Category Archives: Diabetes

Taubes: 10,000 Calories Can Leave You Hungry (If It’s Mostly Carbs). Really?

In the video below, Gary Taubes tells the story of prisoners who were given additional carbs on top of their baseline diet (of about 3000 calories). They ate a lot, “as many as 10,000 calories a day.” “And then they said they’d go to bed hungry.” But when fat was added to their diet instead of carbs … no, they couldn’t add fat to their diet, the prisoners’ eating urge prevented it. (He doesn’t say, but I assume the “baseline” diet was composed of a mix of carbs, protein, and fat in something like the typical American diet: 55/15%/30%, not itself a “low-carb” or high-carb” diet.)

I like this point he raises about appetite. Appetite is a crucial component of our body’s weight management system.

“You can’t divorce the regulation of appetite from the regulation of energy storage. … If you try to force someone to overeat it’s going to feed back on appetite and energy expenditure, in such a way that they’re not going to be able to do it.”

In his example above, Taubes said that carbohydrate doesn’t feed back on appetite, but fat does … that when the prisoners ate fat, their appetite waned, but when they ate carbohydrates, their appetite was sustained. But 10,000 calories and still hungry? I’m having a hard time with that…


Photo of the actual food participants ate during The Evo Diet Experiment. From BBC.

Remember the Evo Diet? A group of volunteers were housed at a British zoo for 12 days and fed “the sort of diet our ape-like ancestors once ate.” Each morning a cooler containing 11 pounds of fruits, vegetables, and nuts was delivered to each participant (see photo). It was a very high-carb, low-fat diet that provided enough calories so that participants wouldn’t lose weight. Well, participants lost weight. Many couldn’t finish their 11 pounds of food.

After just 12 days on the Evo Diet:

  • Cholesterol dropped 23% (e.g. From 210 to 162 mg/dl)
  • Blood pressure dropped from 140/83 to 122/76
  • Weight dropped 9.7 lbs

Barnard et al. found the same thing when he told his study participants, who were not in a zoo but were free-living, and who had diabetes no less, to eat unlimited amounts of whole plant food (cooked or raw).1  That included … potatoes, squashes, corn, rice, oats, wheat, beans, legumes, and all manner of fruits and vegetables.  It was very high-carb, over 70% of their food energy came from carbohydrates.

After 6 months on the whole food plant-based diet:

  • Weight dropped 14.3 pounds
  • HbA1c fell 1.23 points (HbA1c is a measure of blood glucose)
  • LDL cholesterol fell 21.2%

They also experienced reductions in BMI, waist circumference, total cholesterol, had improved kidney function, and many reduced their diabetes medications. They were eating unlimited amounts of food.

It is simply not true that a diet of mostly carbohydrates is not satisfying or cannot contribute to weight loss.

1A Low-Fat Vegan Diet Improves Glycemic Control And Cardiovascular Risk Factors In A Randomized Clinical Trial In Individuals With Type 2 Diabetes, Diabetes Care, August 2006

Animal Fat Is A Natural Reservoir For Environmental Pollutants

BaconFat3With all the debate about weather fat in the diet is good or bad, one morsel getting lost in the discussion is that animal fat is a natural reservoir for environmental pollutants. Persistent Organic Pollutants (POPs) are largely hydrophobic, meaning they don’t dissolve well in water but they dissolve easily in fat. They also bioaccumulate, meaning they are found in higher, more concentrated amounts in animals higher in the food chain (such as tuna, salmon, fish-eating fowl, and farmed animals fed fish meal and other animal products), and, of course, ourselves:

“POPs are lipophilic chemicals that can pass through biological phospholipid membranes and bio-accumulate in fatty rich tissues of humans.”

Consumption of fat and cholesterol has been repeatedly linked to weight gain, arterial plaque buildup, blood glucose abnormalities, even cancer progression. Could it be the chemicals dissolved in that animal fat that are contributing to these ailments? Yes, says researcher Jerome Ruzzin from the University of Bergen in Norway:

Public Health Concern Behind The Exposure To Persistent Organic Pollutants And The Risk Of Metabolic Diseases, BMC Public Health, April 2012

There is now solid evidence demonstrating the contribution of POPs, at environmental levels, to metabolic disorders. Thus, human exposure to POPs might have, for decades, been sufficient and enough to participate to the epidemics of obesity and type 2 diabetes.”

