of 50% alcohol feeding = 90 g/d.  Admittedly, this is a stretch – it’s funny math and comparing two vastly different studies, but it indirectly confirms the rat study: alcohol calories count for less on a high fat diet than on lower fat diet.  CICO is forever bollixed.

Don’t try this at home.  The mechanism has been at least partially worked out (ie, MEOS), and alcohol calories only appear to “not count” in bona fide alcoholics ingesting large amounts of alcohol.  But alcohol is still 7.1 kcal/g, even in bona fide alcoholics  ingesting large amounts of alcohol.

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High MCT Diets Are the Key to Longterm Fat Loss - True or False?

High MCT Diets Are the Key to Longterm Fat Loss - Yes or No?.

Eating tons of medium chain triglycerides (MCTs) will make you lean

Are we, or rather you, my American friend eating too much fat or simply the wrong type of fats? According to a study that was in the SuppVersity news in Nov. 2012, it's the latter the "SAD Diet Has the Optimal Ratio to Induce Diabesity" (learn more)
It depends. While it may be that you can derive certain benefits by kicking out junkfood from your diet and replacing it with MCTs the "fat-burning" effects of medium chain triglycerides (MCTs) wear off after one to two weeks (White. 1999). Unfortunately, this is way longer than the usually cited studies on the direct metabolic effects lasted, so that a cursory look at the research easily fools you to believe that you could effectively burn fat by simply using MCT oils instead of whatever "bad" fat you had been using before.

Moreover, in the aforementioned study that was published in the American Jorunal of Nutrition roughly 14 years ago the postprandial total energy expenditure was already only 3% higher after the MCT meal in the first week. And it's not only that this advantage disappeared within the next 7 days, the respiratory ratio, a measure of the ratio of carbohydrate to fat oxidation, total fatty acid oxidation and carbohydrate oxidation were also identical in the  32% MCT and 32% LCT diets (both diets contained additional 8% of fat from other sources).

But what about all the other research?

While the transient benefits of the MCT feeding on energy expenditure alone are unlikely to have practical relevance there are a good handful of trials, which show some real world benefits in various dieting scenarios. Unfortunately, they are usually too short (Alexandrou. 2007), compare MCTs to beef tallow & co only diets, observe increases in fatty oxidation, which don't translate into changes in body composition (St-Onge. 2003), or have the subjects in the control group use relatively fragile control oils, such as olive oil for frying and cooking (St-Onge. 2008).

Accordingly, you should not be too surprised that the latest review of the effects of dietary intake of medium chain triglycerides on body composition, energy expenditure and satiety concludes: "
Curried Carrot Soup w/ coconut oil certainly qualifies as a good food choice, also bc. it's made with coconut oil, not plain MCTs (more).
"In the present review it was possible to verify that data related to increased satiety after consumption of MCT are quite controversial. Most studies showed no significant difference as to increased satiety and/or satiation related to lipid consumption. [...] A relevant fact in the lack of consensus among the studies concerns the large variation in the amount of MCT provided in different studies due to lack of reference values for a minimum, ideal and maximum consumption in literature. Moreover, there isn’t enough to long-term studies to identify either beneficial effects or potential harmful effects." (Souza. 2013)
If you go through the list of studies included in the review there are a couple other interesting patterns emerging: (a) the effects - if there were any - originated from the gut (mostly greater satiety effects), (b) if there were effects on body composition those often reached statistical significance in the obese individuals, only, (c) the benefits were more pronounced the less the subjects ate (esp. on those 800kcal hunger diets), (d) when the control was not nasty corn oil, or saturated long chain triglycerides (Atkins diet style), the effects were non-existent.

So, if your are lean, your current diet is balanced and your main fat source is neither corn oil nor beef tallow, the chances that you will be better off with expensive MCT oils than with a couple of spoons of coconut oil in your diet probably border zero. You see, it's just as so often not so much about "adding something in", as it is about leaving something else out / replacing it with a better food choice.


The Japanese experience in hemorrhagic str... [J Hypertens Suppl. 1994] - PubMed - NCBI

The Japanese experience in hemorrhagic str... [J Hypertens Suppl. 1994] - PubMed - NCBI


National Cardiovascular Center, Suita, Osaka, Japan.



To review current problems with hemorrhagic stroke in Japan and to explore possible explanations for a change not only in the incidence but also the severity of hemorrhagic stroke in recent years in Japan.


Mortality statistics, community-based registries and hospital records were used.


The age-adjusted stroke mortality rate in Japan has declined over the last 20 years by approximately 75%, a very strong decline compared with other countries. The reduction was much more marked for hemorrhagic stroke than for ischemic stroke. Community-based registries for recent years show that the incidence ratio of brain infarction to brain hemorrhage is 1.5-4.0; this is about one-half, or even less than one-half of the rates reported in Western populations. The incidence of subarachnoid hemorrhage in Japan is 7-12% of total strokes. The growing popularity of antihypertensive treatment and changes in lifestyle, including nutrition, are considered responsible for the marked change observed in the stroke figures. Furthermore, mild to moderate cases of brain hemorrhage have been seen more frequently in recent years than severe cases.
[PubMed - indexed for MEDLINE]

Low incidence of cardiovascular disease amon... [Atherosclerosis. 2003] - PubMed - NCBI

Low incidence of cardiovascular disease amon... [Atherosclerosis. 2003] - PubMed - NCBI


Division for Research in Greenland, National Institute of Public Health, Svanemøllevej 25 Copenhagen Ø, Denmark. p.bjerregaard@dadlnet.dk



The notion that the incidence of ischemic heart disease (IHD) is low among the Inuit subsisting on a traditional marine diet has attained axiomatic status. The scientific evidence for this is weak and rests on early clinical evidence and uncertain mortality statistics.


We reviewed the literature and performed new analyses of the mortality statistics from Greenland, Canada, and Alaska.


The evidence for a low mortality from IHD among the Inuit is fragile and rests on unreliable mortality statistics. Mortality from stroke, however, is higher among the Inuit than among other western populations. Based on the examination of 15 candidate gene polymorphisms, the Inuit genetic architecture does not obviously explain putative differences in cardiovascular disease prevalence.


The mortality from all cardiovascular diseases combined is not lower among the Inuit than in white comparison populations. If the mortality from IHD is low, it seems not to be associated with a low prevalence of general atherosclerosis. A decreasing trend in mortality from IHD in Inuit populations undergoing rapid westernization supports the need for a critical rethinking of cardiovascular epidemiology among the Inuit and the role of a marine diet in this population.

