Insulin Resistance; Dietary Interventions - Higher Carbohydrate, Lower Fat Diets More Optimal

[ShirtTieFitness]

As Peat has routinely emphasized, the macro-nutrient composition of the diet makes a profound impact on the state of the organism. Moreover, Peat goes further to advocate select foods that favor certain compositions; restricting select amino acids like Methionine (abundant in red meat) being one of them. As such, the importance of diet on Insulin and or subsequent Resistance must gain attention.

The following studies (from a multitude on PubMed) provide weight to Peats notion that High-Carb diets do not negatively impact insulin sensitivity, and are more likely preferable. Going further, insulin sensitivity can be improved when select carbohydrates are consumed, whilst high-fat diets impact insulin sensitivity negatively.

It follows that low-glycemic carbohydrates, including fruits and (fibrous starches), are expressed throughout several studies as the basis of the diet.


The role of carbohydrates in insulin resistance, 2001
The role of carbohydrates in insulin resistance. - PubMed - NCBI

Insulin resistance is a metabolic disorder that is increasing worldwide and is associated with some of the most common diseases affecting modern societies including diabetes, hypertension, obesity and coronary heart disease. Although pharmacologic approaches to managing insulin resistance are being advocated by some, public health approaches involving changes in diet and physical activity are attractive because of their lower cost and risk. We briefly summarize some new information on the mechanisms that mediate insulin's many biological actions and examine the effects of dietary carbohydrates on insulin sensitivity. Specifically, we summarize some of the information available on the effects of simple sugars, complex carbohydrates including fiber, slowly digested starch and the general concept of glycemic index. The available data support the idea that consumption of diets high in total carbohydrate does not adversely affect insulin sensitivity compared with high fat diets.

Insulin resistance, low-fat diets, and low-carbohydrate diets: time to test new menus.
Insulin resistance, low-fat diets, and low-carbohydrate diets: time to test new menus. - PubMed - NCBI

PURPOSE OF REVIEW:
Insulin resistance increases the risk of cardiovascular disease and diabetes, and the risk of cardiovascular disease increases further once diabetes has developed. As insulin resistance is a precursor to diabetes, it is critically important to identify cost-effective means, such as dietary changes, by which to reduce insulin resistance. The purpose of this review is to evaluate recent findings concerning dietary composition and insulin resistance, with particular focus on low-fat diets compared with the currently popular low-carbohydrate diets.

RECENT FINDINGS:
Recent findings indicate little support for the value of low-carbohydrate diets as therapies for insulin resistance. In contrast, the limited data available suggest that the higher fat content of typical low-carbohydrate diets may exacerbate insulin resistance in the long term. Preliminary data indicate that proteins from different sources may have differing effects on insulin resistance. Preliminary data also suggest the potential value of whole grains, fruits and vegetables in therapeutic diets to reduce insulin resistance.

SUMMARY:
Current evidence supports the inclusion of whole grains, fruits and vegetables, and lean sources of animal proteins including low-fat dairy products in dietary therapies for insulin resistance. Those who wish to follow a low-carbohydrate diet should be encouraged to follow a new menu low in fat, and with most of the protein derived from plant sources.

A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain
A high-fat, ketogenic diet causes hepatic insulin resistance in mice, despite increasing energy expenditure and preventing weight gain

In conclusion, the present study shows that a high-fat KD causes hepatic insulin resistance in mice, which can be attributed to an increase in hepatic DAG content, leading to PKCε activation and subsequent impaired insulin signaling. Moreover, this study found that a KD increases energy expenditure, which results in weight loss. Given the widespread use of KD in the treatment of obesity and the role of NAFLD and hepatic insulin resistance in promoting type 2 diabetes, these results may have important clinical implications, as obese patients on such diets could lose weight but develop NAFLD and hepatic insulin resistance.


Consumption of a High-Fat Diet Induces Central Insulin Resistance Independent of Adiposity
Consumption of a High-Fat Diet Induces Central Insulin Resistance Independent of Adiposity

These studies also assessed whether a short period of prior access to a HF diet is sufficient for central insulin resistance to develop; importantly, 72-hrs consumption of a HF diet was found to be sufficient to reduce central insulin sensitivity, independent of statistically significant changes in body weight or body adiposity

Previous studies have demonstrated that a reduction of dietary fat is able to improve peripheral insulin sensitivity in humans (59, 60). In rats, reducing dietary fat from 40% to 30% of total energy rapidly restored peripheral insulin sensitivity (34). Hence, the present findings are consistent with the more general hypothesis that dietary fat induces both central and peripheral insulin resistance, and that this is independent of body adiposity.


