Can high insulin make you fat?

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In summary: HDL cholesterol...In Summary, the study suggests that high insulin levels may be directly responsible for obesity, independent of brain insulin production.
  • #1
bohm2
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Can high insulin make you fat directly?

I thought this was a very interesting study because it seems to question the usual relationship between insulin levels, insulin resistance and obesity:
Hyperinsulinemia is associated with obesity and pancreatic islet hyperplasia, but whether insulin causes these phenomena or is a compensatory response has remained unsettled for decades...we provide genetic evidence that pathological circulating hyperinsulinemia drives diet-induced obesity and its complications.
Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production
http://www.cell.com/cell-metabolism/abstract/S1550-4131(12)00453-6

When we eat too much, obesity may develop as a result of chronically high insulin levels, not the other way around. That's according to new evidence in mice reported in the December 4th Cell Metabolism, a Cell Press publication, which challenges the widespread view that rising insulin is a secondary consequence of obesity and insulin resistance...The new study helps to solve this chicken-or-the-egg dilemma by showing that animals with persistently lower insulin stay trim even as they indulge themselves on a high-fat, all-you-can-eat buffet. The findings come as some of the first direct evidence in mammals that circulating insulin itself drives obesity, the researchers say.
Could High Insulin Make You Fat? Mouse Study Says Yes
http://www.sciencedaily.com/releases/2012/12/121204145549.htm
 

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  • #2
Assuming this model pans out, it will be interesting if insulinogenic food indexes like below will be used to monitor insulin-releasing responses of different foods as a means to limit weight gain/maximize fat loss? Then again, I'm not sure because other studies suggest total calories is king. Nutritional research is very confusing:
The results of this study confirm and also challenge some of our basic assumptions about the relation between food intake and insulinemia. Within each food group, there was a wide range of insulin responses, despite similarities in nutrient composition. The important Western staples, bread and potato, were among the most insulinogenic foods. Similarly, the highly refined bakery products and snack foods induced substantially more insulin secretion per kilojoule or per gram of food than did the other test foods.
An insulin index of foods:the insulin demand generated by 1000-kJ portions of common foods.
http://ajcn.nutrition.org/content/66/5/1264.full.pdf

Beyond Glycemic Index: New food insulin index
http://www.nutrientdataconf.org/PastConf/NDBC35/4-2_Sampson.pdf
 
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  • #3
All of human nutrition is extremely complex for both very sound scientific reasons and sometimes political or religious reasons. We understand rat nutrition pretty well compared to some aspects of human nutrition because studies can do things with rats that should never even be contemplated for humans. So a lot of studies are like the ones you cited, more like clinical investigations. There are some population studies, like the ongoing Framingham study.

http://www.framinghamheartstudy.org/

So what you're seeing is interesting but not surprising. There is sort of a dichotomy in the current nutrition world view. This book:

Gary Taubes 2008 'Good Calories Bad Calories and the Controversial Science of Diet and Health' explains it and how it got the way it is.

Taubes is a science reporter, but this does cite quotations from interviews with scientists, peer reviewed papers, so in that sense it is reasonable. But you can see from this book that how we view Nutrition Science and what makes us fat are both undergoing a major reconsideration. Exactly how science works.

The dichotomous view is centered around fat and calories in the diet. As a simplification you can view it as:
1. A Low fat, high carbohydrate paradigm
2. A low carbohydrate, higher fat & protein paradigm

Both of these versus the "Western diet". The Western diet is the bad guy, and everyone pretty much agrees with that. They usually mean the 'Pizza Hut-McDonalds-KFC-Dunkin Donuts' diet. Lotsa fat, lack of veggies, and lotsa simple carbs. My favorite!

The choice between #1 and #2 is the issue. On a popular level, if you want to read about #1, any of the Dean Ornish books explains that point of view. If you want to go for #2, any of the "Paleo Diet" books deals with it. Example: 'The Paleolithic Prescription', S Eaton, et al 1989.
 
