The adipogenic effect of omega-6 polyunsaturated fats

More beating up on vegetable oils to come.  But first, let’s tie off a couple of loose ends from the last post and throw some additional information into the mix.

Lucas made this comment regarding the statistical analysis of risk from the Ramsden meta-analysis of n6 PUFA and CHD risk;

“For non-fatal myocardial infarction (MI)+CHD death, the pooled risk reduction for mixed n-3/n-6 PUFA diets was 22 % (risk ratio (RR) 0.78; 95 % CI 0.65, 0.93) compared to an increased risk of 13 % for n-6 specific PUFA diets (RR 1.13; 95 % CI 0.84, 1.53).”

The RR is only 1.13, and the CI includes 1. This means that it’s equally probable that there were no differences between those eating more PUFAs and those who doesn’t.

“RCT that substituted n-6 PUFA for TFA and SFA without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance (RR 1.16; 95 % CI 0.95, 1.42).”

Same as above, the CI, in my opinion, is too close to 1 to make strong assumptions.

Lucas is absolutely right, from a statistical standpoint, the numbers are weak.  But there seems to be not a day goes by where there isn’t a headline published damning the likes of animal fats or meats for some equally weak link to chronic disease.  Have a look at Tom Naughton’s great post regarding the supposed link between processed meat and pancreatic cancer risk, taking note of the relative risks and confidence intervals.  If we are going to condemn the likes of bacon for having an association with increased pancreatic cancer risk (let’s just abbreviate that to “red meat causes cancer”), based on such numbers, then surely we need to be instilling the same fear of margarine based on equally weak numbers?  I don’t think it is good enough to build public health guidelines around weak association when it comes to things we “know” are bad for us, such as meat and animal fat, but dismiss links between the likes of n6 PUFA and heart disease because the numbers aren’t overly strong.

Yesterday, from Matt Metzgar’s blog, we have a link to this recent paper;

Why Has the BMI Gone Up So Drastically in the Last 35 Years?


We attempted to answer the following questions: Why has the body mass index (BMI) increased so dramatically in the last 35 years? Are some food groups or additives more responsible than others?


Data for per capita food production available for consumption after spoilage for different food groups and additives from the US Department of Agriculture were used as independent variables to predict BMI increases. The heights and weights were taken from the Centers for Disease Control and the US Census Bureau for the years 1970 to 2004.


The additives of fats and sugars in combination, not separately, best predicted increases in BMI accounting for 97% of the variance in the linear regression analyses. When all food groups were entered into regressions to predict increases in BMI, fats and sugars in combination accounted for 96% of the variance for women and 97% for men, with the other food groups adding very little. Path analyses showed that fat and sweeteners had direct effects on BMI and were also the mediators of increased caloric consumption.


In line with the major physiological theories emphasizing palatability as the addictive stimulus in models of incentives and addiction, fats and sugars in combination rather than calories per se or particular food groups accounted for the increases in BMI. These empirically based theories and data suggest that one should focus on palatability and addictive models in dealing with the increasing problem of obesity in the United States.

The whole is greater than the sum of its parts… When we look at how food consumption has changed over the last 35 years, it doesn’t take much to figure out that we have increasingly shifted toward the consumption of ever increasing amounts of processed and fast-food.  A quick scan of the ingredients on the packet, box, or tin, and you will most likely see that you are consuming varying combinations of sugar and vegetable oil.  Go to the fast food joints and you are consuming your order of choice, fried in vegetable oil, and most likely washed down with a gallon of liquid sugar.

This brings me to the two papers I want to summarise for today’s post.  The first looks at the adipogenic (body fat-inducing) nature of omega-6 polyunsaturated fatty acids and ties in nicely with the paper mentioned above.