Effects of an ad libitum, high carbohydrate diet and aerobic exercise training on insulin action and muscle metabolism in older men and women.

Effects of an ad libitum, high carbohydrate diet and aerobic exercise training on insulin action and muscle metabolism in older men and women. - PubMed - NCBI

BACKGROUND:
Previous studies have demonstrated that aerobic exercise training and weight loss have independent effects on insulin-stimulated glucose disposal (ISGD). We hypothesized that ad libitum consumption of a high-carbohydrate diet would result in weight loss and improved ISGD, and that aerobic exercise training would facilitate greater improvements in ISGD compared with diet alone.

METHODS:
Older participants (13 women, 9 men; age = 66 +/- 1 year) with impaired glucose tolerance were randomly assigned to an ad libitum diet alone (18% fat, 19% protein, 63% carbohydrate) or this diet plus aerobic exercise training (4 d/wk, 45 min/d, 80% VO(2peak)) for 12 weeks. ISGD, abdominal fat distribution, muscle glycogen, and glycogen synthase activity were assessed pre- and postintervention.

RESULTS:
Consumption of the diet resulted in significant weight loss and an improvement in ISGD. Consumption of the diet plus exercise training also resulted in weight loss and increased ISGD, but results were not significantly different from those in the diet-alone group. Mean abdominal visceral and subcutaneous adipose tissue cross-sectional areas were smaller postintervention compared to baseline with no difference between groups. Exercise training and consumption of the diet increased muscle glycogen content (344.7 +/- 21.3 to 616.7 +/- 34.4 micromol.g(-1)) and decreased glycogen synthase activity (0.21 +/- 0.02 to 0.13 +/- 0.01) compared to the diet alone.

CONCLUSIONS:
These results demonstrate that consumption of an ad libitum, high-carbohydrate diet alone or in combination with aerobic exercise training results in weight loss and improved insulin sensitivity. Furthermore, exercise combined with this diet appears to limit additional increases in insulin sensitivity due to muscle glycogen supercompensation with a concomitant adaptive response of glycogen synthase.


Meat Intake and Insulin Resistance in Women without Type 2 Diabetes

In conclusion, it appears that meat intake, particularly red and processed meats, is associated with higher levels of insulin resistance in middle-aged women without type 2 diabetes. Among the many potential confounders examined in this study, BMI and body fat percentage influenced the association significantly. Consequently, both a lower meat intake and lower levels of body fat appear important in reducing the likelihood of insulin resistance, especially in this sample. Consumption of very lean meats (VLM) does not seem to play a role in insulin resistance. To decrease the likelihood of insulin resistance, prudence in the amount and type of meat consumed may be helpful.

 

[Ella]

Given the widespread use of KD in the treatment of obesity and the role of NAFLD and hepatic insulin resistance in promoting type 2 diabetes, these results may have important clinical implications, as obese patients on such diets could lose weight but develop NAFLD and hepatic insulin resistance.

thank for posting all these studies. I needed a good reminder that it's the fat and not the carbs.

 

[Wagner83]

From the first one (this is worth a read for the sucrose/fructose/glucose battle):

"
Simple sugars
Simple sugars include the monosaccharides (glucose, fructose and galactose) and the dissaccharides (sucrose, maltose and lactose). Many animal studies have examined the relationship between insulin action and high intakes of fructose and sucrose (15). Studies in rats have generally demonstrated that high intake of sucrose (18–70% of energy) or fructose (15–60% of energy) produce a decline in insulin sensitivity in the liver and later in peripheral tissues (16). An exception to this finding is a study done in female rats that found no association between increased consumption of sucrose and insulin resistance (17). In general, these studies have demonstrated that the adverse affects of sucrose and fructose are a function of the dose used and duration of exposure such that if a lower dose is used, the duration of exposure must be longer to produce the effect. In addition, the effects of sucrose on insulin action appear to be less in older obese rats that already have a moderate degree of insulin resistance, and in rats that are already insulin resistant as a result of consumption of a high fat diet (18). Fructose appears to be avidly taken up and metabolized by the liver. This uptake and metabolism produce a metabolic state characterized by increased glucose uptake by the liver, which leads to a variety of cellular events, such as changes in the expression of the gluconeogenic enzymes that produce insulin resistance.