“The general population is exposed to sufficient POPs, both in term of concentration and diversity, to induce metabolic disorders. This situation should attract the greatest attention from the public health and governmental authorities.”

No mincing of words there!

What are POPs?

“Persistent organic pollutants (POPs), including dioxins, furans, polychlorinated biphenyls (PCBs), and organochlorine pesticides, are chemicals mainly created by industrial activities, either intentionally or as by-products [13]. Because of their ability to resist environmental degradation, these substances are omnipresent in food products, and found all around the world, even in areas where they have never been used like Antarctica [14]. Thus, virtually all humans are daily exposed to POPs.”

What foods contain the most POPs?

“In the general population, exposure to POPs comes primarily from the consumption of animal fat like fatty fish, meat and milk products; the highest POP concentrations being commonly found in fatty fish [15–26].”

Some diseases linked to POPs (from a variety of studies: humans, animals, cell models):

Bio-accumulation of PCBs has been linked to non-alcoholic fatty liver disease (NAFLD) and elevated blood pressure.

Animals exposed to environmental levels of POP mixtures through the intake of non-decontaminated fish oil (obtained from farmed Atlantic salmon) exhibited insulin resistance, glucose intolerance, abdominal obesity and NAFLD [44]. In rats fed decontaminated crude salmon oil, which contained very low levels of POPs, these metabolic disturbances were almost absent.

The presence of POPs in farmed Atlantic salmon fillet was found to accelerate the development of visceral obesity and insulin resistance in mice.

Another important issue is the regulation of organochlorine pesticides, which are chemicals strongly linked to type 2 diabetes [29, 32, 33, 37, 44, 45] as well as breast and prostate cancer [94] and Parkinson disease [95]

It looks like we can’t get away from DDT, even though it was banned here in 1972:

“Not surprisingly, a recent US monitoring study revealed that DDT and its metabolites as well as endosulfan and aldrin, are still largely present in food, and daily consumed by humans.”

Children are at greater risk of exposure:

“Because of their high food intake per kilogram body weight required to maintain whole-body homeostasis and growth, children are likely to be at higher risk for environmental pollutant exposure. Not surprisingly, many scientific studies have highlighted that children are over-exposed to dioxins and dl-PCBs, and exceed the TDI of 2 pg/kg body weight.”

SalmonFillet3Finally, here’s a list of limits set by the European Union:

  • Ruminants: 4.5 pg/g fat
  • Poultry and farmed game: 4.0 pg/g fat
  • Pigs: 1.5 pg/g fat
  • Marine oils: 10 pg/g fat

You can see that the limit for marine oils is double that for fat from land animals. Why? They need to get together on this and create standards that apply across the board, and are based on public health, not commerce. Speaking of salmon, he says that “eating 1 g of fat from a fatty fish fillet could induce an exposure to 70 pg.”

What are Paleos eating? I mean, you can’t be Paleo and vegan at the same time. How do you avoid all these dissolved POPs?

Regulating vehicle emissions, pesticides, and industrial wastes is at odds with economic growth. Which is why I think pollution and its attendant chronic disease load is here to stay.

The Link Between Dietary Fat And Diabetes

FatsVisibleInvisible2I often read in comments elsewhere that people don’t understand how the fat we eat affects blood glucose levels. Here’s a recent one I saw:

“I still can’t figure out HOW meat and fat are supposed to cause diabetes when it has a practically zero effect on your blood sugar.”

They talk about carbohydrates, but fat and protein, they say, have no effect … that you can eat as much fat, as much saturated fat, as you want and it won’t affect glucose levels or glucose uptake.

Truth be told, everything we eat affects glucose clearing in one way or another. The macronutrients … carbohydrates, fat, and protein … all contribute to glucose clearing in unique ways.

Regarding dietary fat, Ricardi et al., in their review…

Dietary Fat, Insulin Sensitivity And The Metabolic Syndrome, Clinical Nutrition, 2010

… Describe several mechanisms for how dietary fat impacts glucose uptake. I’ll highlight two of them.

