It is commonly asserted in journal articles and on the internet that saturated fat reduces insulin sensitivity. The idea is that saturated fat reduces the body's ability to handle glucose effectively, placing people on the road to diabetes, obesity and heart disease. Perhaps this particular claim deserves a closer look.
The Evidence
I found a review article from 2008 that addressed this question (1). I like this review because it only includes high-quality trials that used reliable methods of determining insulin sensitivity*.
On to the meat of it. There were 5 studies in which non-diabetic people were fed diets rich in saturated fat, and compared with a group eating a diet rich in monounsaturated (like olive oil) or polyunsaturated (like corn oil) fat. They ranged in duration from one week to 3 months. Four of the five studies found that fat quality did not affect insulin sensitivity, including one of the 3-month studies.
The fifth study, which is the one that's most commonly cited, requires some discussion. This was the KANWU study (2). Over the course of three months, investigators fed 163 volunteers a diet rich in either saturated fat or monounsaturated fat.
The SAFA diet included butter and a table margarine containing a relatively high proportion of SAFAs. The MUFA diet included a spread and a margarine containing high proportions of oleic acid derived from high-oleic sunflower oil and negligible amounts of trans fatty acids and n-3 fatty acids and olive oil.Yummy. After three months of these diets, there was no significant difference in insulin sensitivity between the saturated fat group and the monounsaturated fat group. Yes, you read that right. Even the study that's commonly cited as evidence that saturated fat causes insulin resistance found no significant difference between the diets. I'll be generous and acknowledge that the small difference was almost statistically significant (p = 0.053).
What the authors focused on is the fact that insulin sensitivity declined slightly but significantly on the saturated fat diet compared with the pre-diet baseline. That's why this study is cited as evidence that saturated fat impairs insulin sensitivity. But those of you with a science background may be able to spot the problem here. You need a control group for comparison, to take into account normal fluctuations caused by such things as the season, eating a new diet provided by the investigators, and having a doctor poking at you. That control group was the group eating monounsaturated fat. The comparison between diet groups was the comparison that matters most, and it wasn't quite significant. I think the most you can say about this study is that it provides weak evidence that saturated fat decreases insulin sensitivity.
So we have five studies through 2008, which overall offer little support the idea that saturated fat reduces insulin sensitivity in non-diabetics. Since the review paper was published, I know of one subsequent study that asked the same question (3). Susan J. van Dijk and colleagues fed volunteers with abdominal overweight a diet rich in either saturated fat or monounsaturated fat. I e-mailed the senior author and she said the saturated fat diet was "mostly butter". After 8 weeks, insulin sensitivity was virtually identical between the two groups. This study appeared well controlled and used the gold standard method for assessing insulin sensitivity, called the euglycemic-hyperinsulinemic clamp technique***.
The evidence from controlled trials is rather consistent that saturated fat has no major effect on insulin sensitivity in humans, at least on time scales of a few months.
UPDATE: other trials have added to this finding. The large European LIPIGENE randomized controlled diet trial found that substantial differences in SFA intake had no effect on insulin sensitivity over 12 weeks in people with the metabolic syndrome (3b).
* For the nerds: euglycemic-hyperinsulinemic clamp (the gold standard), insulin suppression test, or intravenous glucose tolerance test with Minimal Model. They didn't include studies that reported HOMA as their only measure, because it's not very accurate.
*** They did find that markers of inflammation in fat tissue were higher after the saturated fat diet.
79 comments:
Great job of dissecting the research Stephan, as usual! Why do you think that markers of inflammation in fat tissue were higher after the saturated fat diet? Could it be that the fat was from grain-fed animals Or, whatever else was in the margarine?
It raises my hackles to even see the word "margarine" in a test of saturated fat - rigged from the start!
Thanks! I have spent a lot of time looking at the KANWU study but didn't find the catch...
I'm interested in the inflammation finding as well...that's another criticism anti-saturated fat proponents use...
Stephan, a masterful job as always! The dubious claim that "saturated fat causes diabetes" has always intrigued me but I have never been able to find an answer to it. Now I have. Many thanks for your great work.
Caffeine may definitely be more significant than you think. Consider simply the conclusions of the first student of hyperinsulinemia, Seale Harris:
“As [Dr. Seale Harris] pointed out, overindulgence in caffeine is a common cause for [hyperinsulinism]. Harris conducted his research in Birmingham, Alabama, the heart of the South, where various beverages consisting of sweetened and flavored water ‘spiked’ with caffeine are water substitutes. Hyperinsulinism may be induced in persons predisposed to the condition by the very combination of caffeine and sugar found in these beverages.”
-From E.M. Abrahamson's Body, Mind, and Sugar (1951)
If sat-fat does cause a bit of inflammation, couldn't that then result in at least some degree of malfunction, of the body's ability to handle glucose in the LONG term?
Kinda the same way fructose appears "harmless" in the short-term, but we now know it messes with ya in a more roundabout, long-term way?
I would also wonder if inflamed fat tissues would screw up testosterone to estrogen ratios a bit?
I wonder what is the magnesium intake of hunter-gatherers?
Animal foods don't contain much of magnesium, and I have gotten the impression that hunter-gatherers weren't really into low-calorie vegetables. Even so, only certain vegetables are rich sources of magnesium and probably not every group had access to them.
Perhaps the normal required daily intake is low, but something is increasing the need for it, because I can't imagine a hunter-gatherer getting a lot of it.
Or did they get it from the water they drank?
@Matt
In the South, "sweet tea" is a tradition. And when I say sweet, I'm talking syrup here. People who drink something that sweet have no problem consuming lots of other sweet stuff, including a big piece of pie for dessert. Small wonder that AL is second only to MS with the highest rates of obesity (read insulin resistance).