The effect of dietary fat on human health is not solely a matter of quantity but depends also on the nature of the fatty acids. The current recommendation is to replace saturated fat by polyunsaturated fatty acids (PUFAs). Today, more than 85% of the total dietary PUFA intake in Western diets is n-6 PUFAs, mainly linoleic acid, a precursor of arachidonic acid, whereas the consumption of n-3 PUFAs has declined. Since the high intake of n-6 has been associated with childhood obesity, concerns regarding this matter have been raised.

There are two ways in which your fat mass can increase.  First up, we have hypertrophy, where your existing fat cells (adipocytes) store more fat within themselves.  Then we have hyperplasia, where your body makes new fat cells in order to give you more storage capacity.  Dietary components that are able to induce an increase in adipocyte cell numbers are known as adipogenic.  This paper seeks to reconcile whether omega-6 PUFA’s are pro-adipogenic, inducing immature pre-adipocyte cells to become fully functioning fat cells.  As I can hopefully show, context matters…

CAUTION: Animal Study Ahead

In vivo, the obesigenic action of n-6 PUFAs is determined by the balance between dietary carbohydrates and protein. A high carbohydrate/protein ratio translated into a high plasma insulin/glucagon ratio, and in this setting, dietary n-6 PUFAs promoted strongly adipose tissue expansion.

That is pretty much our money-shot there folks.  Whether or not dietary n-6 PUFA’s increase your fat cell numbers is contingent on the balance between your carbohydrate and protein intake.  A high-carbohydrate diet promotes high insulin levels (relative to its opposite hormone, glucagon), which in turn promotes the expansion of your fat mass.

Conversely, a high protein/carbohydrate ratio translated into a high plasma glucagon/insulin ratio and enhanced cAMP-dependent signaling. In this setting, COX-mediated prostaglandin synthesis was enhanced, and dietary n-6 PUFAs decreased white adipose tissue mass. The decreased obesigenic action of n-6 PUFAs in mice fed a protein-rich diet did not result from increased dissipation of energy by uncoupled respiration but rather reflected increased energy expenditure in relation to gluconeogenesis and urea formation.

Here we effectively have the opposite effect occurring.  Under the influence of a high protein to carbohydrate diet, say one that is along similar lines to most iterations of the paleo/primal diet, n-6 PUFA actually leads to a decreased fat mass, partly by way of the increased energy expenditure required to convert protein (amino acids) to carbohydrate (glucose).

Let’s put a bit more context around these two statements.  In the context of a typical Westernised eating pattern, one that is higher in carbohydrate and lower in protein, the predominant n6-PUFA that is likely to be consumed is the rather large quantities of vegetable oil-derived linoleic acid.  In the context of a higher protein, lower carbohydrate paleo-templated diet, I would venture to suggest that the predominant n6-PUFA consumed would be the animal-fat derived arachidonic acid.  This effectively gives us the scenario of “eat more vegetable fats on top of your high-carbohydrate (sugar) diet = gain fat” or “eat more animal fat on top of your high-protein (low-sugar) diet = lose fat”.

Which of those two scenarios is the dominant player in our modern world?

The following is a good summary of the relevant findings for those who don’t want to wade through the details of the full paper;

The Effect of Corn Oil on Body Weight and Adipose Tissue Mass Is Regulated by the Balance between Carbohydrate and Protein in the Feed

As for in vitro studies, fundamentally opposite effects of n-6 fatty acids on adipose tissue development in vivo have been reported. Some studies have demonstrated that a diet enriched in n-6 PUFAs decreases adipose tissue growth, whereas other studies have associated dietary n-6 PUFAs with an increased propensity to obesity. Since the adipogenic potential of n-6 PUFAs is dependent on the cAMP status in vitro, we hypothesize that the hormonal status, such as the glucagon/insulin ratio in particular, might be of importance in regulating the effect of n-6 PUFAs on adipose tissues also in vivo. Since the glucagon/insulin ratio is altered in response to intake of carbohydrates versus protein, we predicted that the adipogenic effect of n-6 PUFAs might be determined by the ratio between carbohydrates and protein in the feed.