Is the "Omega-6 Fats Cause Inflammation" Argument Too Simplistic? - PaleoHacks.com

Is the "Omega-6 Fats Cause Inflammation" Argument Too Simplistic? - PaleoHacks.com

As far as I can tell, some sort of stimuli, whether it be an injury or just a need to constrict or dilate something causes various phospholipases to hack a fatty acid out of the membrane of a cell for conversion into an eicosanoid. These phospholipases have very specific tasks that they are sent out to accomplish:
alt text

Those are the actions of 4 different ones. When that fatty acid is released it can then become the corresponding signalling molecule. The only way that I can see for the system to break down is if there is a dietary deficiency in either the n-3 or n-6 fats that would make it difficult for these phospholipases to find their targets. Assuming that you met the minimums for these fats (whatever they may be), the signalling would proceed as designed.

According to S. Guyenet, the amounts of both of these have increased in the American diet (with much more being n-6 of course). This would indicate that a deficiency has probably not worsened.

If you look at this:

alt text

Grain-fed beef has less n-6 fats than wild game. I'm not saying this is anything near the SAD, just that the real difference appears to be less n-3. Indeed, the seasonal consumption of nuts could skew this temporarily. If hunter-gather's have to eat a high n-6 fat diet temporarily, do they experience more inflammation during that period?

The "n-6 fats cause inflammation" idea implies that all of it is instantly converted into inflammation signalling molecules as it is digested, but really, they're just getting packed into fat cells or oxidized in mitochondria like any other fat until they are called upon to be converted. The composition of our diets is reflected in the fatty acid composition of our depot fat, but to say that a particular fatty acid stored in an adipocyte is more or less inflammatory than another is baseless, as far as I can tell.

To be clear, I'm not saying that industrial seed oils are healthy by any means. I think they are unhealthy because of possible oxidation/rancidity and because their chain lengths could make them more conducive to lipogenesis. I just don't see how a particular tribe focusing on bison and brains is going to have less inflammation than one focusing on elk + nuts. It simply doesn't make sense provided that they both hit the minimums.

It seems to me that a greater risk is in a deficiency of either one, or in a less than optimal starting point for synthesis (i.e. linoleic acid instead of arachidonic acid) but if you ate enough arachidonic acid, maybe that there is so much more linoleic acid wouldn't matter. I'm assuming that cell membranes would be constructed of the optimal components if enough of them are consumed, even if less optimal components are consumed as well.

I haven't really thought about this before, so if I'm missing something let me know.


From my rudimentary understanding, this is roughly true. That is, the argument is too simplistic (for example, arachidonic acid supplementation can often lead to good things). But I'm not sure about a couple of your points. For example, cell membranes can look dramatically different depending on the ratios of fatty acids we eat. Also, excess omega-6 can inhibit the usage of omega-3 because they use some of the same enzymes, no? – Kamal Sep 8 2011 at 5:01

n-3/n-6 ratio is the issue as Kamal noted. From there on out it's minimizing oxidative damage and ALEs. – No more. Sep 8 2011 at 5:14

Also, I'm not sure most people assume this: "The "n-6 fats cause inflammation" idea implies that all of it is instantly converted into inflammation signalling molecules as it is digested". People complain of acute reactions to sugar and gluten, but not vegetable oil so much in my experience. – Kamal Sep 8 2011 at 5:18
I don't have a paper for that, but I have two similar examples in mind. First of all, n6/n3 ratio is derived from red cell membranes, and is extremely variable between people (e.g. mine is around 3:1, some people are 18:1). Second, a controlled experiment feeding people butter vs soybean oil significantly changed the fatty acid composition of adipocyte cell membranes. Also, n3 PUFA gets incorporated into tumor cells and changes their composition. But none of this specifically addresses your point, so you could very well be right. – Kamal Sep 8 2011 at 6:05
I want Chris Masterhacks thoughts on this STAT! – Patrik Sep 8 2011 at 6:12
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3 Answers

You're right that it isn't just omega-6 = more eicosanoids = more inflammation, it's not linear and levels out, and in fact we want a little more than that because we need those eicosanoids. You are also right that a deficiency in omega-3 fats is behind the obscene excessive inflammation that causes disease. The ability to signal "off" or protect the body is the most important factor. There are other factors, and certainly the increased need for the immune system plays a role. An infection or a gluten allery would do it, so would anything that incites the immune system to a degree. This is unwanted inflammation, but isn't caused by omega-6.
But high-dose omega-6 is not innocous, since it causes a DHA deficiency. Excess omega-6 impairs ALA conversion, and it competes for space in cellular phospholipids with DHA. There is a scientist named Bill Lands who talks about this a lot. Stephan has also written about it. So mega doses of omega-6 certainly aren't off the hook. They are anti-anti-inflammatory in the most important sense. You might see short-term benefit via certain mechanisms, but the effect is a J curve (http://healthcorrelator.blogspot.com/2011/09/nonlinearity-and-industrial-seed-oils.html), if you want the best of the best inflammatory signaling you want to keep omega-6 below 4% of calories so that it doesn't cause an omega-3 deficiency. And of course you want more omega-3.
This should explain many paradoxes. It's really all about the "omega-3 index", the available omega-3 in the cells to do anti-inflammatory heavy-lifting. If two groups have similarly poor omega-3 intake (like 95% of rat studies) then you will likely not see a difference, or you might even see a higher omega-6 group do better due to GLA and DGLA, possibly. But if you have a fixed amount of omega-3 across all groups and an obscene amount of omega-6 in one of them, the omega-6 group will be worse because the omega-3 index will be lower due to the omega-6 in the diet. The only desirable diet is one that has a reasonable amount of omega-6 and sufficient omega-3, change either variable and you're headed downhill. Studies that demonstrate that halfway down the hill is better than all the way down the hill lying on some broken bottles with a twisted ankle do nothing to help us, and waste lab rats.
Dietary ratio is a useful tool and is predictive, but it isn't air-tight. Cellular ratio is better and predicts many diseases. http://omega-6-omega-3-balance.omegaoptimize.com/

Welcome to Stabsville, fool. (that's what you can say when you post a good answer) – Kamal Sep 8 2011 at 5:27

So, an increased n-6 intake would create a moving target for the minimum amount of n-3, but it wouldn't ensure added inflammation. In theory, DHA supplementation could negate the effects of added LA for example, right? I just think that a view that assumes that phospholipases say "good enough for government work" when hunting for an n-3 fat and cleave out an n-6 instead is impossible. – Travis Culp Sep 8 2011 at 5:37