For any investigator to single out the combination of caffeine and sugary beverages as anything more than an "association" is unwarranted.
PS: I have lived in the South for about 50 years, and about 15 in the West and New England.
Andy,
I believe nuts are high in magnesium. I think I have seen studies where they questioned the participants whether they ate nuts regularly as an estimation of higher magnesium in the diet.
Thanks, Stephan! As you might remember, this is a question that's been on my mind.
I'd like to just revel in these results, but, as I've mentioned in a comment before, I had gestational diabetes and saw my insulin requirement plummet when I cut way back on fat - all fat - in the last few weeks of my pregnancy. I had no idea it would have that effect - I was avoiding fat because of a pregnancy-related liver problem I thought I was developing, cholesostasis of pregnancy. (The test results would have come after the due date, so I had to act "as-if.")
So, it could be that fat (not necessarily saturated) reduces insulin sensitivity OR that reducing fat increases it short-term in diabetics. But then there's the example of our friend Matt Stone (hi, Matt) reducing his fasting blood glucose on a Joel Fuhrman-type ultra low-fat diet, and he was not diabetic.
The stuff about caffeine makes some sense, but I've also heard off and on through the years that coffee-drinkers have a lower risk of diabetes. It could be other things in the coffee - it has a lot of magnesium, for instance. But could it also be that caffeine mobilizes glycogen in the liver in order to boost blood glucose? And that this might help prevent fatty liver? I'm not sure it does this, but it's a guess. Could it be good for preventing diabetes but bad once you have it? Here's a link to a popular web article on that theme. http://www.diabetesselfmanagement.com/Blog/Amy-Campbell/caffeine_friend_or_foe_part_2/
Also, I've heard that saturated fat increases inflammation but have never seen it backed up. I looked on PubMed once, but that doesn't mean it wasn't there. Yet, I've heard time and again on this and like-minded blogs that PUFAs are highly inflammatory, with some saying that saturated fat is the safest fat. I don't know about MUFAs. I personally seem less inflammed, judging from my allergies, with more saturated fat and less PUFAs, but it might just be the less PUFAs having this effect.
Thoughts?
'Long-chain saturated fatty acids such as palmitic acid induce insulin resistance and NF-kappaB activation in skeletal muscle cells'
in "Trans Fatty Acid-Induced NF-kappaB Activation Does Not Induce Insulin Resistance in Cultured Murine Skeletal Muscle Cells"
Lipids, february 2010
I continue believing a diet based on monounsaturated fats as Mediterranean is healthier than based saturated fats.
I think Evelyn Tribole also thinks is better a diet based on MUFA instead of SFA when talking about fats.
My experience with diet high in SFA is so bad, with inflammatory pains I have forgot removing them and coming back to my almost only MUFA-based diet (along with fish fats).
Omega 6 are the real evils, of course, but maybe Dr Weston Price should have known better mediterranean fats.
i too have heard that coffee drinkers have less rates of metabolic disorder.
@Jim That's what I was thinking, too. Sweet tea is usually little more than hummingbird food with a little Lipton for color. I would hardly call it "spiked" with caffeine, especially compared to your average cola product.
Highly concerned about the caffeine as i love my cup of java w/ heavy cream in the morning- I did a quick search online. One thing mentioned was the difference between caffeine and coffee. It is NOT the same thing and there is much more to coffee obviously then just caffeine. That would lead to different results when testing- its two different things~
I wanted to add your blog is one of my favorites! It is one of the 'go to' sites for me. You are a master of breaking the medical studies down for some one like me, smart- but not that smart! :)
I send links to your articles all the time- especially to the people that argue with me. I do not have the finesse you have at explaining the data. Thanks so much and please dont ever stop!!
The Archives of Internal Medicine reported just last month that coffee consumption is associated with lesser risk of developing type 2 diabetes: 7% less risk for each cup daily.
Details here:
http://advancedmediterraneandiet.com/blog/?p=258
@Adolfo
Can you briefly outline how your idea that 'MUFAs are healthier than SFAs' makes sense in the light of evolution?
Great post as usual Stephan. I can't help thinking though that coffee / caffeine isn't quite as harmless as many in the paleo community (using the term loosely) would wish. I'm a big fan (addict?!) but I'm not going to kid myself that it's a neutral factor in my own attempts to achieve, as best I can, the paleolithic metabolism.
Stephan, awhile back (September '09) when you wrote about palmitic acid, you agreed that it likely causes at least a temporary, reversible insulin resistance. Long term effects aside, if someone is trying to lose weight in the short term, would these IR effects of palmitic acid slow down the weight loss?
I ask because I have now seen several people totally fail to lose weight on a standard low-carb diet, yet subsequently drop the weight easily by limiting sat fats to coconut oil and avoided sources of palmitic acid. I have always preached sat fat goodness, and cannot explain this anomaly that I've witnessed several times now. Any thoughts?
Thanks for the excellent (as usual) deconstruction of another saturated fat scare.
All these studies about saturated fat in the diet ignore the elephant in the room; Mammals typically derive 50% to 80% of their energy intake from saturated fat. Comparing health effects of a totally inadequate saturated fat intake to a slightly inadequate intake is kind of fruitless, but it's what happens when the baseline for the studies is our lipophobic conventional wisdom.
Maybe saturated fat can cause inflammation in the presence of too much omega 6 and too little epa+dha.