To test this hypothesis, obesity-prone C57BL/6J mice were fed an energy-dense high fat diet enriched in n-6 fatty acids (corn oil), supplemented with either protein or sucrose for 53 days. The C57BL/6J mice were chosen in order to limit adaptive thermogenesis that occurs in most mice strains when fed an energy-dense diet. Corn oil was chosen as an n-6 fatty acid source, since this oil is enriched in linoleic acid, the predominant PUFA in Western diets. Analysis of the diet confirmed that more than 50% of the fatty acids in the diets were linoleic acid. The diet did not contain arachidonic acid, but analysis of the fatty acid composition of red blood cells confirmed conversion of the dietary n-6 PUFAs to arachidonic acid. The corn oil-enriched diets were isocaloric and contained a total of 24.3 ± 0.3 and 24.9 ± 0.1 weight % fat, respectively. It should be noted that the sucrose-enriched diet contained 20 weight % protein and hence was not protein-deficient.

Mice fed the sucrose-supplemented corn oil diet ad libitum gained considerably more weight than mice fed the high protein-supplemented corn oil diet. The higher total body weight gain in mice fed corn oil in combination with sucrose was to a large extent due to an increase in white adipose tissue mass.

To evaluate whether the different effect of the diets could be explained by altered energy expenditure and/or voluntary activity of the animals, the mice were individually housed in metabolic cages. No difference in oxygen consumption was found between the two groups, butthe respiratory exchange rate was lower in mice fed corn oil in combination with protein than with sucrose, indicating that relatively more fat and possibly protein were used as substrates for oxidation. However, no increase in expression of key enzymes involved in fatty acid oxidation in muscle or liver was observed. In fact, a lower heat production, indicating lower total energy expenditure, was observed in mice fed the protein-supplemented diet. This was not an effect of reduced animal activity but could partly be explained by the observed lower food intake.

A high protein intake is known to increase satiety and thereby to reduce energy intake. Thus, in order to exclude the possibility that reduced adipose tissue mass in mice fed corn oil and protein ad libitum was simply due to reduced caloric intake, a third set of mice was pair-fed the same diets for 56 days. The mice fed corn oil in combination with sucrose gained an average of 11.3 g of body weight and became visibly obese.The mice fed corn oil in combination with protein gained on average less than 1.8 g of body weight during the 56 days of feeding and had small amounts of white adipose tissue. In fact, the weight gain and amount of body fat in mice fed a high corn oil diet supplemented with protein was comparable with the body weight gain and adipose tissue mass in mice fed an energy-restricted low-fat chow diet.

So, the mice on the high-corn oil/high-sugar diet were not protein deficient.  In fact, at 20% protein, they were probably consuming more protein than most New Zealanders (The 2008/09 NZ Adult Nutrition Survey found we are averaging just 16.5% energy from protein).  This was also an ad libitum feeding study, meaning the mice get to eat when and where they like, similar to free-living humans.  Whilst the fat+sugar mice became noticeably obese, the fat+protein mice gained relatively little body fat and tended to metabolise more fat and protein for energy.  They also tended to be more satisfied by less food than those eating the fat+sugar and had comparable body compositions to the mice fed Jenny Craig their energy-restricted, low-fat chow diet.

The authors make the following statement that seems to make a mockery of the calories-in, calories-out meme that is typically floated by conventional wisdom… you know the one – “as long as you balance your calories in and out, then what you eat doesn’t really matter…”

Our in vitro results and feeding experiments suggest that the adipogenic potential of n-6 PUFAs can be determined by the hormonal status of the animals.

So it becomes less a case of the number of calories consumed when it comes to body fat, and more a case of what hormonal response will be triggered by the foods that those calories are sourced from… quality trumps quantity.  This is highlighted further by the following comment from the authors;

We observed a remarkable difference in feed efficiency between mice fed the protein-enriched versus the carbohydrate-enriched diet. In the high protein group, 467.8 kcal were needed to produce a weight gain of 1 g, whereas the high carbohydrate group only needed 67.8 kcal to produce the same weight gain, which almost exclusively represented an increase in adipose tissues.