Yes but how much fish oil are you going to slug? There are detriments to too much omega-3 as well. Best to keep them both to a reasonable amount. I think the answer you're looking for is that 3% of energy as LA isn't necessarily more inflammatory than 2%, which is the case. Get way up there with the soy oil and all hope of optimal inflammation vanishes. – Stabby Sep 8 2011 at 5:42
"And of course you want more omega-6." Should that not say omega-3 there? – Matt Sep 8 2011 at 13:41
I highly doubt that omega-6 deficiency is causing Japanese people to have a higher rate of hemorrhagic stroke. In fact, I highly doubt that 99.99% of Japanese people have an omega-6 deficiency. – Kamal Sep 8 2011 at 23:18
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Stephan seems to think so:
Honestly, the basis for saying that n-6 causes inflammation is mostly hypothetical. I've come to realize that the case based on eicosanoid formation has been overstated. The strongest piece of evidence is that excess n-6 seems to suppress n-3 elongation and accumulation, and we know that n-3 is important in resolving inflammation.
I think Dr. Willett is correct that the evidence has been exaggerated that higher LA will lead to higher production of inflammatory eicosanoids. At least above a certain threshold, it doesn't seem to matter much.
August 23, 2011 11:52 AM
I'm also reminded of this:
In a 1993 trial, a low-magnesium diet reduced insulin sensitivity in healthy volunteers by 25% in just four weeks (8). It also increased urinary thromboxane concentration, a potential concern for cardiovascular health**.
** Thromboxane A2 is an omega-6 derived eicosanoid that potently constricts blood vessels and promotes blood clotting. It's interesting that magnesium has such a strong effect on it. It indicates that fatty acid balance is not the only major influence on eicosanoid production.

More omega 6 over 3 does cause inflammation.
Try an experiment: Eat oatmeal that is HIGH in 6, and watch your inflammation spike.

Oats are like 5% omega-6 by calories, I don't anyone but the hardcore Peat-heads would say that's high in 6. – Mscott Apr 26 at 21:20

If you are speaking of the immediate reaction, I think you might be confusing inflammation with bloat. If you eat too much or they aren't soaked and cooked fully, the oats soak up liquid in your gut can cause a distended belly. Long term though, there could certainly be some inflammation issues. – Happy Now Apr 26 at 22:34


I Ate 36 Eggs A Day

by Derek Johanson

I just arrived in Iguazu, Argentina today. I went to the grocery store and bought a frozen bag of peas. I ate them, frozen, on the street enjoying every minute. This reminded me of something else ‘crazy’ I did in Panama. I consumed 36 eggs every day for 2 weeks.

It’s no secret amongst my friends and family that I love eggs. One of my roommates used to yell, “Eggs!” whenever I went in the kitchen to cook. My flat-mates in Cordoba, Argentina called me the “Hombre de Juevos” (Egg Man).

In late 2007 I was eating, by normal standards, an astronomical 12 eggs a day. Most health organizations recommend no more than 4 eggs per week while I was averaging 84! Accordingly, people were constantly warning me that I should get a blood test and check my cholesterol. I took them up on it.

When I got the results, my HDL cholesterol levels were incredibly high while my LDL levels were below average – this is a good thing. My triglyceride level was off the charts good at 52. I remember the nurse reading the results was in disbelief. “That’s incredible,” she said.

The blood test results further solidified my belief that eggs are to me, like spinach is to Popeye. So taking the leap to 36 eggs a day wasn’t a difficult or scary step for me.

Why 36 eggs 

In Panama, Clay and I decided to do a bit of experimenting with bodybuilding and diet. My weight had dropped down below 165, the lowest it had been in awhile. I wanted to put on some muscle mass.
After sifting through a lot of diet programs we settled on what is known as the Hormone Precursor diet designed by the famous bodybuilder coach Vince Gironda. His ideas were radical, but the quick transformations and astehically pleasing figures his athletes developed were enough to convince us it was worth a try.

Gironda believed that eggs were a) the most perfect food and b) they had a steroid like effect on the body releasing growth hormones necessary for building muscle. He recommended that the bodybuilder make 3 special eggs drinks and sip them throughout the day in-between meals.

Vince’s special protein drink:

12 (raw) eggs
6 oz heavy cream
1 banana
1/3 cup of milk-and-egg protein powder
(if you’ll notice, this is similar to my Best Breakfast Recipe Ever post)

The idea here is to keep the body in a constant state of positive nitrogen balance. This is achieved by ingesting 30-50 grams of protein at least every 3 hours to keep your blood-suger levels with a constant supply of protein. Doing this puts your body in an anabolic state by releasing growth hormones.

Working Up To 36 Eggs A Day

We began by half-ing the initial recipe in order to slowly work up to 36 eggs. We drank Vince’s special protein drink (with 6 eggs) 3 times a day for 2 weeks. For the second 2 weeks we bumped it up to 24. The next 2 weeks 30. Then for the final 2 weeks of our program we ate 36 eggs a day.
Breakfast was the largest meal – one whole drink 12 eggs in all. The rest of the day was spent sipping on the drinks to down the other 24.

Positive Effects

My time spent building muscle in Panama was very effective. I went from 165 lbs. to 180 lbs. upon waking. This was over an 8 week time period. By a mirror test, I’d say 10 of those lbs. were muscle and the other 5 were fat. I could have exercised more to keep up with the calorie consumption and minimize fat gain.

Negative Effects

1) By the time we reached 36 eggs a day both of us were feeling quite bogged down by the amount of food we were eating. Along with eggs, we were both consuming at least 2 lbs. of beef as well. We had to make sure to get plenty of exercise during the day, on top of the normal workouts.

2) During this period I noticed an unusual amount of blemishes popping up. I attribute it to the increased amount of hormones running through my body. When we completed a five day fast afterward, my skin felt and looked a lot better (until I reached Argentina were there’s beef, beer, and all night discos).

Derek Rant

It amazes people when I tell them that I did this. They’ll say, “That’s so bad for you,” as they shove another buttery croissant down their face. People are so afraid of cholesterol and eggs because it’s been conditioned (mainly by the cereal companies).

Of course 36 eggs in a day is extreme. It’s not a diet I would consider keeping for the rest of my life. In fact, some of you may be shocked to know I’m thinking of beginning a vegan diet later this year.
It’s not too crazy if you think about it:

Calories in 36 eggs: 2160 kcals
Calories in Macaroni Grill Spaghetti and Meatballs with Sauce: 2,430 kcals

And that’s one meal.