  • #4
I'm hypersensensitive to carbs and was diagnosed as having had metabolic syndrome since I was very young. I was was a total mess until I went on the Atkins diet. Been doing it for two years and am now relatively fit and trim [lost over 50 pounds] for the first time since I was in my twenties. I also feel better than I ever have, ever! My life has always been plagued with low blood sugar problems, passing out, uncontrollable weight gain [since my early 30s], the whole works, until now.
 
  • #5
Thanks, I have read some of Taubes, Eaton's and Atkin's suff. I think what is interesting about the papers I've linked above is that some proteins appear to elicit significant insulin secretion while fats may blunt the response. Consider this interesting comment in a more recent paper by some of the same authors:
Interestingly, in the present study, the fat content of the mixed meal showed a significant inverse relation (r = 20.60) with observed insulin responses and was a more reliable predictor of insulin demand than the amount of carbohydrate. This finding is consistent with our previous study of 38 single foods. The explanation may be the reciprocal relation between fat and the sum of the other 2 macronutrients, protein and carbohydrate. Although carbohydrate is the primary stimulus for insulin secretion, insulinotropic amino acids and bioactive peptides are also potent stimulators of insulin release (11, 19, 20). Because protein stimulates insulin secretion, particularly when combined with carbohydrate (8, 20), the meals with the highest protein and carbohydrate content (and hence lowest fat content) produce the highest insulin responses.
Food insulin index: physiologic basis for predicting insulin demand evoked by composite meals
http://ajcn.nutrition.org/content/90/4/986.full.pdf
 
  • #6
I'm always very skeptical about this stuff but this was another study somewhat related to this thread (e.g. Atkins diet) that came out today arguing for a potential benefit of ketone production seen in hypocaloric and low-carb diets:
Scientists at the Gladstone Institutes have identified a novel mechanism by which a type of low-carb, low-calorie diet-called a "ketogenic diet"-could delay the effects of aging... In the latest issue of the journal Science, available online December 6, Dr. Verdin and his team examined the role of the compound β-hydroxybutyrate (βOHB), a so-called "ketone body" that is produced during a prolonged low-calorie or ketogenic diet. While ketone bodies such as βOHB can be toxic when present at very high concentrations in people with diseases such as Type I diabetes, Dr. Verdin and colleagues found that at lower concentrations, βOHB helps protect cells from "oxidative stress" -- which occurs as certain molecules build to toxic levels in the body and contributes to the aging process.
How Calorie Restriction Influences Longevity: Protecting Cells from Damage Caused by Chronic Disease
http://www.sciencedaily.com/releases/2012/12/121206142025.htm

The original paper:

Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor
http://www.sciencemag.org/content/early/2012/12/05/science.1227166
 
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  • #7
bohm2 said:
I'm always very skeptical about this stuff but this was another study somewhat related to this thread (e.g. Atkins diet) that came out today arguing for a potential benefit of ketone production seen in hypocaloric diets and low-carb diets:

I'd be cautious about recommending such diets to the general Western population. There's ample evidence that the antioxidant content of a variety of foods (but not supplements) has a beneficial effect. Caloric requirements vary considerably based on life style and other factors. The Inuit people, prior to receiving the "benefits" of westernization, survived on a high fat, high calorie diet with virtually no fruits or vegetables. I don't think that's a reason why the Inuit diet should be recommended for the typical consumer of a Western style diet either.

http://ajcn.nutrition.org/content/84/1/95

http://ajcn.nutrition.org/content/78/3/517S.long
 
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  • #8
I think many vegetables are encouraged in low-carb diets? It's the bread and cereal group that is not recommended but I guess there are different versions. Personally, I think the vegetables and fruit group should be at the bottom of the pyramid not the bread and cereal group as is typically recommended. The former are nutrient-dense with fewer calories.
 
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  • #9
bohm2 said:
I think many vegetables are encouraged in low-carb diets? It's the bread and cereal group that is not recommended but I guess there are different versions. Personally, I think the vegetables and fruit group should be at the bottom of the pyramid not the bread and cereal group as is typically recommended. The former are nutrient-dense with fewer calories.

