“… serum insulin levels are driven by the carbohydrate content of the diet.”
Many people think this. As you know, it is inaccurate. Dietary carbohydrate is not the sole driver of serum insulin. But it persists in people’s minds. It is the reason people go on low-carb diets … thinking they can reduce their blood glucose and insulin by eating fewer carbs. Unfortunately, that means eating more fat and…
High-fat diets have been shown to increase insulin levels, because fat (especially saturated fat) can decrease insulin sensitivity. When cells become resistant to insulin, the pancreas produces more insulin to compensate, resulting in high serum insulin levels or hyperinsulinemia.
Also, when cells becomes resistant to insulin, glucose in the blood can’t enter cells so blood glucose levels rise.
Here’s an unfortunate result … high insulin levels can feed insulin resistance, which can feed high insulin, which can feed insulin resistance … in a self-propagating manner:
With 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:
“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 . 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 . 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 . 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  and Parkinson disease 
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.”
Finally, 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.
“Atherosclerosis and vascular calcification are usually regarded as circulatory phenotypes associated with advanced modern lifestyles. However, although rare, such conditions have been identified in human remains from some early societies. Examples occur in an elite Chinese burial (c. 700 BCE), and among Canadian Eskimos (c. 400 CE to c. 1520 CE) whose diet was almost entirely meat. They have also been reported since the early 20th century in the mummified remains of the rulers and elite of ancient Egypt.
Interpretation of the hieroglyphs indicates that the diet consisted mainly of beef, wildfowl, bread, fruit, vegetables, cake, wine, and beer. Many of these food items would obviously have contributed to an intake of saturated fat, and our analyses of the individual meat and wildfowl they consumed would demonstrate that all provided greater than 35% of energy from fat. Goose, which was commonly consumed, contains around 63% energy from fat with 20% being saturated, while the bread that was eaten differed from that consumed today, often being enriched with fat, milk, and eggs. The cakes were typically made with animal fat or oil. Although it is difficult to calculate exactly how much was consumed in terms of portion size, variance in food storage, preparation, and cooking methods, it is still evident from a conservative estimate that the dietary energy was more than 50% from fat with a significant portion of this coming from saturated fat.
It is important to point out that there was a marked difference between the mainly vegetarian diet most Egyptians ate and that of royalty and priests and their family members whose daily intake would have included these high levels of saturated fat. Mummification was practised by the elite groups in society, ensuring that their remains have survived to provide clear indications of atherosclerosis; by contrast, there is a lack of evidence that the condition existed among the less well-preserved remains of the lower classes.
The explanation for these frequent pathological findings almost certainly resides in a diet rich in saturated fat that was confined to the elite, while most of the population remained vegetarian. In consequence, there is unequivocal evidence to show that atherosclerosis is a disease of ancient times, induced by diet, and that the epidemic of atherosclerosis which began in the 20th century is nothing more than history revisiting us.”
It is credible to me that a mummy earned the right to be embalmed because of his or her status in the community. And that status may have afforded the person access to foods that weren’t available to the masses.
So, atherosclerosis, or as my mother called it, hardening of the arteries, isn’t new. It’s likely a result of lifestyle, specifically a diet high in animal foods.
… 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.)
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.
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.
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.
This was a prospective study from Taiwan, 1833 men and women (average age 60) were followed for about 10 years. The relative risk (RR) of death in the highest quartile compared with the lowest quartile (of fatty acids in their blood) was:
1.33 for saturated fats (95% confidence interval [CI], 1.01–1.75, test for trend, P = 0.015)
1.71 for trans fats (95% CI, 1.27–2.31, test for trend, P = 0.0003)
0.77 for EPA (95% CI, 0.59–1.00, test for trend, P = 0.048)
0.89 for DHA (95% CI, 0.68–1.18, test for trend, P = 0.354)
Note that there was a higher risk of death for only saturated fats and trans fats (the RR was above 1.00). Note also that even though the RR was below 1.00, that is, appeared to show protection for the omega-3 fatty acids EPA and DHA, it did not rise to a level of significance, especially for DHA.
“CONCLUSIONS: Our data provides strong evidence to support that plasma saturated fats and trans fats can predict all-cause death and CVD [cardiovascular disease] more effectively than other fatty acid markers.”
As people age, they lose muscle mass. That muscle loss is called sarcopenia. Inflammation and oxidative stress are thought to be at the root of sarcopenia. Dr. Holly Van Remmen’s research focuses on how oxidative stress damages mitochondria, and:
“The impaired function of mitochondria also has a detrimental effect on the way motor neurons ‘talk’ to the muscle to achieve muscle contraction,” Dr. Van Remmen said.
This new study now implicates dietary fat in these processes:
“Age-related loss of skeletal muscle mass results in a reduction in metabolically active tissue and has been related to the onset of obesity and sarcopenia. Although the causes of muscle loss are poorly understood, dietary fat has been postulated to have a role in determining protein turnover through an influence on both inflammation and insulin resistance.”
Dietary fat is linked to inflammation and insulin resistance, evidence for which I’ve given over the years.
“This study was designed to investigate the cross-sectional relation between dietary fat intake, as dietary percentage of fat energy (PFE) and fatty acid profile, with indices of skeletal muscle mass in the population setting. Body composition [fat-free mass (FFM; in kg)] and the fat-free mass index (FFMI; kg FFM/m2) was measured by using dual-energy X-ray absorptiometry in 2689 women aged 18–79 y from the TwinsUK Study and calculated according to quintile of dietary fat (by food-frequency questionnaire) after multivariate adjustment.”
Quintiles. Did you see that? They divided the women into 5 groups based on fat intake. Why didn’t the saturated fat study use quintiles? Or quartiles? When you want to see difference among groups, the more groups the better. (The Sat Fat study used 3 groups.)
“Positive associations were found between the polyunsaturated-to-saturated fatty acid (SFA) ratio and indices of FFM, and inverse associations were found with PFE, SFAs, monounsaturated fatty acids (MUFAs), and trans fatty acids (TFAs) (all as % of energy). Extreme quintile dietary differences for PFE were −0.6 kg for FFM and −0.28 kg/m2 for FFMI; for SFAs, MUFAs, and TFAs, these were −0.5 to −0.8 kg for FFM and −0.26 to −0.38 kg/m2 for FFMI. These associations were of a similar magnitude to the expected decline in muscle mass that occurs over 10 y.”
So, as the polyunsaturated-to-saturated fatty acid ratio went up, muscle mass went up. As total fat, saturated fat, monounsaturated fat, and trans fat intakes went up, muscle mass went down.
“To our knowledge, this is the first population-based study to demonstrate an association between a comprehensive range of dietary fat intake and FFM [Fat Free Mass or muscle mass]. These findings indicate that a dietary fat profile already associated with cardiovascular disease protection* may also be beneficial for conservation of skeletal muscle mass.”
That profile which protects against heart disease and now sarcopenia is:
Low dietary fat – of all types.
High polyunsaturated-to-saturated fatty acid ratio, which is … more plant food, less animal food.
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.