Dr. Jade Teta, Naturopath, author and podcast host, joins our ambassador Emma Sutherland, as he describes the connection between metabolism, hormones and weight management.
Working to define metabolism, Jade debunks the calorie-in vs calorie-out paradigm often relied on for weight management, replacing it with a holistic view of metabolism as a sensory apparatus within the body operating to respond to multiple stimuli including stress, hormones and temperature. Describing the difference between metabolic flexibility and inflexibility, Jade highlights the benefits of both a short and extreme diet and a gentle and prolonged diet for weight management.
Turning to hormonal influences, Jade and Emma discuss the role of leptin, insulin, oestrogen and progesterone on metabolism and in turn, weight management.
Covered in this episode
[00:48] Welcoming Dr. Jade Teta
[02:06] Metabolism is more complex than ‘calories in and calories out’
[08:13] Metabolic flexibility and adapting to stressors
[12:57] Assessing metabolism in patients
[18:00] How we can combat leptin resistance
[26:33] The Goldilocks Principle of cortisol
[35:28] Hot and cold therapy and cortisol levels
[37:54] Oestrogen and its effects on weight and metabolism
[48:17] Thanking Jade and final remarks
- Metabolism can be thought of as a sensing apparatus that responds to stimuli by influencing the activity of hormones including oestrogen, progesterone, testosterone, leptin and insulin. Stimuli can include environmental cues such as light, temperature, season, stress, food security, nutrient status, body health among others.
- Hormonal imbalances can lead to dysregulated weight gain/loss.
- Metabolic flexibility or an adaptive metabolism should be the focus of weight management. Rigid routines throughout the day and around eating, exercise and other metabolic stimuli can reduce metabolic flexibility.
- Calorie reductions of 30-50% are considered extreme and may only be suitable for short periods of time as the metabolism will adapt to this. Reductions of between 30-10% are considered less intense and may be done for longer periods.
- Weight loss success is defined as a 10% loss in body weight sustained over a year. Of this, only 5% of people are able to achieve and sustain successful weight loss.
- Metabolic assessment is best done by reviewing the patient’s signs and symptoms including:
- Weight loss and body composition during weight loss program
- Pathology including HbA1C, fasting insulin, thyroid panel, heart rate variation, CGM data
- Leptin is released by adipocytes and signals satiety and adequate fat stores to the brain prompting it to stop seeking food. Leptin also functions to stimulate the adrenal and thyroid glands to increase the basal metabolic rate to burn fat.
- Leptin and insulin resistance and an inflexible metabolism may impede the body’s ability to undergo beta oxidation with liberated fat, causing the fat be stored again rather than used for energy.
- High levels of circulating leptin, like insulin, can result in leptin resistance, reducing the satiety signalling to the brain, preventing the brain from shutting down the hunger sensation. Leptin resistance therefore can lead to increased or insatiable hunger, reduced thyroid and adrenal function and changes to reproduction.
- Cortisol is naturally anti-inflammatory, that with chronic stress can cause the hypothalamus to become less responsive, and is antagonistic to insulin and insulin receptors. Eating, sleeping and exercise in line with the circadian rhythm is important for cortisol regulation.
- High intenisity exercise is associated with an increase in cortisol levels. When this continues for an extended period, or too hard or often, this may contribute to dysregulated cortisol levels.
- Temperature regulation can contribute to cortisol regulation, with hot and cold therapy influencing cortisol levels.
- Oestrogen and progesterone can influence fat distribution and deposition, insulin resistance, cortisol regulation, neurotransmitter levels, thyroid function and tissue growth amonth other factors that can influence metabolism, which can be seen during menopause.
Resources Discussed and Further Reading
Dr. Jade Teta
|Dr. Jade Teta|
|Books by Dr. Jade Teta|
|Article: ‘The Law of Metabolic Individuality’, Metabolic Living, 2021|
|Article: ‘The two factors needed for weight loss’, Metabolic Living, 2021|
|Article: 'Why dieting doesn’t work’, Metabolic Living, 2021|
|Research: ‘Immunometabolic links between estrogen, adipose tissue and female reproductive metabolism’, Biology, 2019|
|Research: ‘Effect of circadian rhythm on metabolic processes and the regulation of energy balance’, Annals of Nutrition and Metabolism, 2019|
FX Medicine acknowledges the traditional custodians of country throughout Australia where we live and work, and their connections to land, sea, and community. We pay our respects to their elders past and present and extend that respect to all Aboriginal and Torres Strait Islander peoples today.
I'm Emma Sutherland and joining us on the line today is Dr. Jade Teta, Naturopath, author, and podcast host. Jade's primary area of specialty is integrative endocrinology, and more specifically, hormones and metabolism. Jade's latest book is called Next-Level Metabolism, and in it he discusses how to heal metabolic damage, balance hormones, and successfully lose fat.
