Loose Fat and Avoid Disease. – The Current Evidence for Diet: Strategies III
This is the 9th newsletter concerning fat loss and disease avoidance from the modern perspective of Insulin Resistance. To understand this highly complex area, it may help to start with the list below in order if you haven’t already read the previous issues: The Insulin Resistance Series:
1. You need to eat 5000 calories per day
2. Why can’t I lose weight?
3. Osteoarthritis, Inevitable or Preventable?
4. Dementia – will it affect you?
5. Lose Fat and Avoid Disease. The Current Evidence for Exercise
6. Lose Fat and Avoid Disease. The Current Evidence for Diet: Overview
7. Lose Fat and Avoid Disease. The Current Evidence for Diet: Strategies I
8. Lose Fat and Avoid Disease. The Current Evidence for Diet: Strategies II
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Or…if you want to miss the reading part, just watch this series. If you implement just 10% of what is discussed I’ll be very very happy!
In this episode we will take a deep dive into carbohydrates and insulin resistance. Should you stop eating them completely or be more focused on the make up of the particular carbohydrate? To answer this we will explore the difference between Glycaemic Load (GL) and Glycaemic Index (GI) and how they may help us make a more informed decision. Fats will also come under investigation where we will discuss what the current nutritional science suggests are good and bad fats.
Our investigation will also discuss a vital process known as gluconeogenesis (GNG) and how endurance sports such as cycling, swimming and running rely on the conditioning of this system. Finally, one key aspect of our nutritional puzzle is the individualised insulin responses we seem to have to foods, and for this we turn to the Gut Bacteria debate.
Carbohydrate Restriction…. As the avid reader will have come to understand, once we appreciate that too much insulin is a main driver of insulin resistance and therefore weight gain and disease, the chain of events suggesting a solution is too obvious:
Eating fewer processed carbohydrates* = reduced blood glucose = reduced blood insulin = improved insulin sensitivity
* especially the Ultra-Processed Foods (UPF’s) we discussed in: The current evidence for diet: Overview. For more detail, this article is brilliant: Ultra-Processed Foods: the 19 things everyone needs to know
With a lowering of insulin comes a sort of resetting (re-sensitizing) of the ‘insulinostat.’ To really appreciate the relevance of the food we eat, we need to establish the effect of each macronutrient (fat, carbohydrate and protein) on blood insulin. As you can see from the chart below, dietary protein elicits a mild insulin effect – about two times fasting levels, although this depends on blood glucose levels which is highly influenced by what other types of macronutrients you have eaten and what order they have been eaten in – i.e. fats, carbohydrates (complex) or carbohydrates (refined). Further, recall from Strategies I, eating carbohydrates last does decrease the overall insulin response.
Carbohydrate (particularly refined aka ultra processed foods (UPF’s)) on the other hand, can elicit a remarkable increase in insulin: more than 10 times above normal, with the height and length of the spike highly variable depending on the carbohydrate and a person’s insulin sensitivity.
Dietary fat elicits no insulin effect at all as eloquently discussed in the paper ‘Metabolic control of macronutrient intake’. Thus, a diet that limits the insulin spiker (carbohydrates, especially refined UPF’s) and increases the insulin dampeners (protein and fat, especially unrefined) is one that should improve insulin sensitivity. And—as we will see—it does.
Protein
The overwhelming consensus with dietary protein is that it causes a significant spike in insulin when combined with refined carbohydrates i.e. a big Mac or Whopper. Thus, the size of the ‘insulin spike‘ is highly dependent on the need for gluconeogenesis (GNG). GNG is the process whereby the liver naturally makes glucose for the body when there isn’t enough coming from the diet. Due to GNG, eating refined carbohydrates is unnecessary. When a person who eats a refined high-carbohydrate diet ingests protein, they experience a robust rise in insulin. However, in a person who eats relatively fewer processed carbs, they have little or no insulin response to protein as documented in the paper Insulin-Glucagon Ratio. The main reason for these different insulin responses is likely based on whether or not GNG is needed. When we eat less glucose, GNG picks up the slack, keeping our blood glucose perfectly normal.
Carbohydrate Intake and Insulin Resistance Restricting carbohydrates was perhaps the first modern documented intervention to control diabetes and weight, accepted as fact throughout Western Europe in the early and mid-1800s. Why such a paradigm fell out of favour, to be replaced with the current recommendations that those with insulin resistance and type 2 diabetes should avoid fat and eat starches, is puzzling (reading our Cholesterol Series should clear up the mystery!), but the shift in guidelines was dramatic.