Studies in humans examining the ability of dietary sucrose to produce insulin resistance have not been nearly as convincing (3). Studies in both normal adults and adults with type 2 diabetes have fairly consistently shown no effect on insulin sensitivity of isoenergetic substitution of sucrose or fructose for starch. Many of these studies had relatively few subjects and were of short duration. Isolated studies have shown adverse effects of dietary sucrose, but these are the exception rather than the rule. Both fructose and sucrose are associated with lower glucose excursions after ingestion, and some recommendations have even advocated the use of fructose as a beneficial sweetener for individuals with type 2 diabetes. The most recent nutritional recommendations of the American Diabetes Association do not advocate or discourage the use of these sweeteners on the basis of available data. They do caution about the development of hypertriglyceridemia with high fructose diets. Epidemiologic studies have also failed to show a relationship between fructose or sucrose consumption and the development of type 2 diabetes.

How can the discrepant results in animals and humans be reconciled? The studies done in rats suggest that if a low dose of sucrose or fructose is used, prolonged exposure is necessary to produce insulin resistance. In addition, the animal studies suggest that if adult animals or animals with preexisting insulin resistance are examined, the effects of these nutrients are reduced. Because most studies in humans have been done in older adult populations and many of the studies have been done in subjects with type 2 diabetes whose liver glucose production is already markedly elevated, it is perhaps not surprising that no effects of these nutrients has been seen.

In summary then, if sucrose has deleterious effects in humans, they are most likely to be produced in younger individuals with moderate-to-high sucrose and fructose intakes over a prolonged period. Information from human studies is not sufficient to conclusively demonstrate any adverse affects of sucrose or fructose in the diet. However, studies adequate to test this idea in younger individuals have not been done."

 

[ShirtTieFitness]

Your welcome @Ella . You'd be surprised at how many studies draw these same conclusions. A simple "insulin resistance high fat diet" search into PubMed will give you many more and some. The studies cited above gained my attention via the specific parameters used and are good examples of the general trends across the studies.

 

[ShirtTieFitness]

@Wagner83 Thanks for highlighting the sucrose/glucose debate. The impact of Fructose in Rat Vs Human was also something witnessed in the research for this post. Sucrose clearly has detrimental effects in Rats but this has not, as far as I can find, been clearly demonstrated in studies on Humans. At least no firm conclusions have been made.

The studies clearly state, in terms of recommendations that for Humans, Fruit is a favored Carbohydrate. One can infer that Fructose is thus best consumed alongside the many vitamins, minerals and electrolytes such as Potassium, Magnesium. This will enable the Fructose to be effectively processed.

It looks as if that is the disconnect with pure sucrose - whether or not the vitamins/minerals/electroyltes are required at the same time to prevent detrimental effects. This is all of course speculation and is still subject to debate.

For the most part, in terms of recommendations, and what falls in line with Peat, is that if one wanted to 'play it safe' they should get their fructose only from fruit and sugar minimally or as a last resort. This quote springs to mind:

"Refined granulated sugar is extremely pure, but it lacks all of the essential nutrients, so it should be considered as a temporary therapeutic material, or as an occasional substitute when good fruit isn't available, or when available honey is allergenic."

 

[Ella]

You'd be surprised at how many studies draw these same conclusions. A simple "insulin resistance high-fat diet" search into PubMed will give you many more and some.

I know, but lately the whole ketosis, high fat, low carb bull**** has been doing my head in. I feel I am living in some parallel universe. A stranger in a strange land where bull**** baffles the brains of all the people around and I am the only been given the truth serum.

 

[ShirtTieFitness]

@Ella, fully understand your frustrations and confusions. What I've come to realise; is that the reasoning behind High Fat Diet recommendations in the fitness or health space, usually comes from an aesthetic orientation. The common held belief being that a low body fat percentage is always or inherently healthy. The ironic thing to observe here, is that being overtly lean (if dieting down or following a strict KD diet - that lowers ones weight beyond that persons natural set point), is ironically the sign of a depressed and stressed metabolism. That emaciated concentration camp survivor look often witnessed on those following a KD or extreeme diet springs to mind.

You can be lean and and insulin resistant, just as you can be lean and diabetic.

Whilst insulin resistance is multi-factoral, excercise, environmental stress, emotional stress etc all playing a part in the absence of or increased resistance, looking from a purely nutritional standpoint as the studies above suggest, carbs would be your best bet (in parallel to a decline in your Fat consumption)

There will also be an adaption period, and it would not be advised to go from a full blown insulin resistant state (high fat low carb diet) to a (high carb low fat diet) overnight.

