Fasting Insulin & Diet ~ Time for some Cognitive Dissonance?

Reader Josh brings this study to our attention:

High saturated fat and low starch and fibre are associated with hyperinsulinaemia in a non-diabetic population

Huh?  They compared dietary intake (24 hour recall) for 1069 non-diabetics (assessed by administering a glucose tolerance test) with fasting insulin levels.  

Subjects were seen for up to three visits from 1984 to 1992. A 24-h diet recall and fasting insulin concentrations were collected at all visits....

... High total and saturated fat intake were associated with higher fasting insulin concentrations after adjusting for age, sex, ethnicity, body mass index, waist circumference, total energy intake and physical activity. Dietary fibre and starch intake were inversely associated with fasting insulin concentrations....

... Associations were similar in men and women and for active and inactive subjects, though associations of fibre and starch intake with insulin concentrations were strongest in lean subjects. 

I'd like to see studies of this nature involve better assessment of dietary intake (weigh/measure/log vs. estimate/recall), but we can't have everything.  The description of the subjects is in the methods section,  the average followup for the study was just over four years.  All subjects had a baseline fasting insulin and dietary recall, the majority had three, and some had two or only one.  They eliminated those who were diabetic at any followup.  This analysis did not report trends over time.  The subjects averaged just over 50 y.o.a. and BMI around 25 at baseline, 47% males/53% female.

In any case, this study is really pretty simple -- look at what a bunch of people habitually eat, break down the diet composition by carbohydrate and fat type, and see how this impacts a biomarker for insulin resistance, that being fasting insulin concentration.  First, the dietary compositions of the subjects are at right.  Granted this was in the mid-to-late 80's, but this is when the obesity epidemic was taking off, right?  I'm always struck by looking at actual data, however flawed, rather than things like NHANES estimates, etc.  Considering these were roughly 50/50 male/female, the daily intake of 8024 kJ works out to just over 1900 cal/day.  And check out the carbs there.  Not the crazy 300-400 g/day we're told, although they were 53g into insidious weight gain terroir by Grokian standards.  In any case, although accompanied by roughly 100g non-starch (aka sugar) carbs, the starch intake here is right in line with PHD, at roughly 100g = 400 cal.  No indication of the nature of said starch.  I would also note that the O6:O3 ratio is ~ 9:1 -- not ideal, but far less than the 15-20:1 and such we're often told is going on.  While we're on the fats, look at that fat percentage:  38%!!  Here I thought we all went low fat....

So, I think the next graphic will -- or at least should -- cause a little bit of cognitive dissonance for the disciples of L.Ron Rosedale and assorted denominations of TWICHOOB's.

Adjusted percent change in fasting insulin concentrations for a given difference in nutrient intake (shown in parentheses under each column). Calculated from the regression model including sex, ethnicity, physical activity, age, body mass index, waist circumference, total energy intake and the nutrient.

Now, I'm sure we'll hear that this would all go away if people ate even more fat and that fat was eaten without the carbs, but one of the knocks against blogs like this one, and scientific research in this realm in general, is that these studies produce no actionable information or relevant information.  I would say otherwise in this case.  It appears that "on average", these subjects were eating the SAD:  47% carb / 15% protein / 38% fat.  It's important to look at those p-values along the bottom row.  Usually statistical significance begins with p<0.05 which is why the authors describe the correlations as follows {I added the p's}:

High saturated fat intake (p=0.02) and low starch (p=0.0007) and fibre (p=0.008) intake, in separate models, were significantly associated with higher fasting insulin concentrations after adjusting for age, gender, ethnicity, vigorous activity, BMI, waist circumference and total energy (Fig. 1). High total fat (p=0.07) and linolenic acid (p=0.07) intakes were marginally associated with higher fasting insulin concentrations.