The mice eating the high-protein diet were able to consume 400 more calories than those in the high-carbohydrate group before gaining an additional gram of weight.  Might this phenomenon explain the observation that those eating a paleo-type diet can appear to be over-eating by conventional standards yet still remain relatively lean?

The authors conclude their discussion with a nice summary paragraph…

Today’s diets are abundant in n-6 fatty acids from vegetable oils (corn, sunflower, safflower, and soybeans) that are used in industrially prepared food. In addition, industrially produced animal feed is also rich in grains containing n-6 PUFAs, leading to meat enriched in n-6 PUFAs at the expense of n-3 fatty acids.

n-6 PUFAs, predominantly linoleic acid, are now the predominant source of PUFAs in Western diets. PUFAs have been considered less harmful to human health than saturated fat, and substitution of saturated fat with PUFAs in general has been recommended by dieticians. If the background diet determines the adipogenic potential of n-6 PUFAs also in humans, this is of great concern, since the intake of refined sugars from sources such as soft drinks has increased dramatically during recent decades.

The findings from this study go some way to answering the question posed by the study Matt Metzgar pointed to – why has BMI [body fat] gone up so dramatically in 35 years?  As the authors of that paper point out, the combinations of high-fat with high-sugar seem to explain the vast majority of the rapid increase in obesity.

But are we seeing something deeper than this going on with the health of our populations?  Are we seeing enhancements in each subsequent generation to become obese when exposed to the same environment?  That is, will Generation-Z become fatter than Gen-Y, who are fatter than Gen-X, even though they all eat much the same stuff?

Another recent (rodent) study poses exactly that question…

A Western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations

The prevalence of obesity has steadily increased over the last few decades. During this time, populations of industrialized countries have been exposed to diets rich in fat with a high content of linoleic acid and a low content of α-linolenic acid compared with recommended intake. To assess the contribution of dietary fatty acids, male and female mice fed a high-fat diet (35% energy as fat, linoleic acid:α-linolenic acid ratio of 28) were mated randomly and maintained after breeding on the same diet for successive generations. Offspring showed, over four generations, a gradual enhancement in fat mass due to combined hyperplasia and hypertrophy with no change in food intake…

So the premise of this research becomes one of each generation becoming further programmed for obesity at lower thresholds than the previous generation.  If indeed this holds true for humans (instead of just mice), you can perhaps see the implications as each generation drifts further away from a diet based around real food and toward a diet that comes almost exclusively from a box, can, or wrapper.

The prevalence of obesity and the risk of developing associated diseases have steadily increased across generations over the last few decades. In addition, these events now emerge earlier in life. This epidemic is not attributable to genetic factors as it has occurred relatively recently and is observed in a wide range of human populations. High-fat diets are considered to be obesogenic in that they produce a consistent increase in fat mass that is directly related to the content of the diet and duration of feeding. However, the contribution of dietary fats compared with an excess energy intake in increasing body weight remains controversial, as no major change in the total amount of ingested fats has occurred in the last two decades.

In addition to caloric excess, a qualitative issue has emerged as a risk factor for obesity in rodents and possibly in humans; i.e., the disequilibrium in polyunsaturated fatty acid (PUFA) metabolism with a high ratio of linoleic acid (C18:2 ω6, LA) versus α-linolenic acid (C18:3 ω3, LNA).

Again, we have another research group here casting doubt on the energy balance hypothesis of our obesity, pointing out that despite rapid increases in obesity rates (which have been systematically blamed on the calorie density of high-fat foods), the total amount of fat consumed by the population hasn’t really changed.  These researchers, like the others already linked in this post, seem to suggest we are dealing with an issue of fat quality and that vegetable oil sources of n-6 PUFA detract from the overall quality of fat in our diet.  This group goes one step further by suggesting that exposure to such low quality fat sources could be leading to the transgenerational enhancements in fat mass we are witnessing in such a compressed time period.