 

[beachbum]

abdominal visceral and subcutaneous adipose tissue cross-sectional areas were smaller postintervention compared to baseline with no difference between groups

Are they saying they didnt lose any fat in the areas mentioned..then what did they lose..sorry confused.. maybe just reading it wrong.

 

[Wagner83]

@Wagner83 Thanks for highlighting the sucrose/glucose debate. The impact of Fructose in Rat Vs Human was also something witnessed in the research for this post. Sucrose clearly has detrimental effects in Rats but this has not, as far as I can find, been clearly demonstrated in studies on Humans. At least no firm conclusions have been made.

The studies clearly state, in terms of recommendations that for Humans, Fruit is a favored Carbohydrate. One can infer that Fructose is thus best consumed alongside the many vitamins, minerals and electrolytes such as Potassium, Magnesium. This will enable the Fructose to be effectively processed.

It looks as if that is the disconnect with pure sucrose - whether or not the vitamins/minerals/electroyltes are required at the same time to prevent detrimental effects. This is all of course speculation and is still subject to debate.

For the most part, in terms of recommendations, and what falls in line with Peat, is that if one wanted to 'play it safe' they should get their fructose only from fruit and sugar minimally or as a last resort. This quote springs to mind:

"Refined granulated sugar is extremely pure, but it lacks all of the essential nutrients, so it should be considered as a temporary therapeutic material, or as an occasional substitute when good fruit isn't available, or when available honey is allergenic."

Yes , I have never heard Ray directly recommend white sugar except acutely for stress as your quote suggest, being that it is highly refined and void of nutrients we enter unknown territory for humans if we use white sugar to replace starch as a good source of calories. There have been studies showing that switching to a high carbohydrate diet overnight can lead to hypertriglyceridemia so that's an other thing to keep in mind. I'm also interested in knowing whether the quantity of fructose (from sucrose or fruits) that can be eaten at a time is an important factor of its potential negative or positive effects.

 

[Ella]

They do caution about the development of hypertriglyceridemia with high fructose diets. Epidemiologic studies have also failed to show a relationship between fructose or sucrose consumption and the development of type 2 diabetes.

I have asked this question before and I'd appreciate anyone that has experienced high TGs can provide some insight. Would it be reasonable to titrate the consumption of fruits, juice and other sugars to levels of triglycerides. How else would you modulate the release of fat while protecting the pancreas and not overburdening enzymes systems.

if sucrose has deleterious effects in humans, they are most likely to be produced in younger individuals with moderate-to-high sucrose and fructose intakes over a prolonged period. Information from human studies is not sufficient to conclusively demonstrate any adverse affects of sucrose or fructose in the diet. However, studies adequate to test this idea in younger individuals have not been done."

It doesn't make it any easier, does it?

there will also be an adaption period, and it would not be advised to go from a full blown insulin resistant state (high fat low carb diet) to a (high carb low fat diet) overnight.

So it would be prudent to follow McDougall's recommendations of not consuming fruit for several weeks or months and sticking to starches while eliminating fat from the diet? If McDougall and others in his camp have built their protocol on the works of Walter Kempnar which combined starch in the form of rice, fruit, juice and SUGAR, why is McDougall now recommending to keep fruit out? Do you think it has to do with increased stored PUFAs of modern times wherein Kempner's time, the diet would have been more replete with SAT fats and less PUFAs?

McDougall has been at the clinical cold front longer than anyone else I know. Peat has been around longer than McDougall, however, Peat does not caution the eating of fruit. He advocates fruit, juice in preference to starches due to detrimental consequences of persorption, bacterial overgrowth and LPS. Fruit instead of starches specifically for the overweight and diabetic individuals because starch is more likely to raise insulin than fruit or sugar. Is the reason for this is that we want very little activity from pancreatic beta cells in producing insulin to give them a chance to repair and rehabilitate? On the McDougall's protocol there would be more insulin triggered by the consumption of starch but then in the absence of meat, eggs etc insulin may still be lower in comparison to animal protein plus fruit.

 

[Wagner83]

I have asked this question before and I'd appreciate anyone that has experienced high TGs can provide some insight. Would it be reasonable to titrate the consumption of fruits, juice and other sugars to levels of triglycerides. How else would you modulate the release of fat while protecting the pancreas and not overburdening enzymes systems.