My point was that a low calorie ketogenic diet is not suitable as a general recommendation and caloric restriction ignores the fact that people vary widely in terms of their caloric requirements. The Atkins Diet restricts vegetables in the induction phase to less than 15 grams (about a half ounce) per day not counting fiber, which is encouraged . Note selected cereals and grains are rich sources of fiber.

http://lowcarbdiets.about.com/od/atkinsdiet/a/atkinsfoodlists.htm

Your previous post suggested that the protective antioxidant effects of ketones is a benefit. I simply countered that there are many foods rich in antioxidants available without resorting to a ketogenic diet.
 
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  • #10
SW VandeCarr said:
Your previous post suggested that the protective antioxidant effects of ketones is a benefit. I simply countered that there are many foods rich in antioxidants available without resorting to a ketogenic diet.
I'm not sure about the ketones benefits, whatsoever, that's why I wrote I was skeptical. Moreover, how compelling is the evidence that increasing anti-oxidants whether as supplements or fruits/vegetables actually increases longevity? I know with supplements it's almost nil. In fact, some anti-oxidant supplements appeared to slightly increase risk of some cancers. Even with fruit/vegetables, some studies suggest that the effects are not as robust as was once thought. I'm thinking about the European cancer reduction study.
 
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  • #11
bohm2 said:
I'm not sure about the ketones benefits, whatsoever, that's why I wrote I was skeptical. Moreover, how complelling is the evidence that increasing anti-oxidants whether as supplements or fruits/vegetables actually increases longevity? I know with supplements it's almost nil. In fact, some anti-oxidant supplements appeared to slightly increase risk of some cancers. Even with fruit/vegetables, some studies suggest that the effects are not as robust as was once thought. I'm thinking about the European cancer reduction study.

The second link in post 7 summarizes the case for the benefits of antioxidants in foods. There is a list of references. If you're arguing that a ketogenic diet is sustainable over a lifetime and would increase longevity, I would like to see valid references. Sustained ketosis is not a physiologic state in humans and ketones are toxic at certain levels. How does one assuredly regulate the level of ketones resulting from a diet?

In treating obesity, these diets may have a place, but I don't think they can be justified in healthy people as a means to achieve longevity based on current science.
 
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  • #12
SW VandeCarr said:
Sustained ketosis is not a physiologic state in humans and ketones are toxic at certain levels. How does one assuredly regulate the level of ketones resulting from a diet?
I'm personally not a fan of any extreme diets including ketogenic diets (but I do have my own biases) because I don't think extreme diets are sustainable over the long-term but I thought I'd comment on this point above. A ketogenic diet or fasting will result in ketone levels between 4-8 mmol. Ketoacidosis is defined as 8 mmol or > and pathological ketoacidosis (e.g. diabetic ketoacidosis), results in ketone concentrations of 20 mmol or >. Ketoacidosis, when it occurs in Type I diabetics and alcoholics which can be potentially fatal, will not occur in nondiabetic individuals due to built in feedback loops whereby excess ketones stimulate the release of insulin which slows down ketone body formation.
 
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  • #13
bohm2 said:
I'm personally not a fan of any extreme diets including ketogenic diets (but I do have my own biases) because I don't think extreme diets are sustainable over the long-term but I thought I'd comment on this point above. A ketogenic diet or fasting will result in ketone levels between 4-8 mmol. Ketoacidosis is defined as 8 mmol or > and pathological ketoacidosis (e.g. diabetic ketoacidosis), results in ketone concentrations of 20 mmol or >. Ketoacidosis, when it occurs in Type I diabetics and alcoholics which can be potentially fatal, will not occur in nondiabetic individuals due to built in feedback loops whereby excess ketones stimulate the release of insulin which slows down ketone body formation.

So we're back to stimulating possibly excessive insulin release. Is this what we want? I will agree that it's better than potentially fatal ketoacidosis.