Taliesen
I am a big supporter of paleodiet concept, but diet did in those days is not perfect. Also, humans have evolved in many ways since those days; many of us can digest with no problems dairy products, probably 15-25% of population has currently not many problems with cereals and starches.
Saying that something is simply good or bad based of paleolithic days is a stupidity. There are thousands of studies about benefits of a diet high in extra virgin olive oil, a antioxidant rich in polyphenols plus antiinflamatory fat. Any other fat is both things at the same time? Also, many paleo advocates like Dr Cordain believe SFA must be mantained low.
My favourite SFA is coconut oil and the only one I consume in very small amounts but also I have known people who develop inflammatory pains in joints with high consume of virgin coconut oil. Lets visit evolution in mediterranean zones (and I am not a supporter of "mediterranean diet" since it has too carbs I think).
"My favourite SFA is coconut oil and the only one I consume in very small amounts but also I have known people who develop inflammatory pains in joints with high consume of virgin coconut oil. Lets visit evolution in mediterranean zones (and I am not a supporter of "mediterranean diet" since it has too carbs I think)."
Very strange...there is no scientific evidence to support that SFA´s is inflammatory. In fact it has found to be anti-inflammatory. PUFA´s (omega6) has been proved to be very inflammatory. And strange also that you can connect those pains with SFA consumption. It could be something else also.
Stephan,
Thanks for this wonderful post. This has come in at a right time for me when I am considering altering the %age of fats being consumed.
Is there a high level guideline that you can suggest or kind of follow for yourself - the %age of different fats everyday?
For example, what %age of SFA, MUFA and PUFA are acceptable in diet in your opinion?
I am a Type II Diabetic, low carber (<30g of carbs everyday), ovo-vegetarian and consume 75% Fat (primarily nuts, cheese and olive oil)in my food everyday.
Thanks
Venkat
@Andy
Bone, and bone marrow, is high in magnesium. Hunter-Gatherers don't, and our Paleolithic ancestors also didn't, simply discard bones the way most of us so-called civilized people do.
Stephan.
Using the hyperglycemic clamp technique, Chiu, Chu, Go and Saad found a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on ß cell function.
5,000iu/day of D3 normalised my abnormal fasting glucose & OGTT results.
Nige.
Stephan,
You beat me to it! I was in the process of writing a critique of this paper for Robb Wolf's blog.
There are a few other things on which I would love your opinion.
1) Data was obtained via surveys
2)This isn’t as much an indictment of saturated fat consumption as it is an indictment of high carbohydrate diets. Note that the observed effects on insulin sensitivity are only relevant when the percentage of energy from fat is 37 or less. Many of us consume diets that are 60–70 percent energy as fat, 20–30 percent of energy as protein, and about 10 percent energy as carbohydrate. The observations simply do not apply to folks on a ketogenic diet.
3)The SAFA group consumed margarine of unspecified composition. Was it mostly palmitate? Did it contain trans-fatty acids? The MUFA group consumed margarine that was oleic acid-based. Oleic acid, which is found in large quantities in olive oil, has known hypotensive effects.
4) This is directly from the paper "Thus, the increase of LDL cholesterol in the SAFA diet was due to an increase among the subjects who took the supplements with n-3 fatty acids (+ 7.8%, p < 0.001). Those subjects, however, on placebo capsules had concentrations that did not change ( + 0.7%, NS). On the MUFA diet, a significant reduction of LDL cholesterol was seen only among the participants who took the placebo capsules (–7.7%, p <0.001) while the mean LDL cholesterol concentrations remained virtually unchanged (–2.7&, NS) after addition of n-3 fatty acids which counteracted the expected decrease of LDL cholesterol.”
Was the observed increase in LDL cholesterol due to increases in pattern A or pattern B LDL?
Caffeine for myself is a major trigger for blood sugar issues, with or without actual sugar involved. To this day I cannot drink a strong cup of coffee without having some major hypoglycemic symptoms show up about an hour later. Not scientific proof on the subject, but proof enough for me to avoid the java.
Stephan,
Do you believe that it is immaterial that SFAs cause a small degree of peripheral insulin resistance because such insulin resistance is not pathological, like liver insulin resistance would be?
I read Peter's discussion of this topic and saw you commented on it, so was wondering about your views. As I understand it, some SFAs, like palmitic acid and MCTs may be bodily triggers for starvation (or at least hypoglycemic conditions), with the result that peripheral cells resist glucose uptake in order to conserve the potentially scarce reserve of glucose for the cells that really need it.
Thanks, Dan
Regarding caffeine and insulin sensitivity, Nephropal had nice discussion on the matter here:
http://nephropal.blogspot.com/2009/10/beans-coffe-and-cacao.html
My guess is the disparity in experience and effects between the various natural caffeine sources could be due to the fact that plant sources of caffeine also contain widely varying mixtures of other xanthine alkaloids, including the cardiac stimulants theophylline and theobromine, and other substances such as polyphenols that can form insoluble complexes with caffeine.
Speaking of saturated fats, I'd love to hear Stephan's thoughts on the following study showing that olive oil consumption leads to higher triglyceride levels than butter:
http://www.sciencedaily.com/releases/2010/02/100209124352.htm
The article amused me in that the researchers sounded quite pained by the results of the study. Perhaps they were up late the night before trying to tweak the numbers another way!
Follow-up: the article uses the term "blood fats." I assume they mean triglycerides?
Olive oil boosts HDL, as is seen in longevity populations. I think its probably the clearest effect of olive oil on blood lipids.
I think there needs to be some caution around the markers of inflammation found with SFA intake. One needs to keep in mind that a degree of inflammation is indeed healthy. No inflammatory response would not be a good thing, just as hyperinflammation is seen as a negative.