Take home message

There are established rules in every aspect of life. A lot of them make sense, and lot should be questioned. Thus, when I wanted to put on muscle quickly I decided to question the norm. And when I questioned and experimented, things turned out great.

Life is a long series of experiments. Why not eat a bag of frozen peas on a hot day? Why not eat 36 eggs in day?


Is Coconut Palm Sugar A Healthy Sugar Substitute? | Upgrade Your Healthstyle | Summer Tomato

Is Coconut Palm Sugar A Healthy Sugar Substitute? | Upgrade Your Healthstyle | Summer Tomato

by | Mar 12, 2012
Photo by Robyns Nest
Photo by Robyn's Nest
Artificial sweeteners and sugar substitutes can be very appealing to people looking to cut their calories or control blood sugar, and I get a lot of questions about them. Generally I don’t recommend processed or sweetened foods and encourage people to break free from regular sugar consumption, but I recently discovered coconut palm sugar and decided to look into it.

Coconut palm sugar has garnered attention as being a low-carb sugar substitute that is more nutritious than typical granulated sugar. Because of its complex flavor it is also gaining a reputation in foodie communities, with establishments like the popular Samovar Tea Lounge in San Francisco switching 100% of its sweeteners over to coconut palm sugar.

Pure coconut palm sugar is a natural product made from the nectar of the coconut palm tree. There are several different varieties of palm (Palmyra, date, etc.), and “coconut palm” specifically refers to the coco nucifera plant.

Most of the “palm sugar” commonly sold in Asian markets is not pure coconut palm sugar but is blended with other fillers such as white cane sugar. Pure certified organic coconut palm sugar is sold under the brand name Sweet Tree in the US, and can be found at some natural food stores. It is also available online at Samovar.

The information in this article applies only to 100% pure coconut palm sugar. Check your labels carefully.

Pure coconut palm sugar reportedly has a naturally low glycemic index (GI)–a measure of how food impacts blood sugar–which has led some people to claim that it is a valuable sugar substitute for people with diabetes or those looking to control blood sugar (the low-carb camp). Indeed, a lower GI may be a good indication that a food is safer for diabetics, though it is not a guarantee.

When I first saw that coconut palm sugar has a low GI I figured it would be composed largely of fructose, similar to the popular sweetener agave nectar (and high-fructose corn syrup). Fructose does not impact blood sugar because it is transported directly to the liver and converted to fat. For an explanation of this mechanism, check out Dr. Lustig’s video on the dangers of fructose.

I was surprised to find, however, that coconut palm sugar is reportedly very low in fructose, and its main sugar component is sucrose (aka table sugar). What confuses me is that the GI of coconut palm sugar is supposed to be 35, while the GI of sucrose is 64. Something doesn’t add up.

I could only find a summary of how GI was measured and not the published study itself. Also, this information was only available on the website of a company that sells coconut palm sugar. This doesn’t mean the number is inaccurate, but it is a little suspicious and I’d like to see the study repeated by another credible source or two before taking it as fact.

(UPDATE: At one time I found reports of newer tests that found discrepancies with the reported GI of Sweet Tree products, but the page has since been taken down)

The number of calories in coconut palm sugar is almost identical to the number in regular table sugar and its closer relative, brown sugar. But coconut palm sugar is notably higher in various micronutrients, probably because it is less processed than industrial sugars.

But does anyone really eat sugar for health benefits?

There are a number of good reasons to consider using coconut palm sugar as a substitute for white or brown sugar in your kitchen. For me the most obvious benefit is that it tastes amazing, similar to brown sugar but with a rich complexity I’ve never tasted in industrial sugars.

Overall coconut palm sugar is a tastier and possibly healthier substitute for granulated or brown sugar. I wouldn’t go so far as to call it a health food, or even low-carb just yet.

Substitute coconut palm sugar for traditional sugar at a 1:1 ratio in normal cooking and baking.

Have you tried coconut palm sugar? What do you think?
Originally published March 10, 2010.

Mark Sisson, BA and Robb Wolf, BS — Paleo Primal Q & A — AHS12

Top Comments

  • troyerjl1
    The difference between the cognitive abilities of these guys versus the vegans I've been seeing on the other channels is astounding. These guys can actually critically think and express themselves in a healthy manner, making actual reasonable claims.
    · 6
  • Drake Santiago
    As seen in this Q & A, Robb Wolf and Mark Sisson approach scientific findings with caution, acknowledging that much of what science has to offer, especially in the realm of nutrition, is tentative. When you hear vegan proponents, they speak with such certitude, as if the science promoting their view is infallible. From their approaches to science alone, you can tell which camp is more motivated by proper science, and which is motivated by dogma and a political/social agenda.

The Paleo Diet Delusion: Paleofantasy's Marlene Zuk on Dietary Myths

Top Comments

  • Matt Santos
    Straw man fallacy? I don't think anyone (ok anyone worth listening to) is arguing that there is a "Perfect" paleo diet or that we haven't evolved at all since paleolithic times.
    · 11
  • Daryl Glen Christensen
    The lady featured in this interview is arguing against the paleo movement, and putting words in its mouth, never really understanding what it is that she is criticizing. She's saying really boring things that people in the movement had been saying three years previous.
    · 7 in reply to Matt Santos (Show the comment)

There's Not Enough Evidence For The Paleo Diet | Lifehacker Australia

There's Not Enough Evidence For The Paleo Diet | Lifehacker Australia

Eating like a caveman is said to improve your lifespan as well as helping you lose weight, but is that actually the case — and did our ancestors actually eat that way anyway? Nutritionist Rosemary Stanton examines the difficulties of the paleo diet.

Over the years, hundreds of diet books have claimed to have the perfect recipe for decreasing the national girth. They manipulate quantities of protein, fats or carbohydrates and most work in the short term because their inevitable restrictions cut energy intake.

But in the long term, few people can stick to most diets for more than a year or two. Indeed, the US National Weight Control Registry reports that only a fifth of those who intentionally lose at least 10 per cent of their weight maintain the loss for at least a year.

Many popular diets are also nutritionally unsound and so their short lifespan is a blessing. Some, such as various paleo diets, however, are recommended for life and claim benefits beyond weight loss. Such diets demand closer scrutiny.

Defining a paleolithic diet is problematic. It’s supposed to be based on what our paleolithic ancestors ate.

Anthropologists have found very different dietary patterns, depending on where our ancestors lived. Most simply consumed what they could find with seasonal variations leading to substantial dietary changes.

From the mists of time?

