Saturated Fat vs. Unsaturated Fat Questions
Hey there!
I had a few quick questionsregarding saturated fat:
In the book, Dr. Rosedale suggests that we limit saturated fat because its 'harder to digest'.
1.) My first question is, what if I am already 'fat adapted' from following an Atkins/Ketogenic diet for 3 months prior? Is it necessary to avoid saturated fats if my goal is to lose body fat?
2.) Dr. Rosedale also mentions that you should limit saturated fats ESPECIALLY if you're trying to lose weight. Could you clarify the reasoning behind this for me? Why would eating saturated fats slow down weight loss?
3.) During a quick search of the support forum, I came across a tid-bit written by Dr. Rosedale that states:
"The important distinction between good and bad fats lies not in whether they’re saturated or unsaturated, but whether they are omega-3 or omega-6. Omega 3 fatty acids, such as those found in fish and flax oils are tremendously healthy and will provide you a great deal of benefit. Omega 6’s such as are found in peanut, soybean and sunflower oils (among others) are almost the opposite. You do need a small amount, but you will get them naturally. The more you willfully eliminate, the better you will be."
In both the book and Dr. Rosedale's website he repeatedly mentions that avocados are an excellent source of dietary fat, however avocados are NIGHTMARISHLY high in omega-6 fatty acids. In fact, a typical fresh avocado has an omega-3 to omega-6 ratio of 1:15.2.
To get a idea of just how 'bad' an avocado's omega-6/omega-3 ratio of 15.2:1 ratio is, consider that partially hydrogenated, industrial soy bean oil has an omega-3/omega-6 ratio of about 1:15.5 - not a big difference you see?
So, in terms of reducing/avoiding systemic inflammation from a dietary imbalance of omega-3 to omega-6 fatty acids, why does the Rosedale Diet emphasize primarily unsaturated fatty acids (like those found in avocados or olive oil) over saturated fatty acids (like those found in butter and red meat), when SATURATED fats typically are much more balanced (omega-3 to omega-6 ratio) than UNSATURATED fatty acids?
4.) Do you have any information regarding DIETARY (not blood concentration) levels of saturated fatty acids and the effect on leptin? I am very curious of what the leptin differences would be in someone who eats primarily saturated fat vs. someone who eats primarily unsaturated fats. I have looked, but all I have come up with is the effect of having high BLOOD concentrations of saturated fatty acids and their effect on leptin, not DIETARY saturated fatty acids and their effect on leptin.
So yeah, those are my questions. I'm sorry if its a lot, I am just throughly confused :( Coming from a Paleo, omega-3 to omega-6-balancing, low-carb perspective, I'm finding Dr. Rosedale's polyunsaturated fat recommendations a bit confusing.
Please help :)
Again, thanks for your help! Loved the book!
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1 Posted by Catherine on 17 May, 2013 02:23 AM
Maahh ha! I found a study! But unfortunately, it has left me with more questions than answers and it was performed using mice so you have to take the findings with a grain of salt :/
You can see the study here: http://www.ncbi.nlm.nih.gov/pubmed/12006366
The objective of the study was to; investigate the effects of changing type and amount of dietary fats on energy balance, fat deposition, leptin, and leptin-related neural peptides: leptin receptor, neuropeptide Y (NPY), agouti-related peptide (AgRP), and proopiomelanocortin (POMC), in C57Bl/6J mice.
"One week of feeding with a highly saturated fat diet resulted in ~50 and 20% reduction in hypothalamic arcuate NPY and AgRP mRNA levels, respectively, compared with a low-fat or an n-3 or n-6 polyunsaturated high-fat (PUFA) diet without change in energy intake, fat mass, plasma leptin levels, and leptin receptor or POMC mRNA. Similar neuropeptide results were seen at 7 wk, but by then epididymal fat mass and plasma leptin levels were significantly elevated in the saturated fat group compared with low-fat controls."
So the level of NPY was SIGNIFICANTLY decreased in the mice fed a SATURATED high-fat diet, but not a high-fat POLYUNSATURATED diet and not surprising, not with the low-fat diet.
Decreasing levels of NPY = decreasing levels of hunger.
But then at week 7, "epididymal fat mass and plasma leptin levels were significantly elevated in the saturated fat group compared with low-fat controls."