This cracks me up: butter was their source of saturated fat according to the study's author, and yet, butter is 50% sauturated and 33% monounsaturated!
Hi Senta, J and Deb,
Regarding the inflammation study. She said the fat was "mostly butter", which is reflected in the fat composition-- roughly twice as much SFA as MUFA. Most animal fats are roughly equal proportions saturated and monounsaturated. The total fat % wasn't reported that I could find, but I have to imagine if these are normal diets that these people were eating a TON of butter. So what caused the inflammation, increasing saturated fat or decreasing monounsaturated fat, or some other difference between the fats? We don't even know that it was the fatty acids themselves that caused the change. It could have been something else, like the fact that the olive oil diet would have been richer in vitamin E.
But that's not all. They said in the paper that the SFA diet caused an "obesity-linked proinflammatory gene expression profile". OK, if that's true, then why is there no consistent association between SFA consumption and fat gain? In the latest and largest study (almost 90,000 participants), higher SFA consumption was associated with a smaller increase in waist circumference in European women over time, compared to other fat types. The trend was the same in men but it wasn't significant.
http://www.ncbi.nlm.nih.gov/pubmed/19828709
I also have to point out that if butter made people fat, the French and the Masai would be a lot fatter than Americans. Yet both have a reputation for leanness. Also, saturated fat doesn't make animals fatter than MUFA or PUFA when the n-6:3 ratio is controlled for, to the contrary. It's fun to look at molecular changes, but at some point they have to intersect with real life.
Hi Andy,
Many foods hunter-gatherers would have eaten are rich in magnesium-- starchy tubers, nuts and bone broths where used.
Hi Helen and Adolfo,
If fat, saturated or otherwise, is giving you glucose intolerance, then maybe you'd be best minimizing it. The evidence linking saturated fat to inflammation in a real live human/animal is pretty minimal. There have been a few controlled diet studies looking at blood markers like CRP and interleukins that found nothing. As far as I know, this is the only study to show a convincing effect. It's also the first study to look at fat tissue by microarray under these dietary conditions.
There's a lot of cell culture stuff but it's not very convincing because they typically use very high concentrations of fatty acids and don't usually control for contamination with inflammatory substances such as LPS in their reagents.
Hi Emily and Steve,
The evidence that coffee is protective of diabetes comes exclusively from observational studies, and the effect is very small. I can't say I believe it, personally.
Hi David,
I was speculating in that post that palmitic acid might cause reversible insulin resistance, but that has never actually been shown in humans. Well I say if your friends were able to lose weight by limiting saturated fat, that's great. The concept doesn't have much support behind it in the scientific lit though.
Hi Stephan,
I plan on getting some test strips to see what different meals do to me now. I suspect that it may be quite different from when I had gestational diabetes. I've also changed my diet since then - less fruit and omega-6.
Peter at Hyperlipid discussed once the finding that a higher-fat diet produces more ROS, but I can't remember the details. I wonder if that's related to the inflammation this study found. It may not all be bad. You also have to take into account things like the 2004 study of post-menopausal women finding that more saturated fat in the diet correlated with less arterial plaque, especially if the saturated fat replaced carbs in the diet. Atherosclerosis is an inflammatory condition, so that's some counter-evidence. In addition, foods with saturated fat may have either inflammatory or anti-inflammatory components as well, so that has to be taken into account. (For instance, butter has both - AA, usually inflammatory, on the one hand, and K2 and butyric acid on the other.)
Stephan, thank you.
You just rocked my world. Learning from our health issues, I'd discovered that my husband and daughter need more magnesium than most people, but I never connected that to the type 2 diabetes that is prevalent in my husband's family. I've seen the mag lower his blood pressure, which also tends to be a problem in his family.
This post really helps me pull together the pieces to understand the health issues that plague his family.
Thank you.
Caffeine-related insulin resistance is likely mediated by high catecholamines, which are lipolytic. It is well known burning fat increases insulin resistance. That's like saying saving your money in the bank results in having less money in your wallet. Without understanding what a bank really does (it saves and adds interest to your money), it sounds as if putting your money in a bank is a bad thing (because it seems to result in less money being in your wallet).
Catecholamines cause body fat to be burned. This causes symptomatic glucose intolerance + elevation, because fat is leaving the fat cell and being burned up in the mit-o-chondriaaa.
Burning fat results in temporary glucose intolerance and elevation.
This is not a bad thing, this is a good thing. Insulin resistance is "usually" bad, but when it results from lipolysis (of body + dietary fat), that's not exactly true anymore.
WHere do you think the energy comes from when you drink coffee? Majik? It comes from catecholamine mediated hypermetabolism. This results in a temporary insulin resistance.
The real problem with coffee is the insulin hypersecretion that tends to occur, as coffee is an adrenal/pancreatic gland stimulant noted to result in a bit of excess insulin release. This will drive people to want to consume sweets after drinking coffee, if they don't know what they are doing anyway.
As long as you don't eat shitty food in response to coffee, you should be o kaaay.
re: sat fat.
If it increases inflammation, it can't be good, as inflammation is at the heart of metabolic disorder/obesity.
Inflammation also plays a role in insulin resistance, so I very much question the finding that sat fat didn't increase IR but DID increase inflammation as that seems illogical.
I find it very probable that sat fat should increase IR and lead to weight gain. Sat fat is a seasonal marker of nutrient availability, it is an animal-form of carbohydrate. The reason we grow fat on carbohydrate is because it is a seasonal marker, we concerved an endocrine/neurotransmitter system that tracks the seasons and responds preemptively. We grow fat on carbohydrate because carbohydrate correlates with fall, and fall comes before winter, and winter is harsh, and a bit of extra padding and inflammation is useful in a harsh winter. Seeing as sat fat is carbohydrate that has been metabolized by animals (usually), it makes sense that sat fat would cause similar metabolic changes as carbohydrate.
re: magnesium...