EDIT: Some diabetics are currently being treated with high fat, low carbohydrate diets (< 50mg carbs/day). This has resulted in good glycemic control with strict compliance, but I'd be concerned about the increased dangers of deviations from strict compliance with diet induced ketotic patients. In addition, many diabetics have, or are prone to coronary artery disease (CAD), and I'm not ready to throw out the lipid hypothesis regarding CAD yet. This is undergoing a rethink at the present time, but the evidence remains that the (total cholesterol)/HDL ratio is a strong predictor of CAD in industrialized nations.

http://thewarper.com.au/Downloads/A%20Low-Carbohydrate,%20Ketogenic%20Diet%20versus%20a%20Low-Fat%20Diet%20To%20Treat%20Obesity%20and%20Hyperlipidemia.pdf [Broken]

http://www.diabetesselfmanagement.c...diet-improves-glucose-control-in-small-study/
 
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  • #14
SW VandeCarr said:
So we're back to stimulating possibly excessive insulin release. Is this what we want? [/url]
That doesn't follow. There's a huge difference in amount of insulin secreted to prevent fatal ketoacidosis versus amounts secreted in gorging on excess calories, particularly ones with a high insulin index.
 
  • #15
bohm2 said:
That doesn't follow. There's a huge difference in amount of insulin secreted to prevent fatal ketoacidosis versus amounts secreted in gorging on excess calories, particularly ones with a high insulin index.

I agree your argument sounds reasonable, but I would appreciate a reference comparing the amount of insulin released in non diabetic persons with a glycemic challenge to that released in non diabetic ketoacidosis induced by a low carbohydrate diet. My interest is not only in the risks of ketoacidosis in such people, but also in the possible effects of hypoglycemia as ketone levels fall.

http://www.nejm.org/doi/full/10.1056/NEJMc052709

Note, this non diabetic patient with low carbohydrate diet induced ketoacidosis required exogenous insulin to stabilize her condition, indicating that her presumably normal endogenous insulin response was inadequate.
 
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  • #16
SW VandeCarr said:
My point was that a low calorie ketogenic diet is not suitable as a general recommendation and caloric restriction ignores the fact that people vary widely in terms of their caloric requirements. The Atkins Diet restricts vegetables in the induction phase to less than 15 grams (about a half ounce) per day not counting fiber, which is encouraged . Note selected cereals and grains are rich sources of fiber.

http://lowcarbdiets.about.com/od/atkinsdiet/a/atkinsfoodlists.htm

Your previous post suggested that the protective antioxidant effects of ketones is a benefit. I simply countered that there are many foods rich in antioxidants available without resorting to a ketogenic diet.
In the Atkins diet, most carbs are supposed to come from veggies. The total of all carbs during the induction phase are supposed to be limited to 25 grams per day. And the induction phase is typically short lived - only a few weeks. I don't understand your point here. The induction phase is only intended to induce ketosis. And it isn't even considered to be absolutely necessary, but the effects are indeed amazing! I stayed ketogenic for over six months [two periods of three-months each] and I was shedding weight so fast that my wife was freaking out.
 
  • #17
SW VandeCarr said:
EDIT: Some diabetics are currently being treated with high fat, low carbohydrate diets (< 50mg carbs/day). This has resulted in good glycemic control with strict compliance,

This is pretty much my program - high protein, high fat [<30% being saturated fats], less than 50 grams carbs per day typically. Not only does it result in good glycemic control, my sensitivity to carbs has decreased significantly. I was told that I could "retrain" my pancreas but took that as just more hype until I actually saw the difference. My sensitivity had reached such a level that just one glass of milk could throw me into a low blood sugar crisis. Now, on those days when I allow myself some slack, I can consume many more carbs than before but never experience a crisis.

The one exception to this was beer; I presume because maltose has a higher glycemic index than does glucose! It only took three beers spead out over five days to ruin an entire Saturday for me.
 
