In parts 1 and 2, we talked about how our evolution has affected the way we eat, and the way we store fat. We talked about how food companies can take advantage of evolutionary traits to create products that we find hard to resist, and how the composition of our meals can further drive us to overeat. Today, we’re going to talk about how our hormones play into all this.
Before we dig in, this aspect of physiology is exceptionally complex. There are hundreds of hormones at work in the human body, and many of them perform multiple functions, interacting and affecting each other in an almost unfathomable series of feedback loops. Clever people study these things for decades, and still don’t know everything there is to know. Needless to say, in order for this to make any kind of sense to you and I, we need to simplify things a great deal and it’s important to acknowledge that.
None of the hormones we’re going to talk about today are ‘bad actors’. It’s become common for some of these things to be demonised, as people look to manipulate their biochemistry, to optimise their physique, wellness or longevity. But evolution has done that work for us, testing the design over and over, and taking the best version forward every time. The result is so graceful, so perfect in its complexity, that our blundering attempts to change it will almost always work out badly. We are not obese because our endocrine system is inadequate. We are obese because we disrupt its proper function.
Let’s start with a hormone that’s been rather unfairly vilified in the low-carb space – Insulin.
Insulin has a number of functions within the body, one of which is to tell cells what to do with energy – whether to store it, or release it for use. If our blood glucose rises too high, it will damage our organs, and vasculature. It’s an emergency that can never be allowed to continue unchecked, and one of insulin’s most critical functions is to move glucose from the blood, into storage in the cells of the liver, muscle and fat. At the same time, it inhibits the processes by which those cells release energy back into the blood for use – processes like glycogenolysis – the conversion of stored glycogen to glucose, gluconeogenesis – the creation of glucose from amino acids, and lipolysis – the breakdown of stored fat into fatty acids.
Different foods require different quantities of insulin to deal with them. Carbohydrates require by far the most, amino acids from protein rather less, and the triglycerides from the fat we eat, almost none – because fat does not need insulin in order to move into the adipose tissue for storage.
So what’s the problem? Well, it’s not so much what insulin has done to us, as what we have done to insulin:
As we’ve allowed hyperpalatable processed food products, the marketing of food, and the notion of food as entertainment to replace our natural pattern of eating, we’ve bought into this idea that people need multiple meals, interspersed with snacks throughout the day. We’re constantly told that we need a given product to ‘get us started’ in the morning, to fill us with energy; a mid-morning snack to keep us going; lunch; an afternoon snack and a cup of tea, followed by dinner, and a treat that we deserve after our hard day. These processed food products – breakfast cereals, pastries, granola bars and energy drinks typically contain high-glycemic carbohydrates – those which spike blood glucose the most, and so require the largest amounts of insulin to control. Even options which most people would consider healthy, can sometimes result in extremely high blood sugar.
As we take in these boluses of carbohydrate, insulin rises sharply, removing glucose from the blood. As glucose falls, so the pancreas stops producing insulin, but there’s a slight lag in that feedback loop, which can result in residual insulin pushing glucose a little low. The result is that a couple of hours later we may experience low blood sugar – hypoglycemia – feelings of weakness, inability to concentrate and distracting levels of hunger. We now physically need the next snack to keep functioning normally. And because insulin inhibits lipolysis, the breakdown of our body fat for energy – we have no choice but to eat again. By choosing foods that cause us to produce large amounts of insulin, we’re artificially creating the need to eat constantly. The more we snack, the more we need to snack.
Some people in the low-carb world are stuck on the idea that insulin, as a regulator of energy storage, is entirely responsible for whether we lay down body fat or not, and that by keeping insulin low, we simply can not get fatter. Their theory is that ‘calories in’ doesn’t matter, that we will simply excrete or burn off any excess energy rather than store it. This isn’t quite right – calories do still matter: if our insulin is low, if we’re not taking in carbohydrate, we must be getting our dietary energy from fat, which does not require insulin for storage. Our fat cells are constantly accepting fat-based energy from the blood.
But it isn’t entirely wrong either, because insulin does inhibit lipolysis: In order for us to burn body fat, insulin must be low, at least some of the time. In that low insulin state, we may still be adding fat into storage, but we will simultaneously be breaking down those fat stores for use. We can burn body fat more of the time.