I base my diet on nuts and have only improved in doing so. Fairly sure the magnesium helps.
John S - I eat the crap out of bones, love marrow, etc. It's great. Chewing on chicken bones. Try to avoid doing it in public, but it's hard, since it is honestly my favorite part (chicken wing bones, and the soft tips of drumsticks... yum).
Re matt stone's lower glucose on low fat.
Lower glucose on a low fat diet in a nondiabetic person is a sign of high insulin, or possibly low calorie intake. Either way, low glucose suggests low fat burning, but it doesn't mean (logically) that the diet will lower glucose in a diabetic person, as a diabetic metabolism is not like a normal metabolism.
High glucose is a sign of high fat burning with insulin inadequate to suppress it, just an FYI. High glucose can be pathological, but it can also be nothing more than a physiologic sign of burning lots of fat.
Glucose follows fat metabolism, FYI. Fat metabolism profoundly affects glucose metabolism and insulin levels. But, for diabetics this comes into play, as well as an additional factor of an absolute carbohydrate intolerance which is NOT FOUDN in a non-diabetic person. Diabetic people are FRANKLY carbohydrate intolerant in a way non-diabetic people aren't. I can eat a low fat diet and I will never get hyperglycemia (I may, however, get lots of hypoglycemia from my tendency to hypersecrete insulin in response to carbohydrate, but I WONT get HYPERGLYCEMIA because my cells respond to insulin normally, if not excessively).
Only a diabetic person is going to have a high glucose on a low fat high carb diet, and that is because the diabetic person lacks an ability to make more insulin to suppress glucose levels (either because of a frank insulin deficiency, or extreme resistance, or both). For a diabetic person, carbs are much worse than they are for non-diabetic people because they lack the ability to hypersecrete insulin and "deal" with them.
The results of a non-diabetic person on a diet change has little to no relevance of how a diabetic person would respond to that same diet change. FYI.
It's like saying "Matt stone drank 10 beers and didn't become an alcoholic... therefore, alcohol has nothing to do with alcoholism!"
If matt stone isn't an alcoholic, he can drink all the beer he wants and not ever develop a pathology from it.
Why do people find it hard to believe metabolic/endocrinological atypicalities exist in people with conditions like diabetes? It's not as simple as not eating wheaties, or eating coconuts.
Hi Stephan,
as far as I know there is only one thing that causes insulin resistance and it is excess avaibility of free fatty acids in the cell.
Caffeine is one of the "culprits" increasing mitochondrial avaibility of fatty acids. That usually leads to down regulation of mitochondrial oxidation of glucose (pyruvate dehydrogenase,PDH) and that is also related to decreased insulin sensitivity since decreased pyruvate oxidation leads to downregulation of Glut-4.
Magnesium deficiency leads also to downregulation of PDH and (as you mentioned) increases insulin resistance. Magnesium deficiency could make cells more dependent on glycolysis and fatty acid oxidation for ATP production.
Fructose is harmful substance which is metabolised in the liver. As a result of high fructose feeding liver PDH activity increases (due to uncontrolled glycolysis of fructose) and fatty acid oxidation decreases. Most of the formed acetyl-CoA is directed to the fatty acid synthesis in the liver but at the same time fatty acid synthesis in the adipose tissue is decreased.
Free fatty acids which should have been allready stored are now directed to the visceral adipose tissue which has bigger activity for FFA uptake than subcutaneous adipose tissue.
Normal function of adipose tissue is very important for healthy metabolism.
Amateur reasoning here, but Peter's (Hyperlipid) discussions about palmitic acid and peripheral temporary insulin resistance make sense to me.
If you eat lots of fat and not that many carbs you can live with some insulin resistance. Your insulin levels won't spike anyway. And eating lots of carbs might not be too bad if you skip the palmitic acid and bad stuff like grains. Perhaps?
Stephan:
"I also have to point out that if butter made people fat, the French and the Masai would be a lot fatter than Americans. Yet both have a reputation for leanness."
When a person is "getting fat" he/she is building fat tissue because every tiny fat cell has quite small capasity to store fat. Lot of new cells/tissue are needed if we want to accumulate fat and restore normal metabolic function.
When we are dividing fatty acids by the degree of saturation like saturated vs. unsaturated fatty we will never understand what is going on. One should take a closer look.
For example medium chain fatty acid octanoate has special properties compared to lets say palmitic acid. Octanoate increases ROS production because it's entry to mitochondria isn't so tightly regulated as long-chain fatty acids. Due to increased ROS octanoate also effects on preadipocyte maturation; it inhibits the growth of fat tissue. So dairy fat or coconut fat could be connected to leanness and that's what we are seeing.
Is that good or bad thing? It depends. Could be both I think.
Type 2 diabetes is usually connected with adipose tissue inflammation which is a result of over grown adipocytes that have died and activated macrophages come to clean the mess. Chronicly this will lead to the situation where the number of anti-inflammatory T-regs will decline. That kind of adipose tissue seems to be very sensitive for proinflammatory stimuli like LPS.
How to overcome this?
One way is building fat with insulin sensitizers (TZDs) which are PPARg agonists and restores normal adipose tissue energy and function. So building fat decreases insulin resistance and glucose homeostasis improves.