  • #18
Ivan Seeking said:
In the Atkins diet, most carbs are supposed to come from veggies. The total of all carbs during the induction phase are supposed to be limited to 25 grams per day. And the induction phase is typically short lived - only a few weeks. I don't understand your point here. The induction phase is only intended to induce ketosis. And it isn't even considered to be absolutely necessary, but the effects are indeed amazing! I stayed ketogenic for over six months [two periods of three-months each] and I was shedding weight so fast that my wife was freaking out.

I already said the Atkins diet and other low carb diets seem to be effective in treating obesity. My arguments are directed toward the claims that it can be a lifestyle that would increase longevity. The case of non-diabetic ketoacidosis described in post 15 occurred after 4 years on a low carb diet.
 
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  • #19
SW VandeCarr said:
I already said the Atkins diet and other low carb diets seem to be effective in treating obesity. My arguments are directed toward the claims that it can be a lifestyle that would increase longevity. The case of non-diabetic ketoacidosis described in post 15 occurred after 4 years on a low carb diet.

The patient strictly adhered to a low-carbohydrate diet for four years, with an estimated carbohydrate intake that was often less than 20 g per day.

That is a Atkins on steroids. And I didn't see anything about her caloric intake, her nutrients, her fluids intake, or the nature of her diet. She wasn't necessarily following any diet but just severely resticting her carb intake. For example, it is considered critical that one consume plenty of fluids. They did indicate that she needed fluids. So it isn't obvious to me at all that this is reprsentitive of a balanced ketogenic diet.
 
  • #20
SW VandeCarr said:
I agree your argument sounds reasonable, but I would appreciate a reference comparing the amount of insulin released in non diabetic persons with a glycemic challenge to that released in non diabetic ketoacidosis induced by a low carbohydrate diet. My interest is not only in the risks of ketoacidosis in such people, but also in the possible effects of hypoglycemia as ketone levels fall.
As I said I'm relatively agnostic about this stuff but there are a number of papers on this topic. You might want to have a look at these and the references listed there:

Low-carbohydrate nutrition and metabolism
http://ajcn.nutrition.org/content/86/2/276.full.pdf

Ketogenic diets for weight loss: A review of their principles, safety and efficacy
http://www.sochob.cl/pdf/obesidad_a...w of their principles safety and efficacy.pdf

Metabolic effects of the Very-low-Carbohydrate diets: misunderstood "villains" of human metabolism
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/pdf/1550-2783-1-2-7.pdf
 
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  • #21
Ivan Seeking said:
That is a Atkins on steroids. And I didn't see anything about her caloric intake, her nutrients, her fluids intake, or the nature of her diet. She wasn't necessarily following any diet but just severely resticting her carb intake. For example, it is considered critical that one consume plenty of fluids. They did indicate that she needed fluids. So it isn't obvious to me at all that this is reprsentitive of a balanced ketogenic diet.

Ketoacidosis is a hyper-osmolar condition that leads to an osmotic diuresis and dehydration. I can't add anything to what the article said. The point is that by shifting the metabolism toward a ketotic state, the risk of ketoacidosis in non diabetics can be expected to increase in the population of L-CHO dieters. 100% compliance in all aspects, all the time and by all participants is an unreasonable expectation, if in fact non-compliance is the problem in this case.
 
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  • #22
Another reason why nutrition science is so confusing. Consider the previous study linked above suggesting that ketone production may be the mechanism by which calorie restriction increases longevity. Now look at the conclusions of this study suggesting that caloric restriction may not, after all, affect longevity in monkeys or humans:
The verdict, from a 25-year study in rhesus monkeys fed 30% less than control animals, represents another setback for the notion that a simple, diet-triggered switch can slow ageing. Instead, the findings, published this week in Nature, suggest that genetics and dietary composition matter more for longevity than a simple calorie count...The molecular effects of caloric restriction have also turned out to be complicated...Meanwhile, there is a dearth of evidence that caloric restriction slows ageing in humans.
Calorie restriction falters in the long run: Genetics and healthy diets matter more for longevity.
http://www.nature.com/news/calorie-restriction-falters-in-the-long-run-1.11297