If we’re cutting out carbohydrate, we’re necessarily removing all hyperpalatable, processed foods, and increasing nutrient density in our diet. Our appetite is going to regulate to some meaningful degree. While this works extremely well for many people, it’s important to understand that it’s likely working because people are satisfied with fewer calories, rather than just because insulin is low. We can still gain fat on a zero carb diet, if we overeat energy.
In the same way that some people gain weight on a zero carb diet, it’s possible to lose it on a high-carb diet, provided calories are controlled. We can lose weight eating only Twinkies, if we eat few enough of them.
So insulin doesn’t make a difference? No, it does:
When we control calories, we control insulin to some degree. We’ll have to eat our Twinkies in very small quantities, or very infrequently to stay within our calorie limit. Even though insulin will spike higher than it would on a low-carb diet, it will still be low at times. There are endless reasons why a Twinky diet is a terrible idea, but the point is that we shouldn’t fear some periodic spiking of insulin – after all we’ve evolved eating boluses of carbohydrates – honey and fruit. If we hadn’t, we wouldn’t have this graceful mechanism of dealing with them. We need to stop second guessing the design. Insulin helps us to gain, and maintain muscle, increasing our metabolic rate. If we stick to evolutionarily consistent quantities of carbohydrates, we don’t need to be afraid of insulin. Needless to say, those quantities are a great deal lower than those of a standard diet, which abuses insulin. Let’s talk about that…
When insulin is always high, some cells may become chronically insulin resistant. They have a limited capacity – they can’t just continue to allow energy to flow in, but not out, so they begin to stop listening to insulin as it nags at them to do so. What then begins is a battle between the fat cell and the pancreas. The pancreas produces ever more insulin in an attempt to force the issue – a state called hyperinsulinemia, and the fat cells become increasingly insulin resistant.
As this battle unfolds, the fat cells get bigger in a process called hypertrophy, and when they can’t expand any more, they become inflamed. Ultimately they completely stop responding to insulin, and regardless of the now massive amounts of the stuff that the pancreas is churning out, they will be constantly leaking energy back into the blood, but now, they will also be leaking inflammatory cytokines. This state is Type 2 Diabetes.
It’s important to note that it’s an oversimplification to say that eating carbohydrates always causes hyperinsulinemia, which always causes insulin resistance, which always leads to Type 2 Diabetes. Hyperinsulinemia and insulin resistance go hand in hand, but insulin resistance has other causes too. It can be driven by cortisol or inflammation. Furthermore, insulin resistance isn’t necessarily bad – it’s normal, essential for cells to become acutely insulin resistant as and when they need to. Again, we have to trust evolution’s design. It’s that chronic state of insulin resistance that we associate with bad outcomes.
Some people don’t suffer damaging enlargement of their fat cells – they are able to simply create more, rather than overfilling the ones they already have. This process of hyperplasia allows them to lay down an extraordinary volume of fat, all of which is functional and healthy. These people are the truly obese, and their physiology protects them against type 2 diabetes. But obviously that level of obesity has other problems of its own.
Most people can’t just create unlimited numbers of new fat cells like the truly obese are able to do. While oestrogen allows adult women to do so around their hips and thighs, typically our fat cells are created during childhood and puberty, and there’s a strong genetic component to that process. We each end up with a ‘personal fat threshold’ – an amount of fat we can healthily store, beyond which our adipose tissue becomes inflamed, and inflammatory. It’s possible to look skinny, but to be diabetic – profoundly insulin resistant. When the fat beneath our skin – our subcutaneous fat stores are full, we begin to deposit fat in and around our organs, and it’s this visceral fat that’s so indicative of serious health problems. People who have no capacity for subcutaneous fat are in serious trouble. They have no leeway to overeat, being unable to store fat anywhere healthy – it all ends up within their body cavity.
These ‘Thin Outside Fat Inside’ and truly obese phenotypes sit at the extremes of the curve. Most people with these sorts of problems are going to look visibly overweight, and they’re going to carry a significant amount of weight around their middle. Their belly might be quite hard to the touch if a lot of that fat is sitting beneath the stomach wall, rather than being located subcutaneously, but either way, waist to height ratio is a fantastic indicator of metabolic health.