Now someone help me decipher this; decreasing levels of NPY is a GOOD THING and is actually seen in people who practice intermittent fasting. Like I mentioned before, decreasing levels of NPY = decreasing levels of hunger, but what I'm hung up on is the fact that leptin levels INCREASED and if leptin resistance is the result of chronically elevated levels of leptin (much like insulin resistance is the product of chronically elevated levels of insulin) then this increase in leptin seen here is a BAD thing correct?
What are the implications of this? Does this imply that BOTH dietary carbohydrate and saturated fat contribute to leptin resistance?
Does this suggest that we should focus more on polyunsaturated fatty acids in our diets even though they are primary contributor to the chronic omega-3 to omega-6 imbalance seen in our population today? What about monounsaturated fatty acids? How do they relate to all this?
Blah, I'm so confused :/
2 Posted by Catherine on 17 May, 2013 02:29 AM
Here's another one: http://jcem.endojournals.org/content/87/11/5008.long
Abstract
The recently discovered hormone leptin is primarily secreted by adipose tissue and serves as an internal signal indicating the size of body fat stores. The aim of the present study was to investigate the impact of the dietary fatty acid composition on serum leptin concentrations. Therefore, serum leptin levels were measured by RIA in healthy nonobese men (n = 30) and women (n = 25). First, all participants received a baseline high-fat diet, rich in saturated fat, for 2 wk and were then randomly assigned to one of three high-fat dietary treatments, which contained refined olive oil (rich in monounsaturated fatty acids, n = 19), rapeseed oil [rich in monounsaturated fatty acids and α-linolenic acid (18:3n-3), n = 17], or sunflower oil (rich in n-6-polyunsaturated fatty acids, n = 19) as the principal source of fat for 4 wk. On the rapeseed oil diet, serum leptin concentrations increased slightly in men [+0.25 ng/ml, T(9) = −2.778, P = 0.021], but decreased distinctly in women [−4.70 ng/ml, T(6) = 5.083, P = 0.002]. Both the olive oil and the sunflower oil diet did not affect serum leptin concentrations. Thus, it is proposed that serum leptin levels were affected by the high amount of α-linolenic acid in rapeseed oil. However, questions remain as to why this diet differently affected serum leptin in men and women.
WHOA. Why would there be a difference seen in men vs. women?
3 Posted by Catherine on 17 May, 2013 02:44 AM
And here it is: http://www.ncbi.nlm.nih.gov/pubmed/9717726
Dietary fat type and energy restriction interactively influence plasma leptin concentration in rats.
Cha MC, Jones PJ.
Source
School of Dietetics and Human Nutrition, Macdonald Campus of McGill University, Ste Anne de Bellevue P.Q., Canada.
Abstract
To investigate whether dietary fat source and energy restriction interactively influence plasma leptin levels and its association of leptin with insulin action, rats were fed diets containing either fish, safflower oil, or beef tallow (20% wt/wt) for 10 weeks. Groups of rats consumed each diet ad libitum or at 85% or 70% of ad libitum energy intake in a design that held fat intake constant. Graded levels of energy restriction caused body weight to decrease (P < 0.001) differently according to the dietary fat provided. Plasma leptin concentrations were 60% higher (P < 0.05) in the groups fed fish oil and safflower oil ad libitum compared with those in the beef tallow group, despite smaller perirenal fat mass and fat cell size in the fish oil-fed animals. Energy restriction resulted in a 62% decrease (P < 0.05) in leptin levels in fish oil- and safflower oil-fed rats, whereas no changes were observed in beef tallow-fed animals. Plasma insulin levels were lower (P < 0.05) in the fish oil group fed ad libitum compared with those in the two other diet groups. These data demonstrate a hyperleptinemic effect in animals consuming diets rich in polyunsaturated fatty acid, which can be normalized to the level of saturated fat consumption by mild energy restriction. Thus, dietary fatty acid composition, independent of adipose tissue mass, is an important determinant of circulating leptin level in diet-induced obesity.