Another interesting review article that goes against the "hyperinsulinemia makes you obese" hypothesis and is at odds with the original suggestion in this thread is an article by James Krieger: "Insulin…an Undeserved Bad Reputation". I didn't want to post here because even though he has a number of publications in both nutrition and exercise science, that piece was not published and would not meet criteria of this forum, although he does provide direct peer-reviewed article links to all his arguments. In it he argues that while insulin injection as used in diabetics can induce weight gain, such effects of insulin injection cannot be compared to normal physiological insulin release, since amylin is co-secreted with insulin from the pancreas and amylin has appetite suppressant and lipolytic effects.
 
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  • #23
I thought this was a relevant and very interesting study that was just published in the NEJM suggesting that a Mediterranean diet fared significantly better for primary cardiovascular disease prevention that a low fat diet. What is interesting is that the effects were so dramatic that the researchers felt obliged to stop the study for ethical reasons. The second link is the full study:
According to the researchers, the results of PREDIMED study are relevant as they prove that a high-vegetable fat diet is healthier at a cardiovascular level than a low-fat diet. The authors state that the study has been controversial as it provides new data to reject the idea that it is necessary to reduce fats in order to improve cardiovascular health.
Mediterranean Diet Helps Cut Risk of Heart Attack, Stroke: Results of PREDIMED Study Presented
http://www.sciencedaily.com/releases/2013/02/130225181536.htm
Our results compare favorably with those of the Women’s Health Initiative Dietary Modification Trial, wherein a low-fat dietary approach resulted in no cardiovascular benefit. Salient components of the Mediterranean diet reportedly associated with better survival include moderate consumption of ethanol (mostly from wine), low consumption of meat and meat products, and high consumption of vegetables, fruits, nuts, legumes, fish, and olive oil. Perhaps there is a synergy among the nutrient-rich foods included in the Mediterranean diet that fosters favorable changes in intermediate pathways of cardiometabolic risk, such as blood lipids, insulin sensitivity, resistance to oxidation, inflammation, and vasoreactivity.
Primary Prevention of Cardiovascular Disease with a Mediterranean Diet
http://www.nejm.org/doi/pdf/10.1056/NEJMoa1200303
 

1. Can high insulin levels cause weight gain?

Yes, high levels of insulin can contribute to weight gain. Insulin is a hormone that helps regulate blood sugar levels, but when there is too much insulin in the body, it can lead to an increase in fat storage. This is because insulin promotes the uptake of glucose by fat cells, leading to the conversion of glucose into fat.

2. How does high insulin affect metabolism?

High insulin levels can slow down metabolism. Insulin helps regulate the metabolism of glucose, but when there is too much insulin in the body, it can cause the cells to become resistant to its effects. This means that the body needs more insulin to do the same job, which can lead to a slower metabolism and weight gain.

3. Can high insulin levels lead to insulin resistance?

Yes, high insulin levels can contribute to insulin resistance. When the body is constantly producing high levels of insulin to control blood sugar levels, the cells can become resistant to its effects. This can lead to a vicious cycle where the body needs more and more insulin to regulate blood sugar, leading to weight gain and an increased risk of developing type 2 diabetes.

4. Does a high insulin diet cause weight gain?

A high insulin diet, which is characterized by consuming large amounts of simple carbohydrates and sugar, can contribute to weight gain. This is because these types of foods cause a spike in blood sugar levels, leading to a surge in insulin production. The excess insulin can then promote fat storage and lead to weight gain over time.

5. How can I lower my insulin levels?

There are a few ways to lower insulin levels, including reducing your intake of simple carbohydrates and sugar, increasing your intake of fiber and protein, and engaging in regular physical activity. These lifestyle changes can help improve insulin sensitivity and reduce the need for high levels of insulin in the body, leading to better blood sugar control and weight management.

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