There are also endogenous or dietary PPARg agonists like oxidation products of linoleic acid. So using linoleic acid and especially highly oxidized form of LA (in heated plant oils) one should see increasing prevalence of adipocity which we certainly do.
Quite interesting stuff and all this should be taken into account if we want to complete this picture we're building.
Side point: as someone from the "Mediterranean", people please let go of the idea that olive oil is the main fat used there. Before the craze of the "Mediterranean" diet came over from the US to the "Mediterranean", olive oil was not used a lot in cooking. Think more duck and goose fat (still sold in large amounts in south of France), lard, lamb fat and ghee. In my region, traditional cooking books call mostly for ghee in cooking as well as cooking every part of the animal (even organs you'd think no one would eat). Olive oil is reserved mostly for cold dishes.
Hi Stephan,
"Insulin sensitivity is a measure of the tissue response to insulin. Typically, it refers to insulin's ability to cause tissues to absorb glucose from the blood. A loss of insulin sensitivity, also called insulin resistance, is a core part of the metabolic disorder that affects many people in industrial nations. "
This statement I feel is misleading. Insulin resistance with regard the response of peripherial tissues is a normal response to a low carb diet and not at all a marker of metabolic disorder.
Insulin resistance with regard to the liver (ie the liver does not stop doling out glucose when insulin is secreted from the pancrease) is the marker of metabolic disorder.
These two types are often confused in the literature.
Hi Djinn,
Yes, most mammals do end up getting many of their calories from saturated fat if you take into account intestinal production of fatty acids. But those are short-chain fatty acids like butyrate, propionate and acetate. Not equivalent to eating longer-chain fats like animal fat.
Hi Venkat,
My only real guideline is to keep omega-6 low and omega-3 adequate. I think very low-carb diets may be problematic for some people, but in the case of diabetes they're likely to be preferable.
Hi M@,
According to the study, trans fats should have been low in both diets. I wouldn't discount the results just because diets were assessed by survey. Surveys might not be a great measure of dietary intake, but I'm willing to believe that they detected significant differences between groups. Clearly it would have been better if the diets were better controlled though.
Hi Daniel,
What's the evidence that SFA cause peripheral insulin resistance in humans?
Hi Westie,
Thanks, that's interesting.
Hi Hkay,
I agree that the Mediterranean diet has been misrepresented by overzealous American cardiologists. Where do you live, if you don't mind me asking?
Nicoretta9,
Do you have references to support those statements? As far as I know, the idea of "physiological insulin resistance" is logical but remains unproven.
Thanks for the reply Stephan.
Thanks, Venkat
I second the suggestion that the discussion of peripheral, i.e., physiological insulin resistance at the Hyperlipid blog is plausible, if not proven. Plausibility arguments abound in the physical sciences (prove to me that the Schroedinger Equation is untrue because "unproven"), so why do we forbid them in the biological sciences, where there are even more factors at play? Said argument asks only that we consider that our cells, depending on what we eat, choose one source of fuel over the other. No more, no less.
Also, is not coffee an excellent source of magnesium?
Westie,
I hold a similar outlook and have been looking at these areas (-:
I found this really useful article on MCTs whilst looking for something else.
http://cpmedical.net/articles.aspx?ProdID=art6564&zTYPE=2
te info on MCTs is interesting as they seem to actfor immediate fuel like carbs but dnt promote insulin jumps... gives coconutoil and nuts a better outlook
Robert,
yes I've read that article for some time ago when I was sucking information on MCT's. Octanoate inactivates PPARg in AT and increases fat accumulation in the liver perhaps by decreasing VLDL excretion from hepatocytes. These all are probably due to increased mitochondrial ROS formation. Increased ROS could also explain why octanoate will decrease pyruvate oxidation and ATP generation which may lead to increased lactate formation.
As I wrote above these can be seen positive or negative things and it depends on the situation. For example type 2 diabetics has decreased pyruvate oxidation, fatty acid synthesis and increased lactate formation in their AT.
So MCT's are not some miracle food but they are good for e.g. activating liver ketogenesis in Alzheimer patients providing food for dying brain cells.
There's still lot of more thinking and reading to do.
Let me get back to you on references..
But offhand, most the studies claming that low carb (or high fat or high protein) diets cause insulin resistance are measuring glucose tolerance.
The fact that diabetics also end up with impaired glucose tolerance is why there is confusion. They're viewing the result (impaired glucose tolerance) as the cause.
The acutal pathology of diabetes results from your body being subjected to consistantly high blood sugar and consistantly high circulating insulin, because the liver has stopped responding to normal amounts of insulin. Result, high circulating insulin, AND higher blood sugar because the liver keeps releasing glucose.
Having impaired glucose tolerance on a low carb diet does not result in these things (because you are not providing the source of the carbohydrate), and is reversible when regular consumption of carbohydrate is resumed, showing that the liver-pancrease messaging is still intact.
Hi nicoretta9,
From what I've read, on average, low-carb high-fat diets improve insulin sensitivity in overweight people. I don't think that's true in lean people though. Rats and mice become insulin resistant and overweight on high-fat diets, which is partially reversible, depending on how long it's been going on.
What you're saying makes sense, I'm just not aware of any direct evidence.
nicoretta9:
"The actual pathology of diabetes results from your body being subjected to consistantly high blood sugar and consistantly high circulating insulin, because the liver has stopped responding to normal amounts of insulin."
If you are saying that liver is a cause for high blood sugar I think you got it wrong. Liver is just doing what the rest of the body "wants it to do".