…by analogy to humans, where consumers have been continuously exposed—from in utero to old age—to dietary fats with a high LA content and a low [omega-3] content and in which the prevalence of overweight and obesity has increased within a few generations, we decided to set up a nutritional model mimicking a human situation.

For this purpose, male and female mice were chronically exposed over four generations to a single Western-like fat diet; i.e., 35% energy as fat with a LA/LNA ratio similar to that found in the most consumed foods. The results show that this condition was sufficient to trigger gradual transgenerational enhancement of the fat mass observed at early and adult ages. In addition to changes in insulin and adipokine circulating levels and to changes in cellularity of adipose tissue, gene expression profiling over generations was used to highlight the major molecular events favoring adipose tissue hyperplasia and metabolic imprinting that lead to an obese phenotype.

So what exactly did these researchers do?

A colony of pure inbred C57BL6/J mice was established by mating four males and four females from the same litter that was fed a chow diet. At weaning, pups were either maintained on a chow diet (STD mice) or fed a high-fat diet (ω6HFD) (HF mice).

…male and female mice were first fed ω6HFD at weaning and later mated to generate HF0 mice, whereas HF0–HF4 male and female mice were fed ω6HFD. In this way, HF0–HF4 mice were continuously exposed over generations to the isocaloric, isolipidic diet.

Think of it this way… A community of Baby Boomer-generation humans, who had previously had no exposure to vegetable oils (either pre- or post-natal) , began consuming these fats and oils early in their childhood life.  Eventually they grow up and have kids of their own (Generation X).  These Gen X kids have been exposed to these evolutionary novel levels of omega-6 PUFA’s since conception.  The Gen X’s have kids – Gen Y – as do the Gen Y’s – the Gen Z’s.  So within this community we have multiple generations exposed to essentially the same diet, with the same level of total calories and the same types of fat.

Highlights from the results…

Body weight and fat mass across generations

…four male and four female C57BL/6J mice from the same litter were mated randomly. At weaning, their pups were fed an LA-enriched diet [termed ω6 high-fat diet (ω6HFD)], which contained 35% energy as fat…

From weaning up to 8 weeks old, body weight was not affected by the diet. However, when the adult male and female HF0 mice on the ω6HFD were mated randomly and produced HF1 pups, the body weight of the male mice at weaning became significantly higher than that of the HF0 mice; this weight difference persisted at the adult age. Suckling HF1 pups from both sexes were fed the ω6HFD at weaning and then mated as above. The difference in body weight both at weaning and at 8 weeks was further increased in HF2 male pups and adults compared with HF1 mice, although no significant weight difference persisted between HF1 and HF2 mice at the adult age.

Let’s use our human generation-game analogy again… Compared to how much the Baby Boomer kids weighed at say, 2 years of age, the Gen X kids were a little bit heavier at the same age.  Then the Gen Y kids were heavier still.  And finally, the Gen Z kids were slightly increased in weight even more.  As they all tracked through to their adult years, they remained heavy but without much difference between the generations.

Lipid profile across generations

PUFA metabolism in the mothers’ milk lipids was altered in response to the linoleic acid-enriched diet but then remained similar across generations. The ω6HFD altered the PUFA composition of milk lipids of HF0 dams. It strongly increased the content of LA…

In contrast, it decreased significantly the content of long-chain polyunsaturated fatty acids (LC-PUFA) of the [omega-3] series, i.e., eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)…

All these observations are in agreement with human studies showing that an increase in LA intake leads to stimulation of [arachidonic acid] and/or inhibition of EPA and DHA synthesis.

Taken together, these results show that the PUFA profile was altered by the diet fat content and that a steady state was then observed across generations.

In other words, the high dietary intake of omega-6 fats was transferred through to the breast milk and the nursing children, with a concurrent decrease in omega-3 content of the breast milk.