We’ve talked a lot about what happens when we drive blood glucose up, but what happens when it falls too low? Well that’s also a potential emergency, and of course the system has an answer in the form of another hormone, cortisol. As well as actively suppressing insulin, cortisol promotes the mobilisation of energy into the blood – it raises our blood sugar, and blood pressure. It also breaks down muscle tissue, and suppresses the conversion of thyroid hormones, lowering our metabolic rate in order to reduce our energy expenditure in times of scarcity. It’s cortisol that gets us up in the morning, cortisol that sustains us when we can’t find food and cortisol that provides the immediate fuel for high-intensity exercise, and our fight or flight reponse. If we find ourselves face to face with an angry rhinoceros, we get an immediate ‘full tank’ of blood sugar, to enable us to do whatever it is one does in a rhinoceros crisis.
So fine, all we need to do is tank our insulin, and raise our cortisol as often as possible, and our fat will melt away, right? Wrong. Cortisol raises our blood sugar, and while that’s entirely appropriate if it’s low, or if we suddenly need to run, what if there is no rhinoceros? It’s not just times of acute stress that raise cortisol – any stress will do it.
Stress is now an epidemic in our modern society. Historically, our lives were hard, but simple. We had only to find food, and have children. Our small communities were limited in size and scope – unconcerned with the complexities of the world as a whole. We knew few people, but knew them well, drawing on our community, our tribe for support and affirmation. Now, we isolate in tiny family units, separated from the direct support of communal living, separated even from our extended families. We concern ourselves with issues of global importance, over which we have no direct control. Our livelihoods are dependent on myriad factors over which, again we may have no control. We know hundreds of people, but can draw little support from any of them. We worry about our past, present and future. Many of us are plagued by chronic sleep problems, lying awake, endlessly scanning the web on our bright, backlit phones. That lack of sleep, and the caffeine we consume in its aftermath, further contribute to these constant spikes in cortisol, resulting in chronically elevated blood glucose. And because we never actually have to run away from a rhinoceros, that glucose needs to be put back into storage, driving up insulin to get the job done.
Furthermore, we all know what happens when we’ve had a poor night’s sleep – it makes us crave sugar. We don’t head down to breakfast thinking about boiled eggs, as much as steaming piles of buttered toast, slathered with strawberry jam. Our poor sleep affects the balance between another pair of hormones that influence our hunger, and satiety – ghrelin and leptin. While we can measure that increase in ghrelin, it isn’t yet clear why that hunger is specifically for such carb-centric foods – but we’ve all experienced that feeling.
Cortisol also drives the deposition of abdominal fat. While this isn’t relevant in the context of infrequent, transient spikes, if cortisol is chronically high, this characteristic drives the apparent migration of fat from relatively safe storage in peripheral areas, to harmful abdominal deposition – it moves our fat to the bad place.
We can’t have a conversation about fat loss, without mentioning thyroid hormones. The thyroid gland is the primary regulator of our metabolic rate. It receives messages from the pituitary gland and the hypothalamus, instructing it whether to turn the wick up or down – whether it’s ok to increase our energy use, or whether we need to restrict it, to hold on to our fat stores. Its activities depend on the complex interaction of a number of thyroid-specific hormones, as well as others like cortisol. By undereating or overtraining, we can provoke a downregulation in thyroid hormone production, slowing our metabolism. Equally, there are a number of diseases that affect us in a similar way, like Hashimoto’s Thyroiditis.
The diagnosis of thyroid problems is tricky, because of the way the various hormones affect each other – a practitioner has to be able to tease out where the problem lies in this complex feedback loop – the pituitary gland? The thyroid itself? Maybe the downstream conversion of T4 to the active T3 hormone?
To muddy the waters even further, low carbohydrate diets may increase the efficiency of thyroid hormones, making adequate levels appear low, while the caloric restriction that these diets can encourage may result in a genuine deficiency – if we don’t eat enough, we will begin to suffer with the symptoms of hypothyroid, something which happened to me while following a calorie-restricted zero-carb diet for a long period of time. I was constantly cold, even in warm weather, tired, lethargic and weak.