Within decades (from the early to the mid-1900s), guidelines for diabetes went from encouraging strict avoidance of bread, cereals, sugar, and so forth, while allowing all meats, eggs, cheese, and the like (per The Practice of Endocrinology in 1951), to just the opposite—encouraging breads and cereals while discouraging meats, eggs, et cetera (per the American Heart Association and, until recently, the American Diabetes Association). And we responded— according to the article ‘trends in intake of macronutrients’, we eat far less fat now than we ate 50 years ago and guess what – the impact of chronic diseases from insulin resistance were practically non-existent compared to todays tidal wave of avoidable ill health especially when you control for smoking.
Endurance Sports and why Zwift (indoor cycling) doesn’t really work….
We have a ‘storage window’ of energy within our muscle cells. The cell engine or mitochondria, stores around 60-90 minutes worth of energy called adenosine triphosphate (ATP) when exercising at moderate intensities. Once depleted you are into gluconeogenesis (GNG) territory. This is an energy switch from storage to manufacture. The more efficient/practiced at manufacturing the better you go after 60-90 minutes of swimming, riding or running.
Whilst short intense sessions have their place in any well considered training schedule, they don’t have time to tap into this system and improve GNG. That’s why the classic ‘Zwifter’ is fast and punchy to begin with, but falls out the back of the group consistently as the ride gets over 2 hours. Their capacity to create energy is not well trained.
There are many, many studies that indicate insulin sensitivity increased more with a lower-carbohydrate diet. Multiple meta-analyses (or statistical analyses that pool the findings from numerous studies), encompassing thousands of patients, unanimously reveal that a carbohydrate-restricted, calorie-unrestricted diet lowers insulin at least as much, and often more, than low-fat, calorie-restricted diets. The study ‘Effects of low-carbohydrate diets versus low-fat diets on metabolic risk factors: a meta-analysis of randomized controlled clinical trials’ pulled huge amounts of data together and confirmed carbohydrate restriction as being the vital component to lowering insulin resistance and controlling weight. Indeed, the sum of evidence is so convincing that the American Diabetes Association updated its ‘Standards of Medical Care in Diabetes’ to include the use of low-carbohydrate diets for controlling type 2 diabetes.
Before we move on, it’s important to acknowledge that the collective evidence supporting carbohydrate restriction should be viewed in the context of insulinand, thus, should not be considered a call to avoid all carbohydrates. Not all carbohydrates are created equal. Whether they are considered ‘good’ should depend on the degree to which the food increases insulin.
Carbohydrates – Quality Vs Quantity…. I encourage you to think of carbohydrates as being on a spectrum with regard to their effects on glucose and insulin. It doesn’t always matter how many grams of carbohydrate you’re eating if the foods you choose have ‘good’ carbs. A useful tool in deciding whether a carbohydrate is ‘good’ or ‘bad’ is by determining its glycemic load, or GL—a number that estimates how much a particular carbohydrate food will raise your blood glucose after you eat it. And, as you know by now, an increase in blood glucose will in turn spike your blood insulin.
It’s easy to confuse the GL with the glycemic index (GI). The GI is simply a measure of how quickly the carbohydrate is broken down into glucose in the blood. GL, on the other hand, actually determines how much carbohydrate is in the food that can become glucose in the blood and therefore cause an insulin spike. .
Let’s take a watermelon, for example. With a GI of 72, watermelon is considered ‘high GI,’ but its GL is remarkably low at 2—this means that even though the carbohydrate in the watermelon can rapidly become glucose in the blood (per GI), the actual amount of carbohydrate is low enough to not really matter (per GL).
To be clear: The problem with the GI is that it doesn’t account for how much potential glucose is in the food you’re eating. GL does. Thus, it’s possible to consume a diet that has a higher amount of carbohydrates and still potentially prevent or improve insulin resistance if the carbohydrate is low GL. Of course, as a reminder, the underlying utility in understanding the glycemic load is to get an idea of what the food is doing to insulin. A GL of 20 and above is usually considered ‘high,’ 11 to 19 is ‘moderate,’ and 10 or below is ‘low.’ This convention is fine; just remember, the lower the better. It can be difficult to calculate GL on your own, but there are several online and smartphone app resources that you can use to determine the GL of the foods you’re eating.
High-GL foods include sugary drinks and sweets, white pasta and bread, and French fries and baked potatoes. Whole wheat pasta, brown rice, sweet potatoes, and fruit juices without added sugar generally fall in the moderate range. Some low GL foods are kidney beans, chickpeas, and black beans; lentils; certain whole-grain breads; and cashews and peanuts. Fibre-rich vegetables and fruits are good examples of low-GL carbohydrates; a diet high in fibre improves insulin sensitivity.