Problem in type 2 diabetes is that there is too much glucose in the body and that is a result of increased gluconeogenic precursor production. Puryvate oxidation is a main highway that takes glucose out of the body and if puryvate oxidation is downregulated (like in T2DM) 3-carbon skeletons (for example lactate for the Cori cycle) are saved.
There are atleast two ways to make situation better. You can decrease the intake of the glucose like on a low carb diet or you can find ways to restore your oxidative metabolism and pancreas function. There may be some difference between these two.
great article, thank you.
This is a great article, and yet another supporting evidence of why I grind my own wheat and make my own bread (with olive oil)! As to what I eat, if I didn't grow it (other than a little meat and dairy), I don't eat it.
- David
Aloe Vera 101
Westie,
Interesting. Where does pyruvate oxidation take place?
Thanks,
Nicoretta9,
as you can easily find out pyruvate is oxidized in mitochondria. It's not all about pyruvate but that is one important part of it.
Read and learn! :)
When my monosaturated fat consumption was highest, my HDL never rose about 48. Replacing monounsaturated fats with saturated fats raised my HDL to 70. This is a dramatic increase from 10 years ago when my HDL was 25.
I'm not sure I understand why anyone would study the effect of saturated fat on insulin sensitivity in the first place, unless it's to be thorough. What is the suspected mechanism here?
I have had insulin resistance for 5 years and after trying EVERYTHING, I am finally losing weight and feeling better with the extra virgin raw coconut oil. I too have eliminated every other saturated fat (besides a small amount of real butter now and then) and the only other fat/oil I use is cold pressed Extra Virgin Olive Oil. The first week or so my weight stayed the same, I maybe even gained a pound or two... but my weight did seem to shift slightly and I have more energy and I don't feel as swollen/inflamed. Now a couple weeks later it's slowly coming off.
FINALLY!
I have been very strict with diet and exercise and I've gained or stayed the same for several years until now.
Oh, and as a side note... I have been using it as a moisturizer as well and it has almost cleared my Keratosis Pilaris (and my husband's Psoriasis).
:) Heather
"The Archives of Internal Medicine reported just last month that coffee consumption is associated with lesser risk of developing type 2 diabetes: 7% less risk for each cup daily."
Hahahaha if that was true then I'd not only be cured I'd be curing other people through touch . . .
. . . seriously though has anyone done a statistical breakdown of coffee/caffeine studies? My impression is they balance out about 50% pro and con.
"I'm not sure I understand why anyone would study the effect of saturated fat on insulin sensitivity in the first place, unless it's to be thorough. What is the suspected mechanism here?"
Er . . . fat people become diabetic. Fat people must eat fat (doctrine of signatures) therefore eating fat must cause diabetes. Simple.
Anecdotally my IR dropped like a stone from reducing carbs (totally expected) and didn't change much from eating more sat fats, the HDL went up at the expense of LDL but the trigs also seem to have increased so the ratio stayed around the same.
Not everyone appears to react the same to different dietary fats though, some individuals actually do worse on sat fats while others don't. I'm coming to believe that the entire mechanism of metabolism is an intersection of a whole bunch of J curves. What I'd like to see is studies where individual responses are plotted, it may well be that a single or a few individuals within a study totally bias the results while the majority react quite differently. After all there must be reasons for so many studies "proving" things that don't actually occur in the Real World.
I'm having a heck of a time determining if saturated fat is bad or not.
Dr. Mary Enig Ph.D is in favor of saturated fat.
Dr. Suzanne Craft Ph.D is not. She studies how insulin resistance plays a role in developing Alzheimer's. http://www.hbo.com/alzheimers/supplementary-the-connection-between-insulin-and-alzheimers.html
She says that consuming saturated fat causes a rise in insulin.
Well, does it or doesn't it? I'm tearing my hair out trying to make sense of this.
I must be the latest temporarily confused person out here--I read this story (http://yourlife.usatoday.com/fitness-food/diet-nutrition/story/2011/06/DNA-based-diet-assists-with-disease-prevention/48287254/1), and it says that saturated fats are responsible for insulin resistance. If that's true, then why are doctors pushing the Mediterranean diet as a "gold standard" for the way we should eat--it's loaded with olive oil, avocados, fish, etc. All are Omega-3's, which are SATURATED! Without these foods, how are we supposed to control inflammation without rotting our stomachs out eating aspirins all day?
Somebody's obviously wrong.
what has been helping me these past several months with my metabolic syndrome and all it's nasty side affects, is low carb low gi diet.
slowly I have lost mass, clothes are getting to big for me (I dont weight myself those numbers drive me crazy)people have commented too even strangers who see me in the neighborhood too, slowly I started to sleep better, not having low hypo symptoms in the middle of the night like I used to, tho I still have occassions, my energy levels are increasing slowly, but i have noticed the tendency to feel funny, like I am sick but not really at times, like I have the flu but not really. it passes.
I did notice last week that when my gi went up on some meals it was starting to affect me negativly, It past once I got back on the lower gi scale. it did take a few days for the negative affects but only a day or so to get back on track.
naturally my saturated fats have increased to compensate for the otehr caloires missing, especially dairy, I add cream to my milk to up the fat and notice I can drink less of it (milk) for satiaty.
i use coconut oil sometimes, lots and lots of real butter and dairy of course and I love my berries and I still use oranges and pineapple and grapefruit if I have a craving for it, but as time went on I noticed less craving for it and it still stays within my overall low gi reading and lower carb (30 percent of total calories or less depending on hunger).
it is the first diet I have been able to stick to for many many months, like four months, never been on a diet that long, without getting those binging episodes and I do not have to use willpower not to eat higher carbs stuff that I usually love like ice cream and double layer chcolate cake tho I am considering ordering low carb flours but how do you do a low carb icing?
anyway I am defintly calmer inside, not have minor quacks all day long, that is what is feels like inside, like I have been taking adrenalin or too much caffeine even tho I don't take that stuff but occassionally.
now I am more relaxed mentally and physically. I think maybe the world needs to reconsider it's understanding of how our bodies really work under present world conditions.
saturated fats I believe were demonized because of either the veggie oil industry (which was throwing it out as a waste product before finding a new market) or because they do know saturated fats make you healthier and we can't have that now can we?
rosa
Have you ever considered that all fats are a problem - so that it is not about whether it is saturated or not? I am about to try to RAVE Diet which is a very low fat diet with no animal protein at all. It's a diet that has been shown to reverse cancer which is my main concern at the moment.