The first of the popular paleo diets (dubbed the stone-age or caveman diet) was published in the 1970s by Walter Voegtlin, a gastroenterologist.

Although Voegtlin had published papers on various topics in his field during the 1940s and 1950s, by the 1970s he had come to believe humans should adopt a carnivorous diet because he considered our teeth and digestive tract were “more like a dog than a sheep”.

Before his death in 1975, Voegtlin published a diet book that recommended meat protein and fat, but no dairy products, no salt and minimal plant-based foods (especially grains and sugar).

In the late 1980s, Boyd Eaton published a somewhat different version of the paleo diet, based largely on the diet of our East African ancestors. It featured low saturated-fat content (in keeping with the flesh of wild animals) and a one-to-one ratio of energy from plant and animal foods.

This version of the paleo eating pattern supplied moderate amounts of carbohydrates from fruits, roots and shoots.

Eaton’s ideas have been amplified and publicised widely by Loren Cordain, an exercise physiologist from Colorado State University, whose website claims he is the founder of the paleo diet movement.
Cordain’s paleo diet is based on grass-fed meat, poultry, eggs and seafood, fruits and non-starchy vegetables. Fats are not restricted, but grains, legumes, potatoes, dairy products and sugar are all off the table.

Cordain’s group claims our ancestors were not only lean but had no cardiovascular diseases, type 2 diabetes, cancer, autoimmune diseases, osteoporosis, acne, myopia, varicose veins, gastric reflux or gout.

This is supposedly due to their lack of grains, legumes, dairy products and potatoes. Oh for some proof!

Not so fast

Some notable experts have begun to speak out about paleo diet claims. Evolutionary biologist Marlene Zuk, from the University of California, has written a book titled Paleofantasy in which she debunks many myths about the paleo diet.

You can read about it on Scientific American or New Scientist. Or you can watch this: http://www.youtube.com/watch?v=nkQhSMnRwpI#at=159

Anthropologist Christina Warinner from the University of Oklahoma and the University of Zurich notes that most versions of the paleo diet are closer to an early 20th century affluent farmer’s diet than that of our paleolithic ancestors.

Here’s her recent TEDxOU talk about it:http://www.youtube.com/watch?v=nkQhSMnRwpI#at=159

Another anthropologist, Katherine Milton, claims that much of what has been ascribed to hunter-gatherer populations is inaccurate. Milton notes the very different dietary patterns among groups living in different parts of the world.

She has also documented the role that both animal and plant foods have played in human evolution.

Ancient vs modern

Paleo diets recommend against the highly-processed foods rich in sugar, saturated fats and salt that characterise the modern Western diet; for this they deserve a tick.

But they ignore the benefits of many plant-based foods and some dairy products. You should check the evidence report of the Australian Dietary Guidelines for these.

Most importantly, however, the paleo diet pushes a pattern far removed from that of our ancestors. Even if domesticated animals are grass-fed, their flesh is unlike that of wild animals — kangaroo being the exception.

Free-range poultry don’t just forage but are fed grains, unlike wild birds. Wild-caught fish are an option, but there are simply not enough of them to go around. Around 70 per cent of seafood consumed in Australia is also imported, often from countries where the diet of the local population desperately needs it.

Modern fruits and vegetables are also unlike those consumed in paleolithic times.

Paleo enthusiasts sometimes cite several relatively recent studies to justify their recommendations, but without exception, these are short-term and involve only small numbers of subjects. They do not constitute adequate proof of benefit or balance.

Those following the paleo diet could have low calcium and dietary fibre. Fruits, vegetables and nuts are the only sources of fibre, and calcium is found in almonds, seafood (especially prawn shells) and Asian vegetables.

Oxalic acid in vegetables such as spinach prevents absorption of its calcium and iron. Accurate nutrient levels in Australian foods are available here.

Remember too that processed meats and a weekly intake of more than 450 grams of red meat (including pork) increases the risk of colorectal cancer.

Rosemary Stanton is Nutritionist & Visiting Fellow at University of New South Wales. She does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.

The ConversationThis article was originally published at The Conversation. Read the original article.


Saturated fat is bad for you…….really??? | The Science of Human Potential

Saturated fat is bad for you…….really??? | The Science of Human Potential

by Grant Schofield and Helen Kilding

Addendum note from Grant: This post has generated an enormous amount of debate – see the comments section.  Its interesting as the authors of this study came back into the debate early.

Another study, this time it’s my colleagues much closer to home in New Zealand, and they received quite a bit of media space from it. The authors sought to estimate the potential impact on cardiovascular health of modifying dietary intake of saturated fat across the New Zealand population, and whether this would be appropriate and feasible.

They decided that while there was no evidence that fat intake affected health, substituting saturated fats with polyunsaturated fats would be of use and is “feasible” for the health of New Zealanders.
Here’s the paper. “Review of the evidence for the potential impact and feasibility of substituting saturated fat in the New Zealand diet (Rachel H. Foster, Nick Wilson, Burden of Disease, Epidemiology, Equity and Cost-Effectiveness (BODE3) Programme, Department of Public Health, University of Otago – Wellington, New Zealand).

They concluded that “Replacing 5% of daily energy consumed as saturated fat with polyunsaturated fats would be expected to reduce cardiovascular events by about 10%.”

Here’s what the media made of it - The New Zealand Herald, and Stuff.co.nz

And I got more than a few questions from readers….for example:
Hi Grant 
What’s your take on this study? (see attached) 
Many of the fats they mention as bad I have been eating for the past two months and have lost weight and improved cholesterol! This is an actual result and if anything by default resulted in me consuming less of their so called good fats i.e canola oils, polyunsaturated oils etc. 
No wonder it  is hard for people to make informed decisions about diet with so much conflicting information. End of the day I decided to see for myself and make myself the test subject on a LCHF diet and continue to be thankful I did.

So what do we make of all this? First, they actually found no association between fat intake and disease outcomes in their meta-analysis. So great, fat isn’t a risk. But they did conclude that because replacing saturated fat reduces risk, that saturated fat must therefore be a risk factor.

I guess they haven’t considered the latest meta analysis in the American Journal of Public Health (2013)  ”Food Sources of Saturated Fat and the Association With Mortality: A Meta-Analysis “.

 This specifically looks at saturated fats. They show very limited evidence for most saturated fats foods having any association with CVD or cancer. Probably processed meat is the strongest association. In this sort of food product, saturated fat isn’t the only metabolic ingredient.