1. “Consumption of energy-dense/high fat diets is strongly and positively associated with overweight that, in turn, deteriorates insulin sensitivity, particularly when the excess of body fat is located in abdominal region.”

That’s an indirect method. The middleman there is overweight.  But what if you delete the middleman? What if you eat a high-fat, particularly high-saturated-fat diet but keep your weight within a healthful range? Can it still lead to insulin resistance? Yes. Studies have shown it can.

The composition of our cell membranes is determined, in part, by the amount and type of fat we eat. Saturated fat is less flexible than unsaturated fat, and will contribute to less flexible, or less ‘fluid’ cell membranes. (e.g. less saturated vegetable oils are more fluid at room temperature than more saturated butter and lard.), and:

2. “Given that insulin signaling and recruitment of GLUT4 to the cell membrane in skeletal muscle are largely membrane-associated events, a more fluid membrane might be expected to be associated with improved insulin sensitivity.”

Indeed, Ricardi cites studies, including intervention studies, that bear this out … the more saturated fat in the cell membrane (and the more saturated fat we eat), the more insulin resistant the cell. (GLUT4 is a glucose transporter or “door” for glucose to enter the cell.)

I’ll add a third mechanism that they don’t address but I’ve read about (e.g. Polyunsaturated Fatty Acids: From Diet To Binding To PPARs And Other Nuclear Receptors, Genes and Nutrition, 2006).

3. Fatty acids (FAs) themselves can affect the expression of genes. For example, FAs can bind to proteins in the nuclear membrane, acting as transcription factors. (A group of these transnuclear proteins are known as PPARs. Some of the best known PPAR ligands are the thiazolidiediones … a class into which the diabetes drugs Avandia and Actos fall.) By controlling gene expression, FAs can and do control many processes, from lipid storage (lipid synthesis) to lipid oxidation (lipid breakdown), which, taken together, affect insulin sensitivity.

In sum:
1. Fat can affect body weight and body composition, which can affect insulin sensitivity.
2. Fat can make cell membranes more or less fluid, affecting insulin sensitivity.
3. Fatty acids can control how genes get expressed, affecting insulin sensitivity.

There must be something else working too, something more immediate, because when you give people with type 1 diabetes a high-fat meal and a low-fat meal, they need more insulin to cover the high-fat meal, even though both meals contain the same amount of carbohydrate and protein.

Dietary Fat Acutely Increases Glucose Concentrations and Insulin Requirements in Patients With Type 1 Diabetes, Diabetes Care, April 2013

I thought this was interesting, from Ricardi, about omega-3 (n-3):

“The n-3 very-long-chain polyunsaturated fatty acids characteristic of fish intake were weakly negatively associated with insulin sensitivity. This tends to confirm earlier findings that n-3 polyunsaturated fatty acid intake can impair insulin sensitivity.”

So, fish oil may contribute to insulin resistance as well. It’s already been shown to increase LDL cholesterol.1

There has been a lot of study in the area of diet and insulin resistance.  That’s why comments like the one at the top of this post surprise me. There remain questions, but the body of evidence so far points to the notion that high-fat, especially high-saturated-fat diets increase insulin resistance, affect blood glucose levels, and contribute to the development of type 2 diabetes.

* “Insulin sensitivity” refers to how sensitive cells are to insulin, and how well cells take up glucose. If cells are insulin sensitive, that’s good. If cells are “insulin resistant”, that’s not good. It means cells are resistant to taking up glucose from the bloodstream, which can lead to high blood glucose and over time diabetes.

1 Effects Of Dietary Saturated, Monounsaturated And N-3 Fatty Acids On Fasting Lipoproteins, Ldl Size And Post-prandial Lipid Metabolism In Healthy Subjects, Atherosclerosis, 2003.

Animal Protein But Not Plant Protein Increases Risk For Diabetes

AnimalFoods2Diets high in animal protein – meat, eggs, seafood, cheese, yogurt and other dairy products – were associated with an elevated risk for type 2 diabetes. That was the finding of this new study:

Dietary Protein Intake and Incidence of Type 2 Diabetes in Europe: The EPIC-INTERACT Case-Cohort Study, Diabetes Care, 10 April 2014

It was large with a long follow up:

“The prospective European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct case-cohort study consists of 12,403 incident type 2 diabetes cases and a stratified subcohort of 16,154 individuals from eight European countries, with an average follow-up time of 12.0 years.”