In the study I mentioned in the other thread, gradually transitioning from high fat - low carb to high carb - low over a period of weeks allowed patients to not experience hypertriglyceridemia.

 

[Ella]

Even though I have been doing lots of fruit, sugar, carbs and milk, I'd be surprised to find that my TGs were high, but you never know. I don't want to shock my dr just in case. I think I can handle it but she is going think I am mad, if I tell her what I have been up to. She is on this whole low carb bandwagon and how much weight she has lost. She grew up with a diabetic mum so I know she will freak. Christ, this is crazy, I feel like I have been doing drugs and I don't my dr to find out. I am going to have to suck it and see.

I just listen to Jason Fung promoting fasting for the overweight and diabetics. I don't feel comfortable with the whole idea of fasting, skipping breakfast or skipping lunch to free up time in your schedule. This is precisely the way I got fat. Fasting induces autophagy breaks down protein. Autophagy triggers adrenaline which we know breaks down protein.

http://www.economist.com/news/scien...cancer-researchers-now-understand-why-run-day

Isn't the release of adrenaline precisely what we are trying to prevent by increasing salt and sugar and eating every 3 hours?

He says that if someone has high cortisol then it would be stupid to fast them because cortisol is going to go higher. However, he does not test for cortisol because it is too tricky, too expensive; he just knows from experience. So what is the difference between someone that has high cortisol and a diabetic. They both will have high glucose levels. He says diabetics are overfed and will not die if they are starved. So diabetics are the ones eating Maccas and cream puffs???

So if you are fat with high cortisol you should not be fasted; however, if you are fat and have diabetes you can be fasted. How does he tell?



I thought I heard McDougall mention somewhere about the benefits of water-fasting.

 

[lollipop]

I thought I heard McDougall mention somewhere about the benefits of water-fasting.

Check out @Westside PUFAs comments. He has posted several times on well monitored water fasting...

 

[UberNova]

Hello everyone!

I just found this forum and read the article.
I am not sure whether should I create a new post or not, because my question is related to this topic.

I am female and 29 yo.
I was diagnosed with reactive hypoglycemia a year ago but I hadn't have insulin resistance at that time.
My endocrinologist said that I shouldn't gain weight otherwise I will end up with insulin resistance and diabetes as well.
Anyway,
I wanted to prevent this situation by following keto diet.
I got blood work after 3 months of keto diet and my levels was good(fasting and not fasting insulin levels and glucose).
I was suspicious about this diet because I also have hashimoto and hypothyroidism as well.
But my old endocrinologist said that this diet is totally fine and ok for me.
I was skinny and feeling healthy.
Before starting keto diet I wasn't eating junk food(actually I have never had junk food in my all life, it is rare habit for to consume fast foods and junks foods where I am from)
I was consuming gluten-free diet.
And I was eating lots of cheeses and my homemade yogurt and potatoes, buckwheats vegetables fruits.
At some point I was ok with simple sugars like honey but when I eat it afternoon(I mean except morning)
So without intention I was eating low GI foods I suppose, for to prevent sugar crashes.
I changed my diet approximately 7 months ago and transformed into the ketogenic diet.
As I already said first two months I was super.
At the fifth or sixth month I started to feel awful. I increased fats I gained 10 kgs in just 2 months.
I changed my doctor and he runned new blood test.
And ta-da!
I am insulin resistant now, my thyroid levels screwed up and he increased my thyroid medicines.
My vitamin d level is also dropped and I developed pcos.
I really don't know which cause to which.
Nowadays I am using metformin and returning back to my old eating habits slowly.
But I just want to know that if my insulin resistance can be reversible?
Thank you for the patience.

 

[tara]

Hi UberNova,
I am no expert, but I think there is a chance you may be able to recover from your period of 'keto' dieting. From reading various stories here, it seems that the high fat diet can tend to increase insulin resistance, and some people do seem to have trouble readapting to more carbohydrates again after they stop. Some seem to recover well. Being relatively young may work in your favour.

If you have not read about the 'Randle cycle', you may find it interesting. When there is a lot of free fatty acids circulating and available to burn for fuel, many tissues in the body tend to burn less glucose. Under normal conditions, the reverse is also true: when the free fats are low, many tissues tend to burn glucose more easily.
Your previous diet that you are returning too looks more nutritious to me.

I'm not sure how your reactive hypoglycemia was diagnosed. It is possible to get hypoglycemic by eating too little or too infrequently, or maybe too high protein: carbohydrate ratio or other imbalances. I wonder if any of those could be at play.

Good luck.