Importantly, for people with insulin resistance (recall our questionnaire in the first newsletter on Insulin Resistance), keeping the GL low is significantly more effective at improving health compared with a simple low-fat diet. Focusing on the GL of foods becomes particularly valuable if your diet is based mostly on plants and plant products (so read closely, vegetarians and vegans). In general, most plant foods are lower in protein and fat and contain mostly carbohydrate that is low GL (obvious exceptions are ‘fatty fruits’ such as avocado, olives, and coconut). Nevertheless, some plant foods are great sources of dietary fibre that can help control their glycemic effect. Many of us have heard that plant-based diets are inherently healthier and more effective at preventing disease, though this isn’t without debate. Regardless, a plant-based diet isn’t necessarily better when it comes to insulin resistance.
The simplicity of eating ‘low-carb’ discourages a person from eating any insulin-spiking packaged snacks and treats, such as crisps. However, such foods could very easily be acceptable on a vegetarian/vegan diet, insofar as they may not contain any animal products. Your best guide is the GL of the product.
Fats – explained…
Low-carbohydrate diets are often (not always!) high in animal fat and protein. Many people who avoid animal fat do so out of fear of saturated fat. ‘The saturated fat will clog your cells and block insulin from working!’ is the common cry. There are a few scientific problems with this sentiment. First, animal fat is never exclusively saturated—it’s a broad mix of saturated, monounsaturated, and polyunsaturated. Second, according to the article Skeletal muscle lipid content and insulin resistance the muscle of insulin-sensitive athletes is just as ‘fat filled’ as the muscle from obese,insulin-resistant people.
However, fat does matter—just not the kind you think. The most likely fat that matters is a type called ceramide, and it’s not one you worry about in your diet; it’s one you make in your cells. Ceramide production is activated by inflammation; once turned on, the cell will turn an innocent saturated fat into ceramide, and the ceramide then makes the cell less sensitive to insulin.
Critically, according to the study ‘Muscle ceramide content after 3 weeks’ consumption of fat or carbohydrate’ ceramide levels are not increased in the tissues of people who adopt a carbohydrate-restricted, fat-liberal diet.
Equally important, saturated fat in the blood is NOT increased in people adhering to a high-fat diet. In the study ‘Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet’ the low-carbohydrate group, despite eating three times more saturated fat than the low-fat group, not only had a much greater drop in fasting insulin but also a two to three times greater reduction in saturated fats in the blood!
Interestingly, the study ‘Palm oil and olive oil cause a higher increase in blood lipids compared with lard’ showed that adding saturated fat to a meal (like lard) actually reduces blood fats to lower levels compared with adding unsaturated fats (like olive oil).
According to the Sydney Diet Heart Study, one of the dangers with avoiding saturated fat is what we replace it with. Our collective fear of saturated fat has led to an embrace of polyunsaturated fats, derived industrially from seeds. Interestingly, replacing saturated fat (e.g., lard, butter, tallow, etc.) with polyunsaturated fat (e.g., soybean oil, corn oil, rapeseed oil, safflower oil, etc.) may actually do more harm. However, these findings don’t apply to all seeds—the polyunsaturated fat (alpha-linolenic acid) from flax seed improves insulin resistance.
Gut Bacteria
You may recall the work of Professor Eran Segal in our newsletter What is the best Diet for Humans? The biggest nutritional study featured some ground braking results, namely, GL is an individual reaction! His work suggests that differences in gut bacteria could explain how some people are able to readily use carbohydrates and others aren’t. That’s right—the billions and billions of bacteria in your intestines that help you digest food may be the strongest distinguishing factor that determines how intensely your glucose and insulin respond to a carbohydrate-rich meal. Scientists at the Weizmann Institute found that a person’s gut bacteria determined the glycemic load of a food, and that some people had a fairly minor response to things like ice cream, while others had dramatic glycemic responses to common foods like wheat bread.
So to conclude, I hope, as these newsletters build upon one another that they help dispel some of the dietary and health myths that bombard us in modern society. Human science is full of error, it’s really shades of grey, not black and white. There are always variables we cannot account for when studying humans and sadly it is exactly this aspect that is manipulated by much of the misleading dietary and health advice we receive – even from traditional sources (i.e. Health Professionals whom still recommend outdated low fat diets for high cholesterol!!!)
Thanks for reading. The next newsletter in our Insulin Resistance series will consider the place of Ketogenic diets and what the evidence tells us about weight control. The article will also unearth what fat cells do and discuss fat cells that actually help us burn fat! We will end with a discussion on how diet and insulin resistance affects:
- Heart Disease & blood pressure
- Reproductive Health
Happy Christmas…..
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