It found:

“After adjustment for important diabetes risk factors and dietary factors, the incidence of type 2 diabetes was higher in those with high intake of total protein and animal protein. Plant protein intake was not associated with type 2 diabetes.

In view of the rapidly increasing prevalence of type 2 diabetes, limiting iso-energetic diets high in dietary proteins, particularly from animal sources, should be considered.”

It’s not news on this blog that animal foods raise the risk for diabetes. This study just adds to the growing body of evidence. Eat plants.

Does The Type Of Fat You Eat Affect Blood Glucose?

FingerStick4If you give a group of men one of three meals…

1. High in saturated fat (SFA)
2. High in monounsaturated fat (MUFA)
3. High in polyunsaturated fat (PUFA)

Will there be any difference in blood glucose levels after the meal? (All meals contain the same amount of fat (61% of energy), carbohydrate (33%), and protein (6.3%).

If you answered yes, which group had higher or lower blood glucose?

Here’s what this study* found:

  • Ingestion of the PUFA meal resulted in an improved postprandial insulin sensitivity compared with SFA.
  • Insulin and glucose concentrations were higher after the SFA meal than after the PUFA meal, with intermediate values for the MUFA meal.
  • These data suggest that the effects of replacement of SFA by PUFA may contribute to lower uptake of lipids in skeletal muscle and therefore may protect against the development of insulin resistance in humans.

* PUFAs Acutely Affect Triacylglycerol-Derived Skeletal Muscle Fatty Acid Uptake And Increase Postprandial Insulin Sensitivity, American Journal of Clinical Nutrition, February 2012

Saturated fat comes primarily from dairy products (cheese, butter, cream, milk) and animal foods. The fat in plants tends to be more unsaturated, PUFA and MUFA.

Diets High In Animal Protein, But Not Plant Protein, Linked To Cancer, Diabetes, And Earlier Death


Want protein? Eat beans.

I just posted about mice that lived longer and healthier lives when they ate low-protein, high carbohydrate diets.  Because people will say “Great for the mice!” here’s a brand new study in humans that found the same thing:

Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population, Cell Metabolism, March 2014

Mice and humans with growth hormone receptor/IGF-1 deficiencies display major reductions in age-related diseases. Because protein restriction reduces GHR-IGF-1 activity, we examined links between protein intake and mortality. Respondents aged 50–65 reporting high protein intake had a 75% increase in overall mortality and a 4-fold increase in cancer death risk during the following 18 years.

These associations were either abolished or attenuated if the proteins were plant derived.

There was also a “5-fold increase in diabetes mortality across all ages.”

This was an epidemiological study that tracked 6,381 US men and women, 50 and over (NHANES III), for nearly 2 decades. It included a variety of ethnicities, education levels, and health conditions.

A few more excerpts from the study:

  • Notably, our results showed that the amount of proteins derived from animal sources [meat, fish, cheese, milk, eggs] accounted for a significant proportion of the association between overall protein intake and all-cause and cancer mortality. These results are in agreement with recent findings on the association between red meat consumption and death from all-cause and cancer.
  • Previous studies in the U.S. have found that a low carbohydrate diet is associated with an increase in overall mortality and showed that when such a diet is from animal-based products, the risk of overall as well as cancer mortality is increased even further.
  • The progression of both melanoma and breast cancer was strongly attenuated by the low protein diet, indicating that low protein diets may have applications in both cancer prevention and treatment.
  • In mice, the changes caused by reduced protein levels had an effect potent enough to prevent the establishment of 10%–30% of tumors, even when 20,000 tumor cells were already present at a subcutaneous site.

So, you can have cancer, but prevent it’s progression by eating a low-protein diet.  Dr. Campbell, author of The China Study, must be breaking out the champagne.

Note, though, that when someone reached their mid-60s, a higher protein diet was found to be beneficial:

“Both high and moderate protein intake in the elderly were associated with reduced mortality compared to that in the low protein group, suggesting that protein intake representing at least 10% of the calories consumed may be necessary after age 65 to reduce age-dependent weight loss and prevent an excessive loss of IGF-1 and of other important factors.”