Quote from the study posted previously;
"Cha and Jones (7) observed in rats that a diet rich in n-6- and n-3-polyunsaturated fatty acids (PUFA) led to higher serum leptin levels than a diet rich in both saturated fatty acids (SFA) and monounsaturated fatty acids (MUFA). In contrast, Reseland et al. (10) showed that a high intake of n-3-PUFA decreased leptin gene expression both in vitro using a human cell line and in vivo in rats. Our group recently observed that serum leptin levels decreased in hypertriglyceridemic patients after dietary SFA had been replaced by marine n-3-PUFA and MUFA (11). However, in this study, the diet also differed, in several other regards, from the habitual diets of these patients (for example it contained more vegetables and more complex carbohydrates). Also, this diet resulted in dramatic decreases in serum triglycerides and a small, but significant, drop in body weight; and thus, the changes in serum leptin levels could not be exclusively attributed to the changes in dietary fat quality. Thus, there is still a lack of knowledge, with regard to the impact of dietary fatty acid composition on serum leptin levels, particularly in humans."
..."The present study showed that a diet rich in MUFA and α-linolenic acid, compared with a SFA-rich diet, distinctly reduced serum leptin concentrations in women and slightly increased serum leptin levels in men. However, the latter effect was only small and supposedly of marginal clinical significance, particularly when the inconsistent nature of the changes in this group are taken into account. Nevertheless, these findings raise the interesting hypothesis that serum leptin concentrations in men and women respond differently to diet..."
4 Posted by martschuffing on 19 May, 2013 08:58 PM
Yeesh, is someone going to decipher what this all means in layman's terms? Your confused Catherine!!! My eyes fell out.
Support Staff 5 Posted by Dr. Rosedale on 29 May, 2013 09:24 PM
This, like the vast majority of so-called "high-fat" diet studies, is nothing of the sort. In this study, the "high-fat" diet was 38% of calories from fat and 48% of calories from carbohydrates, i.e. still a high carbohydrate diet and effectively making sure that fat was not the primary fuel being burned.
Support Staff 6 Posted by Dr. Rosedale on 29 May, 2013 09:24 PM
What I have mentioned is that saturated fats are harder to burn then unsaturated fats and this is true. This is especially true when one is not fat adapted. Therefore I limit saturated fats (certainly do not forbid them) for the first several months until one is used to burning fat after which it makes much less difference. Personally, I need lots of butter.
The same is somewhat true for polyunsaturated fats also. Certainly I have long cited the detriments of omega six fatty acids for 20 years and have said to limit their intake. However, the detrimental omega six fatty acids also becomes somewhat less of a concern if one is adapted to burning fat (and one does not eat glucose forming and insulin and leptin raising) carbohydrates, as one will more likely burn them before they become incorporated into membranes or has other harmful inflammatory producing effects. Virtually all of the research and information being perpetuated about the so-called omega 6/omega-3 ratio has been done in high carbohydrate eating individuals. Leptin plays a far greater role in inflammatory response than that ratio. Furthermore, the total amount of omega 6 oils is, to me, far more of a concern then the ratio. The total amount of omega 6 fatty acid in an equivalent amount of avocado compared to soybean is significantly less, and the amount of monounsaturated fats very much higher.
Also, I have long advocated using fish oil as a supplement to complement my diet that would lower any omega 6/omega-3 ratio.
I will be talking about many myths circulating around the Paleo (and natural health) community at the next AHS meeting in Atlanta. Perhaps I will include this topic also.
Thank you for the fine questions.
7 Posted by Catherine on 05 Jun, 2013 06:11 PM
Thank you Dr. Rosedale. Your response has really helped put some of my concerns to rest.
I did not consider the potential effects omega-3/omega-6 misbalances in fat-adapted persons and since researchers are still demonstating the inability to understand that it takes several weeks (if not months) for the body to become fully fat-adapted, I doubt there is any good research published (or being done for the matter) on excessive omega-6 intake in these individuals. I would be very interested in these findings.
8 Posted by taiairam on 12 Jan, 2014 02:59 AM
Hi
I, too, am interested in understanding the difference/problem with eating (excellent sourced) saturated fats such as grass-fed beef tallow, raw dairy butter and cream, pastured chicken fat etc.
So, how does one know when one's body has become "fat adapted"?
I am beginning the Rosedale Diet soon - not to lose weight as much as to decrease my insulin resistance. I am completely on board with eating low carbohydrates.
9 Posted by Gunnar on 12 Jan, 2014 01:56 PM
Thank you Dr Rosedale for your answer.
I have been interested to know if Omega-6 fats are so bad when the body is fully adapted to burning fat. I have guessed that it might not be so harmful and your answer has given me a crystal clear answer to that issue.
Your answer was very helpful.
//Gunnar