Within this SAD-eating population, fasting insulin levels decreased with 10g increments in starch intake and 5g increments in fiber intake, and increased with 5g increments in saturated fat intake.  Now, it's important to interpret this properly, this doesn't say that if an individual increases their sat fat intake by 5g, or decreases their starch intake by 10g they'll see their fasting insulin rise, and vice-versa.  But it does show, at least in this population, that diets higher in starch and lower in sat fat resulted in lower fasting insulin levels.    The linolenic (omega 3) acid bar is a bit shocking, even with the marginal p=0.07.  Also the trend for MUFA and oleic acid in particular trended towards increasing fasting insulin.  Here's what they had to say about this:

MUFA:  ... to the extent that people reporting high saturated fat intakes also eat more monounsaturated fats, the apparent adverse association of monounsaturated fat with insulin concentrations may be due only to its association with saturated fat intake (Table 3). When saturated fat was held constant by adding it as a term in the regression model with oleic acid (the primary monounsaturated fatty acid in the diet and more strongly related to insulin concentrations in Figure 1 than total monounsaturated fat), the oleic acid effect was reduced by 73 % to near zero (p = 0.74).

Omega 3 PUFA:   The effect of linolenic acid was only reduced by 18 % (p = 0.15) after further adjustment for saturated fat intake. Animal studies have suggested that linolenic acid in the absence of linoleic acid [O6] may improve insulin sensitivity. However, a scatter plot of linoleic acid intake by linolenic acid intake revealed that there were no subjects with high linolenic acid intakes in the absence of linoleic acid intakes to allow us to test this hypothesis.

I've actually seen some studies that finger O3's with decreasing insulin sensitivity.  Interestingly while paleo diets are lowER in O6's, many are not so much so as they might think if they're eating a lot of nuts and avocado without eating a lot of oily fish or popping fish oils.  But there's lots showing the opposite. 

Anyway ... also from the discussion:

There was no apparent interaction between saturated fat and fibre (or starch) intake, suggesting that the positive association between saturated fat and fasting insulin concentrations was present at all levels of fibre intake (data not shown). 

Perhaps this is why, in SAD-styled dietary interventions we don't see fiber doing its thing.  Next up, sucrose:

It was also of interest to explore the apparent lack of effect of sucrose on insulin concentrations, since sucrose has been implicated in the development of insulin resistance. When both carbohydrate and energy were held constant in the model, high sucrose intake was significantly associated with higher insulin concentrations. This suggests that eating sucrose instead of other sources of carbohydrate may be detrimental to insulin sensitivity.

This is in agreement with what most studies seem to show because the 50% fructose content of sucrose does not elicit an insulin response.  Those fructose and glucose bars off on the right of the figure above are a bit misleading, p=0.74-0.75!  

To further determine if this was due to beneficial effects of starch or adverse effects of sucrose, terms for starch, sucrose, fructose and glucose were simultaneously included in the model predicting fasting insulin concentrations. In this model, starch remained significantly and inversely related to fasting insulin concentrations, and sucrose, glucose and fructose were not associated with fasting insulin.

Let's go back to the combined sugar intake of this population.  Combining 1/2 sucrose + fructose, they averaged around 40g fructose per day.  Now this was the 80's, but to flirt with the 100g/day dose so often used in studies to produce some degree of IR, you would be talking a doubling of this intake.  Not unlikely if one is guzzling sodas, but many MANY of those who've gotten hyperinsulinemic/IR through the path of obesity, sugar sweetened beverages are not part of the equation.  More importantly, the beneficial effect of starch consumption remains.

OK, lastly, how about these associations taking BMI into account?  The figure at right shows the fat and carb effects for different BMI's.  The black bars = all BMI, the center-slashed bar = BMI of 22, right-dotted bar = BMI of 28.  For total and sat fats, the differences are not significant, but they are for all carb, starch and fiber (the p-values are for comparison between BMI levels).  It seems that starch and fiber are insulin sensitizing (lowering fasting insulin levels) over the range of BMI's, that persists, if significantly less in the highest BMI group.   What we do not see, that is important to point out, is where starch consumption negatively impacted insulin in the high BMI group.  

The evidence mounts folks.  Indeed, I've yet to see evidence supporting the notion that postprandial carb-induced insulin has any negative bearing on insulin sensitivity and basal insulin production.  Wait, we did have the Grey & Kipnis metabolic ward study where fasting insulin levels plummeted with an essentially ZC diet and skyrocketed with an essentially ZF diet (high sugar) ... but even those levels seemed to be returning to baseline after 3-4 weeks following the abrupt and extreme changes.  

The  "carbs causes insulin/hyperinsulinemia causes insulin resistance" is not supported by the research, or in an analysis of "real people" in this case.  It's time for those who propagate this mistaken notion to revisit the science.