I reread this post you forgot some other things that cause the dreaded insulin resistance (from the livers standpoint)
* calcium deficiency saturated fat increases absorption including fat soluable vita/min
*vita d deficency (no one likes ot sun bath anymore without sunscreen)
*sulfer defiency (for vita d production)
*high gi carb intake with low fat intake that buffer the glucose
*artifical saturated fats (margerine, crisco which are only damaged rancid polyunsaturated fats deguised as saturated fats no wonder they cause inflammation they are rotten oils)
*basic malnutrtion that leads to resistance that leads to hyperinsulinemia which leads to binging episodes on high gi foods because the glucose set point has been raised, and high gi foods raise it quickly as the brain has triggored an alarm.
insulin resistance is a natural process when the brain does so to conserve glucose for itself like when your sleeping or exercising hard that sorta thing. as long as the liver responds to basal insulin there is no problem.
basal insulin prevents the liver from pouring out sugar when the blood is already high enough my guess it is because the setpoint for glucose (increasing concentration to overcome the resistance somewhat) is set higher than the numbers on a chart say they should be.
rosa
Thanks so much for this article! Yesterday, my nutrition instructor was saying that saturated fat caused insulin resistance because it made the cell membranes too stiff. It went against everything I believed in so I googled this morning and you handed me the science to cite for my Paleo meal plan for blood sugar regulation that includes saturated fat.
This study is in no way conclusive because it takes years not months of eating a diet containing saturated animal fat and oils for diabetes to rear its ugly head. Insulin resistance is caused by the buildup of fat in the muscle cells where sugar is stored for energy bye way of insulin. That's when sugar starts backing up in the bloodstream causing high blood sugar. Get the animal and oil fats out of the diet and diabetes simply disappears. THE END
Debunking the Paleo diet: TED Talks
https://www.youtube.com/watch?v=BMOjVYgYaG8
TED Fellow Christina Warinner is an expert on ancient diets. So how much of the diet fad the "Paleo Diet" is based on an actual Paleolithic diet? The answer is not really any of it.
Dr. Christina Warinner has excavated around the world, from the Maya jungles of Belize to the Himalayan mountains of Nepal, and she is pioneering the biomolecular investigation of archaeological dental calculus (tartar) to study long-term trends in human health and diet. She is a 2012 TED Fellow, and her work has been featured in Wired UK, the Observer, CNN.com, Der Freitag, and Sveriges TV. She obtained her Ph.D. from Harvard University in 2010, specializing in ancient DNA analysis and paleodietary reconstruction.
Wenchypoo said...
"why are doctors pushing the Mediterranean diet as a "gold standard" for the way we should eat--it's loaded with olive oil, avocados, fish, etc. All are Omega-3's, which are SATURATED!"
Omega-3 are not saturated. They are PUFA.
Hey Stephan,
Good post as always. Just curious if you still feel the evidence points to SAFA having no impact on insulin sensitivity?
Have you seen this: http://www.nrjournal.com/article/S0271-5317(14)00120-1/abstract
Just curious on your thoughts. Thanks!
saturated fats are healthy
A Fat Vegan said...
"Have you ever considered that all fats are a problem - so that it is not about whether it is saturated or not? I am about to try to RAVE Diet which is a very low fat diet with no animal protein at all. It's a diet that has been shown to reverse cancer which is my main concern at the moment. "
-----------
See the paper following paper. It's available online for free and has useful references. It discusses the issue of the modern Western diet being relatively high in dietary fat (30% or more) compared to the relatively low levels (10 to 15%) in third world countries such as rural Asia and Africa.and how it relates to the very low cancer risk and high insulin sensitivity seen in those rural populations.
"Insulin and IGF-I as determinants of low ‘Western’ cancer rates in the rural third world" by Mark F McCarty, Int. J. Epidemiol. (2004) 33 (4): 908-910. doi: 10.1093/ije/dyh265 July 15, 2004
Excerpt from the paper:
"...total fat and total protein intakes do not emerge as important determinants of cancer risk in many Western case-control studies. However, this may simply reflect that fact that Third World intakes of fat and high quality protein are usually far lower than the range encountered among free-living Western subjects; rather stringent restriction of fat (especially saturated fat) and protein may be required to achieve substantial down-regulation of insulin and free IGF-I levels."
This recent research finding is interesting as it indicates that there's a role for inflammation:
"Chronic tissue inflammation is typically associated with obesity and metabolic disease, but new research now finds that a level of “healthy” inflammation is necessary to prevent metabolic diseases, such as fatty liver. This finding may explain in part why anti-inflammatory medicines have so far not been successful as anti-diabetic treatments. The effects of interventions that promote local low-level inflammation in fat tissue remain to be determined," researchers said." - Science Daily, June 28, 2016.
Read more here: https://www.sciencedaily.com/releases/2016/06/160628072037.htm
Cjuan
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