The adipose phenotype can be partially reversed at later generations

To assess whether further transgenerational effects of the ω6HFD could be reversed, HF4 mice were switched at weaning to the chow diet.

…adult male and female revHF4 mice were subsequently mated randomly to give birth to the 5th generation of pups. When the litters were fed at weaning either the chow diet (std5 mice) or the ω6HFD, not only were std5 mice heavier at weaning than STD mice, but a large difference in the rate of weight gain could be observed in hf5 mice compared with std5, as early as the first week after weaning and maintained thereafter.

The incomplete reversal of the adipose phenotype at later generations suggested that some transgenerational memory had been acquired, allowing revHF4 mice to respond more rapidly than STD mice to the ω6HFD.

So let’s say we took some of our Gen Z people and put them back on a normal low omega-6 diet early in their life – we’ll call these people reverse-Gen Z, or revGen-Z.  When these revGen-Z people have children of their own, even if these children are fed a normal diet, they still gain weight more rapidly and are heavier than their Baby Boomer relatives were at a similar age.  They are predisposed to gaining fat at a higher rate even though their dietary conditions have improved.

Metabolic changes in plasma across generations

Compared with mice fed a chow diet, those fed the ω6HFD for 19 weeks after weaning exhibited an increase in the plasma level of most parameters traditionally associated with the metabolic syndrome in the first, second, and third generations…

Surprisingly, this inflammatory signature was almost reversed at the fourth generation… leptin levels became dramatically reduced compared with those observed in HF3 mice and became similar to those of STD mice.

Fasting insulin levels followed a pattern similar to that of cytokines but remained significantly higher than those of HF0 mice. These observations indicate that, despite the fact that glycemia in HF4 mice appeared normal at 22 weeks old, continuous exposure to the ω6HFD led to a sustained increase in plasma insulin levels, which strongly suggests the emergence of insulin resistance of adult animals at later generations.

So whilst blood sugar levels appeared normal across the generations, the continuous exposure to high levels of omega-6 fats increased insulin levels suggesting that each subsequent generation was a little bit more insulin resistant than the previous.

Cellularity and cell subpopulations of adipose tissue across generations

Exposing pups at weaning to the ω6HFD led within seven weeks to changes in adipose tissue cellularity. HF0 mice exhibited an increase in the percentage of very small adipocytes (∼20 μm) and a slight increase in that of large adipocytes (40–70 μm).

However, in HF3 mice, a substantial change in cell hypertrophy occurred, with a shift to large-sized adipocytes (50–70 μm) and the emergence of a population of severely hypertrophied adipocytes (80–100 μm). Cell hypertrophy became dramatic for HF4 mice, in which two additional populations of large-size adipocytes, 50–70 and 70–130 μm, could be observed. A fairly large proportion of small adipocytes (20–40 μm) remained detectable in HF4 compared with HF0 mice, suggesting that adipocyte recruitment was still taking place at the fourth generation.

Exposure to the high omega-6 diet over the generations saw increases in both size and number of fat cells contained within each generation.  And being fat cells, guess what they are going to want to do??  Bingo – store fat.

From the discussion…

We and others have pointed out the detrimental effects in humans caused by a dramatic change in the fatty acid composition of dietary fats at a time when the quantitative changes in fat consumption were not observed. Notably, at a time where overweightness and obesity have steadily increased over generations in most industrialized countries, consumption of LA…has increased…

…Our results show that, in a situation of genome stability that is reminiscent of augmentation in the prevalence of obesity observed worldwide, a gradual transgenerational increase in adiposity can occur in mice fed a Western-like fat diet…

…Noteworthy, enhanced adiposity occurs over generations through hyperplasia and hypertrophy despite no significant change in food intake in pups and adult mice…