Nor have they considered that actual experimental evidence through randomized controlled trials (there are more than 20 now) does not show a harm for increasing saturated fat intake in LCHF diets. All the “established” cardio-metabolic risk markers show very favorable outcomes compared with all other diets. No long term outcomes, but these are well known and regarded proxies.

The recently published Sydney Heart study data shows that exactly the opposite happened back in the 1970s, when they replaced saturated fat with polyunsaturated fat and saw things get worse. Here’s the BMJ editorial on this. And here are some results:

“Participants were randomly divided into two groups. The intervention group was instructed to reduce saturated fats (from animal fats, common margarines and shortenings) to less than 10% of energy intake and to increase linoleic acid (from safflower oil and safflower oil polyunsaturated margarine) to 15% of energy intake. Safflower oil is a concentrated source of omega-6 linoleic acid and provides no omega-3 PUFAs. The control group received no specific dietary advice. 

Both groups had regular assessments and completed food diaries for an average of 39 months. All non-dietary aspects of the study were designed to be equal in both groups.

The results show that the omega-6 linoleic acid group had a higher risk of death from all causes, as well as from cardiovascular disease and coronary heart disease, compared with the control group.”

Nor have they considered almost all of the growing mechanistic evidence that metabolic issues, including CVD, are inflammatory based and the evidence points strongly to a myriad of interacting pathways, from gut microbiome, to sugar, to simple carbs, to the stress axis, to VLDL and triglycerides through the liver etc etc. The direct effect of dietary saturated fat is not clear in any of these mechanisms and unlikely to be a factor.

Overall, the evidence from the association studies is weak, equivocal, or inconsistent, depending on what term you like best.  Experimentally and mechanistically it doesn’t stack up.  Come on guys, are you doing your reading? It’s not good enough when there is such a broader amount of evidence. Your study doesn’t lead to a rationale for reducing saturated fat and replacing it with polyunsaturated.

Worse still, you’re promoting the use of manufactured vegetables oils which are high in Omega 6 and likely to be inflammatory, adding further to the problem.  These oils are also quite unstable and easily oxidized further, adding to metabolic problems. Saturated fat is not.

Avoiding fat will likely mean eating more carbohydrate.  For many, this will further dysregulate their carbohydrate metabolism and make them more insulin resistant resulting in a downward cycle with all the direct and indirect effects of hyoerinsulinemia.  These guys just haven’t even thought that the active metabolic ingredient in their weak epidemiology might be something else which they haven’t or can’t control for…..insulin-raising carbs.

  1. Fat contains loads of calories
  2. Fat is an essential nutrient
  3. Highly processed fats are inflammatory
  4. Good quality whole foods, including loads of vegetables, are good for you.  Their fat content appears not to harm you.
  5. Omega 3 fats are good for you. These are poly unsaturated so if that is what they are talking about then great.  But these guys go on to talk specifically about manufactured seed oils – these are not good.
  6. In high carb, insulin-provoking diets, fat seems to add to the insulin response.  This seems to be worse in people who are insulin resistant.  By itself, fat is metabolically benign, at least as far as insulin response is concerned. A good reason to avoid the standard American diet.
  7. Processed meats are likely to be bad for you.  I’m not sure if it’s the actual fat and I’m not sure what the mechanisms might be – inflammatory? We may never know if they are for sure because no one is likely to run an experimental trial where people get a long dose of processed meat.
Take home messages:
  • Don’t believe everything you see in a scientific paper.  Sometimes they go past the evidence.
  • Carry on eating fat, hopefully in the absence of processed and simple carbs as they may harm you in combination.
How did fat get such a bad name in the first place?

We’ve been brainwashed in to thinking that when we eat saturated fat it goes straight into our bloodstream, instantly bonding to the inside of our arteries, eventually clogging them up completely. This is bullshit. Atherosclerosis is caused by oxidised LDL particles penetrating our arterial walls, inciting inflammation and damaging the arterial tissue. And what increases LDL particle number?
  1. Insulin resistance and metabolic syndrome
  2. Poor thyroid function
  3. Infections
  4. Leaky gut
  5. Genetics
Let’s look at that list again…..no mention of dietary intake of saturated fat.

And when we talk about saturated fat, everyone always wants to talk about cholesterol. Dietary cholesterol does not affect total blood cholesterol. In fact, when we do eat cholesterol, our body makes less of it to keep our blood levels in balance.

So even if eating fat doesn’t result in CVD, won’t eating fat make us fat?

No again. As we’ve said before, fat doesn’t make you fat. Fat is very satisfying, especially when paired with low-carb eating. A nice steak rippled with fat is far more filling than some crusty bread spread with butter. You’ll eat a decent piece of the former and be satisfied but could easily polish off half a loaf of the bread with a good helping of butter and still be hungry. It’s difficult to overeat on a high-fat, low-carb diet.

Our bodies want to use fat for energy, but when we eat fat in the presence of large amounts of dietary carbohydrates, it makes it difficult to access fat for energy. On the flip side, dietary fat in the presence of low levels of dietary carbohydrates makes it easier to access fat for energy. It’s also easy to overeat fat and carbs together – think hot chips, buttered toast, milk chocolate.

And let’s think about farming for a second….how do you fatten cattle? You feed them lots of lots of grass (a carbohydrate).

According to a recent post on Christine Cronau’s Facebook page, “70 years ago, farmers tried to fatten their livestock with saturated fat. It backfired! The pigs lost weight and became more active. Of course, the farmers weren’t silly enough to persist with something that didn’t work, yet our conventional health professionals have insisted on doing so!” I’ve tried to source more detail on this but have drawn a blank so far.

Gelatin / glycine (I am going to experiment with purposely eating more) - The Scribble Pad

The Scribble Pad: Tasty things I am eating, low energy snack foods edition. 23andme. Glycine and gelatin - more good advice from George.

I am going to experiment with purposely eating more gelatin / glycine. 

I have long noticed something about broth made me feel "good", and something about certain meats made me feel terribly "bad". I have noticed the following food items are protein based yet agreeable: animal stock/soup broth, animal skins/pork rinds, jello gelatine. I have noticed lean meats often make me feel quite bad. Have intuited it may be defective glutamate processing causing protein intolerance and ketogenic diet helps of course.

I really began to suspect it might be certain amino acids causing the problem when I observed consuming this supplement Prostat 64 significantly and reliably increases energy and mood. The supplement only contains glycerine and various amino acids, namely tons and tons of glycine. It contains about 26 grams of glycine per 100gms of product, which is a huge amount relative to the other aminos...not surprising as it is made of hydrolyzed collagen.