For these authors, less than 10% was considered low-protein, 10-19% moderate protein, over 20% high-protein.  They found that even moderate amounts of protein had detrimental effects during middle age.  However, they are advising people over 65 to get at least 10% of their calories from protein.  Note, however, that risk for diabetes was still 5-fold at those older ages.  So the protein they should be consuming should come from plant sources. Bean, legumes, peas, peanuts, soy products, nuts, and seeds are excellent sources of plant protein.

“These results suggest that low protein intake during middle age followed by moderate to high protein consumption in old adults may optimize healthspan and longevity.”

Here’s co-author of the study, Valter Longo (Professor of Biogerontology at USC Davis School of Gerontology, Director of USC Longevity Institute), from their press release:

“The majority of Americans are eating about twice as much proteins as they should, and it seems that the best change would be to lower the daily intake of all proteins but especially animal-derived proteins,” Longo said. “But don’t get extreme in cutting out protein; you can go from protected to malnourished very quickly.”

“Almost everyone is going to have a cancer cell or pre-cancer cell in them at some point. The question is: does it progress?” Longo asked. “Turns out one of the major factors in determining if it does is protein intake.”


Want To Avoid Diabetes? Eat Plants

Because plants contain flavonoids, and flavonoids are consistently linked to a lower risk of type 2 diabetes in studies. Here’s the latest:

Dietary Intakes of Individual Flavanols and Flavonols Are Inversely Associated with Incident Type 2 Diabetes in European Populations, The Journal of Nutrition, March 2014

“In this large prospective study across 8 European countries, all flavan-3-ol monomers, proanthocyanidins with lower degree of polymerization, and the flavonol myricetin were inversely related to a lower risk of [type 2 diabetes].”

This study says:

“Flavonoids are a large group of secondary metabolites in plants that comprise 6 subclasses: flavanols or flavan-3-ols (flavan-3-ol monomers, proanthocyanidins, and theaflavins), anthocyanidins, flavonols, flavanones, flavones, and isoflavones.”

So the word “flavonoid” is a bucket term; the study found some flavonoids were more protective than others. But all flavonoids are found exclusively in plants. The main food sources of one particularly beneficial flavanol were “tea and some fruit, particularly apples and pears.”


Here’s a study from a few months ago, similar group of investigators:

The Association Between Dietary Flavonoid and Lignan Intakes and Incident Type 2 Diabetes in European Populations, The EPIC-InterAct study, Diabetes Care, December 2013

“CONCLUSIONS Prospective findings in this large European cohort demonstrate inverse associations between flavonoids, particularly flavanols and flavonols, and incident type 2 diabetes. This suggests a potential protective role of eating a diet rich in flavonoids, a dietary pattern based on plant-based foods, in the prevention of type 2 diabetes.”

How do flavonoids protect against diabetes? From the first study:

“Several in vitro and in vivo studies have evaluated the antidiabetic effects of individual flavan-3-ol monomers and flavan-3-ol–rich foods (e.g., cocoa and tea), showing a high range of activities related to improving glucose homeostasis, such as inhibition of glucosidase activity and glucose absorption from the intestine, protection of pancreatic β cells, increased insulin secretion, activation of insulin receptors and glucose uptake in the insulin-sensitive tissues, and modulation of intracellular signaling pathways and genes involved in gluconeogenesis and glycogenesis.”

People underestimate the benefit of a plant-strong diet. They also underestimate the detriment of a meat-and-dairy-rich diet. I’ve had many people ask me, “What I eat doesn’t have anything to do with whether I get diabetes. Does it?” It does.

Dietary Fat Raises Blood Glucose

Here you are. Dietary fat raises blood sugar:

Here’s the study it was based on:

Dietary Fat Acutely Increases Glucose Concentrations and Insulin Requirements in Patients With Type 1 Diabetes, Diabetes Care, April 2013

Each person had a chance to eat the high-fat meal and the low-fat meal. When they ate the high-fat meal they needed more insulin to cover the same amount of carbohydrate. The meals had identical carbohydrate and protein, but different fat content (60 grams vs. 10 grams).