…Despite fat tissue expansion across generations, leptin levels returned to normal. This suggests that hypothalamic leptin sensitivity had somehow been redefined through transgenerational exposure to the ω6HFD. Moreover, the decreased levels of inflammatory adipokines could be regarded as adaptive evolution of the autonomic nervous system output…

The most persistent dysregulation was that of insulin. In the absence of hyperglycemia, this strongly suggests insulin resistance, which is consistent with a progressive loss in sympathetic inhibition of insulin release over generations

Let’s pull this back to the start and wrap it up.  High omega-6 foods are promoted as “heart healthy” on the basis of their effect on cholesterol levels and we are encouraged to reduce our saturated fat intake in favour of these polyunsaturated fats to lower our cardiovascular disease risk.  However, there is enough evidence floating around (and it has been floating around for decades), to cast doubt on this premise.

If the evidence I have presented here is indeed applicable to humans – and we have to be cautious on that front – then it would appear that a food environment rich in omega-6 PUFA, in combination with evolutionary-novel levels of sugar, and sustained over multiple generations, is making it increasingly difficult for individuals to maintain their health and lowering the threshold at which disease can occur.  It may well also be making it very difficult for these people to lose weight based on the many and varied versions of low-fat, low-protein, high-carbohydrate diets which, even if energy-restricted, still emphasize vegetable sources of n-6 PUFA where fats are recommended.

Small amounts of omega-6 PUFA’s derived from meat and nuts may be healthful in the context of a high-protein, low-carbohydrate diet (such as a paleo diet), but otherwise need to be limited.  And depending on where you sit in the generation game, you may have less scope to tolerate combinations of these fats and sugars around the fringe of even a healthy paleo diet.  For those who pad their diets out with large amounts of fruits and nuts (fructose + linoleic acid) in the belief that these foods are paleo, but are struggling to lean out, and who also come from a family with several generations of obesity running through it, you may find that you have to trial restricting this combination and focus on increasing the likes of protein, medium-chain fats, and safe starches, etc.

Let’s leave fat and cholesterol alone for the time being and move on to other things… like getting fit, fast, and strong.

9 thoughts on “The adipogenic effect of omega-6 polyunsaturated fats

  1. mem

    I was writing to someone the other night that I feel your blog is likely under appreciated. This is such an excellent post. Thank you from the many of us who have found experientially, through our bodies, over many years, that what you write is true, Personally, as a 130lb woman maintaining a 106lb weight loss, with 90 of that maintained since 02, I have little to no use for CICO. It is a factor, like many factors, but is nowhere near the “inviolable diety” it is held up to be. Again, thank you for this!

  2. Nigel Kinbrum

    Hi. New reader here (thanks Emily!).
    To me, adipogenicity means a shift in fuel partitioning away from muscle mass towards fat mass which results in a worsening of body composition i.e. a shift towards skinny-fatness.
    I don’t believe that adipogenicity directly affects body weight. To gain weight, energy in has to exceed energy expended. Indirectly, adipogenicity can produce weight gain if it results in increased appetite and/or reduced energy expenditure.
    Cheers, Nige.

  3. bopes

    Fascinating, thanks.

    But are you not concerned that your post may cause food rewardists’ heads to explode? Perhaps a disclaimer is in order.

  4. DoctorSH

    Excellent post.

    Puts together the differences in types of fat and why “fatty” diets have different results in different people.


  5. O Primitivo

    You just have to love the official guidelines, food pyramids and mainstream nutritionists. The’yre really usefull, because if you just do the opposite they’re saying, you should the on the right path!

  6. Pingback: Perfect Health Diet » Around the Web; Why I Blog Edition

  7. george henderson

    Thanks for that. I always suspected it.
    I have another theory as to why PUFAs are fattening; if used for fuel they compete with MUFA for saturase enzymes. You do get a build up of MUFA, relative to SFA, in fatty livers, and this is exacerbated by extra n=6 EFA; not sure about other scenarios, but as half the body’s fat, pretty much, is stored as MUFA, it might be worth looking at.

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