Observing the almost medicinal effects of prostat (radically unlike simply eating "meat" or a high protein food) I began to suspect, then, there might be something to one or more of the amino acids in prostat. I didn't do more research at the time, until George spontaneously informed me that glycine , of which gelatine is quite rich in, regulates methylation and dopamine activity and provided a link to a masterjohn WAPF article regarding such. I admit a bit of skepticism of these claims regarding the exact mechanism of action but at this point I am fairly confident there is something therapeutic for attention/alertness/energy/mood and the answer is glycine. I have replicated the "prostat" effect with gelatin, and in hindsight, I was experiencing this effect very weakly when eating broths and other foods rich in animal collagen.

I must do more research regarding the metabolism and effects of the amino acid glycine, because this potentially holds the key to totally controlling my protein intolerance and a great deal of my mood problems I'm sure as well. It seems to antagonize/correct the constant emotional negativity and energy issues I associate with food and protein in general. Augmenting GABA does not seem to be a likely explanation, because other amino acids like Taurine promote GABA and cannot do what glycine is doing. Taurine is acutely mood stabilizing I find but long term destabilizing unless I take it diligently.

Acutely speaking glycine promotes this feeling of extreme alertness, energy, and wellbeing. It feels somewhat dopaminergic but without any signs of norepinephrine/epinephrine. It also completely squashes appetite and blood sugar instability, perhaps this is via dopaminergic mechanisms in the brain/greater central dopamine sensitivity. All of this is highly speculative at this point but the larger more important piece is that glycine , I am finding, is a common every day nutrient that I need to consciously intake regularly / radically increase dosage of, just like inositol. This is probably a "woo defect" thing normal people likely dont need to concern themselves with as normal intakes of protein provide enough glycine. I suspect I have some genetic liability pertaining to metabolism of glycine, or antagonistic processes, and so benefit very much from purposely increasing glycine.

A fun way to do this is to make a lot of jello and eat it. I have done this and feel much more alert and energetic and mentally centered as I would expect from "prostat". If nothing else, it is nice to have discovered the "prostat" effect is  glycine/gelatin which costs only pennies as much as prostat ;) .

How to Burn Fat and Why You Shouldn’t – 180 Degree Health

How to Burn Fat and Why You Shouldn’t – 180 Degree Health

By Danny Roddy, author of The Peat Whisperer
Traversing through the blogosphere reveals much text, but little art. This is, until you stumble upon the site of low-carb sage Petro Dobromylkyj. Similar to da Vinci’s “David” or Shakespeare’s Hamlet, Petro’s exudes extraordinary vision. One doesn’t have to read past the header for the first glimpse of his contribution to The Great Work:

You need to get your calories from somewhere should it be from carbohydrate or fat?” — Petro Dobromylkyj

If I was forced to interpret Petro’s poem, I would say that he’s trying to tell us that carbohydrates reassure men that they can be masters of their own reality—but then turns around and says that actually, reality is not real.

Another interpretation, which sounds less plausible, could be that one must decide where to obtain their fuel from: carbohydrate or fat.

While the blogosphere has been polluted with the idea that “using fat as fuel” is somehow more desirable than glucose, in this article, I intend to describe how lipolysis (i.e., the liberation of free fatty acids into the blood) is a feature of stress, disease and aging.

Lazy Reader Summary:
  • Glucose and oxygen, which are substrates for efficient energy production, are the two most basic anti-stress substances
  • Carbon dioxide (CO2), which is produced under the influence of active thyroid hormone, is needed to use glucose and oxygen efficiently
  • Stress liberates free fatty acids (non-esterified fatty acids or NEFA) into the blood for use as fuel

    • The use of free fatty acids as fuel supplies less carbon dioxide than the complete oxidation of glucose
    • The liberation of free fatty acids into the blood interrupts the use of glucose in the short- and long-term
    • Over time, free fatty acids damage the cell’s highly evolved ability to produce oxidative energy (i.e., glucose to carbon dioxide)
  • Those with obesity and diabetes have markers suggestive of stress and the production of energy through inefficient glycolysis (i.e. glucose to lactic acid):

    • Increased blood levels of adrenaline
    • Increased blood levels of cortisol
    • Increased blood levels of lactate
    • Reduced respiratory quotient (i.e., less carbon dioxide produced)
    • Increased reliance on free fatty acids as fuel
    • Decreased thermogenesis upon food ingestion (especially carbohydrate)
  • Low-carb high-fat (LCHF) diets may have short-term therapeutic effects (e.g., if one loses weight or reduces allergenic/inflammatory substances that were being consumed previously)
  • In terms of reversing the degenerative effects of stress, LCHF diets are mostly counter-productive as they simulate the stress metabolism
  • People lose fat on diets that aren’t LCHF
  • Calcium, fructose, aspirin, niacinamide, and the fat soluble vitamins are therapeutic aids to restore normal glucose metabolism
 Anti-Stress Factors: Glucose, Oxygen & Carbon Dioxide

In my first guest post on 180 Degree Health we chatted about stress increasing our energy requirements. In this context, glucose and oxygen, which are substrates for efficient energy production, can be thought of as the two most basic anti-stress factors.

We also briefly went over carbon dioxide’s role in stress and how the complete oxidation of glucose (i.e., mitochondrial respiration) supplies more carbon dioxide than the oxidation of fat.

In addition to allowing cells, tissues, and organs to absorb oxygen, carbon dioxide has some other interesting qualities:
  • Carbon dioxide is an anti-inflammatory, opposing the production of pro-inflammatory lactic acid
  • Carbon dioxide has been referred to as a “cardinal adsorbent,” meaning that it has a powerful controlling influence in restoring order and coherence to the entire organism
  • Carbon dioxide maintains cellular ion gradients (i.e., so that the cell retains far more potassium than sodium and is able to excrete calcium while binding magnesium) 
Carbon Dioxide? Big Whoop… Turn me into a fuggin’ Fat-Burning Beast Roddy!

Free Fatty Acids In The Stress Response

As I’ve mentioned previously, Hans Selye first introduced the concept that in response to a wide range of stressors (e.g., darkness, low blood sugar, toxic drugs, loud noises, forced exercise, etc.), the hypothalamic-pituitary-adrenal (HPA) axis is invariably activated and there is an increase in cortisol secretion. This is an adaptive, life-saving reflex in the short-term, but when the exposure to stressors is excessive or prolonged, degenerative processes are set in motion, which is ultimately a result of failing adaptive mechanisms and inability to generate sufficient energy.