I’m not a clinician, and have neither the knowledge nor experience to offer any specific suggestions on the diagnosis and treatment of these sorts of problems. But I can say that if you have symptoms of hypothyroidism, if you’re cold, tired, lacking in energy, or feel that you’re unable to lose fat despite maintaining what should be a calorie deficit, you should get some medical advice. The same goes for any hormonal problems. A doctor who specialises in hormone-related problems has very kindly agreed to come on in a future episode, and talk about these things in more detail. If you have questions, please comment, or get in touch privately.
So what we start to see in this highly simplified depiction, is that the natural ballet of these hormones, their elegant ebb and flow as they maintain homeostasis, becomes replaced with a dysregulated, unbalanced mess. As we repeatedly attack that finely-tuned mechanism with excessive quantities of sugar, chronic stress and poor sleep, we inhibit our ability to burn fat, inflame our fat cells, reduce our metabolic rate and increase the breakdown of that muscle that we so badly need to retain. We ultimately cause a state of serious chronic disease, that due to the complex dependencies within the system, affects almost every aspect of our general health. The very habits that drive us to become obese, upset the balance that enables us to effectively lose fat.
For most of us, the root cause of our problems is not the hormones themselves, but the ways we continue to drive them. While for some people, significant damage has been done, and they need some additional medical intervention to get back on track, all of us need to stop putting the wrong fuel in the tank.
In the next episode we’ll look at what to do about all this – the actionable steps we can take to get control of our bodies, and lose fat.
Disclaimer: I am not qualified to give any sort of medical or dietary advice, and nothing in this material should be considered as such. The opinions expressed here are my own, and for the purposes of discussion only. Please consult a qualified medical professional before undertaking changes to your diet.
Why We Get Sick – Dr Ben Bikman (2021 Benbella Books ISBN 978-1953295774): https://www.amazon.co.uk/Why-We-Get-Sick-Epidemic/dp/1953295770/ref=tmm_pap_swatch_0?_encoding=UTF8&qid=1622802479&sr=8-1
How To Reverse Insulin Resistance, Lose Weight And Thrive, With Dr Ben Bikman – Fast Keto With Ketogenic Girl Podacast: https://podcasts.apple.com/ca/podcast/fast-keto-with-ketogenic-girl/id1344681226?i=1000521137810&fbclid=IwAR19fNERGNbVQlPD79OOyisW5fdmO5-fWO37OD3IZfLrPabTXDV-2zscowk
Does Your Thyroid Need Dietary Carbohydrates? Dr Stephen Phinney: https://www.virtahealth.com/blog/does-your-thyroid-need-dietary-carbohydrates
How To Optimize Your Thyroid, With Elle Russ – Fast Keto With Ketogenic Girl Podcast #21: https://www.ketogenicgirl.com/blogs/fast-keto-podcast/episode-21-how-to-optimize-your-thyroid-with-elle-russ?_pos=1&_sid=8ce7ea9c4&_ss=r
Assorted Diabetes Treatment Research From Virta Health: https://www.virtahealth.com/research#Papers
What causes the insulin resistance underlying obesity? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038351/
Waist to height ratio as a new marker of metabolic syndrome in type 2 diabetic patients: https://www.researchgate.net/publication/303527089_Waist_to_height_ratio_as_a_new_marker_of_metabolic_syndrome_in_type_2_diabetic_patients
Waist-to-height ratio as a risk marker for metabolic syndrome in childhood. A meta-analysis: https://pubmed.ncbi.nlm.nih.gov/29700992/
Waist to height ratio: a better anthropometric marker of diabetes and cardio-metabolic risks in South Asian adults: https://pubmed.ncbi.nlm.nih.gov/23298662/
Chronic stress and diabetes mellitus. Interwoven pathologies: https://pubmed.ncbi.nlm.nih.gov/31713487/
Deconstructing the role of glucocorticoids in adipose tissue biology and the development of central obesity: https://www.sciencedirect.com/science/article/pii/S0925443913001919Cortisol responses
Normal weight individuals who develop type 2 diabetes: the personal fat threshold: https://pubmed.ncbi.nlm.nih.gov/25515001/