Additionally, Selye often pointed out that 1) stress is unavoidable and 2) the impact of stress is proportional to how we perceive it (i.e., stress before a gnarly hot make out is not the same as being hungry and going without food for 24 hours, however both stressors would transiently increase energy requirements).

Meeting these energy demands requires the efficient use of glucose and oxygen by living cells. A deficiency of either one requires a “higher functioning” of our adaptive stress hormones to compensate for the reduced energy supply. A hormone central in this adaptive response is adrenaline.

A healthy person is able to store a meaningful amount of glucose in the form of hepatic glycogen (the muscles use their glycogen for themselves). When a stress is encountered that can’t quickly be overcome, adrenaline, which is released from the adrenal glands (and noradrenaline to some extent, which is predominantly released from the sympathetic nerve endings), stimulates the breakdown of hepatic glycogen, releasing stored glucose into the blood.

At the same time, adrenaline (along with glucagon, which has an inverse relationship with insulin) stimulates fatty acid mobilization, which serves as an alternate fuel source to glucose, from adipose tissue and, in a vicious cycle, activates the HPA axis, amplifying the stress metabolism.

Selye notes in his book The Stress of Life that blood levels of free fatty acids, similar to cholesterol, is a marker for stress:
The elevation in certain blood lipid substances, such as cholesterol and free fatty acids, are comparatively simple to estimate, although they do require a chemical laboratory. Rises in STH, glucagon, insulin and prolactin are not only more difficult to determine, but also less reliable indicators of stress reactions in man.” – Hans Selye
 So “stress” releases fat into the blood… Big deal… Roddy…

In 1963 P.J. Randle and his colleagues described the inhibition of the use of glucose by elevated levels of free fatty acids as an immediate physiological phenomenon.  For example, brief bouts of intense exercise or fasting will raise free fatty acid levels, which will thereafter be used for fuel in preference to glucose, until glucose can be supplied (insulin suppresses the use of free fatty acids).

Over time, however, the chronic exposure to free fatty acids leads to a myriad of toxic effects, such as damage to the energy generating apparatuses of cells and an increase in the prostaglandin modulation of the aromatase enzyme, which creates new estrogen. These are just some of the many long-term consequences.

As evidence for the role of free fatty acids in these long-term degenerative conditions, consider some of the common features between obesity and diabetes:
  • Reduced respiratory quotient (i.e. less carbon dioxide is produced)
  • Increased levels of lactate in the blood of diabetics (i.e., energy production through glycolysis instead of our high evolved oxidative metabolism)
  • Decreased heat production (thermogenesis) upon the ingestion of food, especially carbohydrate
  • Increased levels of free fatty acids (generally)
  • Increased levels of adrenaline, which initiates the stress response
  • Increased levels of cortisol, which sustains the stress response
Is Low Carb a Tool? Possibly Maybe, Probably Not

In a recent article it was mentioned that HFLC diets are simply a “tool in the toolbox” for those who are “metabolically broken”. More specifically that ‘if you are insulin resistant, have fat in your belly or not sleeping well, then you should limit your carbohydrate intake below 50-110g…’

To recap, “stress” is anything that increases our energy demands, and glucose and oxygen are the basic substrates needed for efficient energy production.

A HFLC diet aims to “treat” poor glucose tolerance (a sign of stress) by replacing carbohydrate with fat; however, the excessive oxidation of fats (especially when polyunsaturated) impairs the cell’s ability to oxidatively metabolize glucose to carbon dioxide, water, and hydrogen.

In this context, a HFLC diet can be conceived as a diet that activates the stress metabolism.

Uhhh… Yeah whatever Roddy, I lost fat and I feel fuggin’ so badass on HFLC. Fat FTW!!1
Losing weight is part of the equation, and any diet that induces weight loss is likely to increase metabolic efficiency. However, there may be a couple of reasons for the initial “success” of low-carbers:
  • As Andrew Kim has pointed out, insulin resistance is not necessarily induced on hypocaloric HFLC diets because fatty acid oxidation keeps up with fatty acid mobilization. In other words, you are burning through fat at an accelerated rate.
  • As Matt has written about in Catecholamine Honeymoon, some stress hormones have anti-depressant and anti-inflammatory actions. Similar to fasting, this can provide a false sense security with one’s health (monitoring pulse and body temperature can help one avoid this problem).
  • LCHF diets exclude numerous foods that could cause inflammation or allergies.
Look, Roddy, I get it, but if I don’t use fat as fuel, I will never lose any weight. Everyone knows that.
“Healthy” fat loss is most likely a combination of keeping the metabolic rate up, consuming a nutrient-dense diet, and getting sufficient calories per your needs (e.g., stress and activity levels) – the basic message of Diet Recovery 2 and most of the material on this site.

Suppressing lipolysis doesn’t mean that you will never burn fat for energy. In fact, large skeletal muscles prefer saturated fats as a source of fuel while at rest, as does the heart’s myocardium.

If you take away anything from this article, let it be that the hormones that mobilize fatty acids are the same hormones involved in the degenerative effects of stress.

These hormones have short-term protective qualities (i.e., survival), but long-term negative effects such as immune system suppression (cortisol dissolves the thymus and renders us susceptible to infections and food allergies) and thyroid inhibition (cortisol interrupts the conversion of thyroxine to triiodothyronine).

Practical Application: Niacinamide, Aspirin & Fructose

Simple, yet effective, strategies like consuming more carbohydrate than protein (i.e. protein is insulinogenic and alone uncomfortably lowers blood sugar), avoiding polyunsaturated fats – like corn oil just to name one common source (which damage the energy producing apparatuses of the cell and decrease the rate of energy generation), and, for those who have blood sugar control issues, consuming fat, protein, and carbohydrate together can help to achieve steady blood sugar levels throughout the course of a day.

Niacinamide (not niacin or nicotinic acid) and aspirin (with vitamin K) both suppress lipolysis and can be considered rational treatments for those with advanced cases of insulin resistance.

Despite the irrelevant “evolutionary” interpretation of fructose, in the context of supporting the known factors that influence energy production, fructose (along with glucose):
  • Improves insulin sensitivity
  • Bypasses and activates key steps in glycolysis that are inhibited in people with poor glucose tolerance
  • Restores diet-induced thermogenesis and carbon dioxide levels to near normal more than glucose alone does
Increased parathyroid hormone correlates with insulin resistance and can be suppressed with enough dietary calcium, vitamin D, and vitamin K. Fructose, by depleting intracellular phosphate, decreases blood parathyroid hormone levels, too.