Now today, we're going to deep dive into the world of metabolism, looking at the hormones and the roles they play, as well as so much more. Welcome to FX Medicine, Jade. Thanks for being with us today.
Jade: Thanks for having me. Emma, I'm excited for the conversation. It's going to be fun.
Emma: Yeah, totally agree I can't wait either.
Now, just to set the scene, in June of last year, the World Health Organization stated that worldwide obesity had nearly tripled since 1975. According to Australian Bureau of Statistics data from 2018, 67% of adult Australians are overweight or obese. The link between obesity and chronic diseases like insulin resistance, diabetes, non-alcoholic fatty liver disease, and cardiovascular disease is well known.
Now as clinicians, I'm sure we can all relate to the following scenario. A patient comes in saying “I need to lose weight.” You then look at their food diary and they're not eating that badly and it's mainly pretty healthy food, and they go to the gym regularly. But what is happening hormonally with these patients?
There are well-known drivers for metabolism, including genetics, gut microbiota, sleep, ageing, and excess energy consumption. But today, I want to deep dive into the role of hormones and weight. We know hormones regulate appetite and satiety. But what is happening beyond calories in and calories out?
So let's kick off with some basics. Jade, what actually is metabolism? And what influences it?
Jade: Yeah, well, the best way to think about metabolism in my mind is as a sensing and responding apparatus. And I want to break that down a little bit because if we look at the way it is currently seen, most people…and let's just go through the evolution of this really quickly. When we think about the way metabolism has been described historically, it is usually described in my mind as a metaphorical calculator, right? It's basically this idea of like, we're going to manage our energy resources, and it's calories in, calories out.
Jade: It's an addition or subtraction problem from the old model, the calorie model. Now, the truth of the matter is the metabolism does have some ability to track and sort of count in a rough crude, calorie counting way or calculator way, what is going on with its fat cells. For example, leptin is a hormone that is released from fat cells, and we all know that speak to the brain and say, “Hey, brain, we've got about this much fat on our body.”
The problem is that that model, that calculator model falls apart pretty quickly, once you begin to cut calories and/or exercise more, the metabolism begins to budget itself. And so the calculator model has not really served us. And so a lot of us started to upgrade that model. And we started to talk about the metabolism as more like a chemistry set, where we went to this hormonal model where it's like insulin and leptin and cortisol and oestrogen and progesterone and testosterone. And if we get the hormonal balance correct, we should be able to lose weight. And the fact of the matter is, that also has not really panned out too well for us.
Now, of course, calories matter, and the calculator model is somewhat correct. And of course, hormones matter. And the hormonal model is somewhat correct, but they're both not complete and somewhat incorrect. And so when we think about the sensing and responding apparatus, that is the metabolism, it looks out into the environment. It says “What is out there in terms of light and temperature and season? What is out there in terms of food availability? What is out there in terms of danger?” And then it also takes signals from inside the body and gathers up those things. What does the liver need? What's my nutrient status? What's going on with the signals that the microbiota are sending? What's going on with inflammatory signals and infection, things like this. And it merges those two things to plot a course back to balance.
So, to me, we should never really give a simplistic metaphor for metabolism, because it's too complex. But if we're forced into it, this looks a little bit more like a stress barometer, a pressure barometer, or a stress barometer, and a thermostat. This is more what we should be thinking about with the metabolism, it looks at how much stress is in the environment.
Jade: It looks at how much stress the cells inside the body are under. And then it adjusts and adapts and reacts like a thermostat. And so it does have some calculator-like properties, it does have some chemistry set-like properties. But it probably most resembles a thermostat and a stress barometer.
And so if we understand that, we can start to understand that really, any stress, whether too little or too much food, too little or too much movement, infection, injury, inflammation, social pressure, even if we think...even if we're not under pressure, but we have a perception that we are, this is all registered as stress, and then the metabolism has to respond. And this is how we should be looking at the metabolism. It is not about trying to speed it up. It is about trying to make it more resilient. It's not about having a fast metabolism. It's about having a more flexible, resilient, and adaptive metabolism.
And I think this is the most succinct way, right now, with the limited information that we have about metabolism, this is the best way to look at it. And when we look at it this way, it does begin to change our way of dealing with it because it does start to take into account when we cut calories, why the metabolic rate slows down, why we end up getting excess hunger and cravings. The old models don't really account for that. So that is how I see metabolism and how I think we want to be viewing it moving forward.
Emma: Yeah, I really love that analogy. And I agree, that stress barometer, which adapts according to internal and external cues, in order to maintain balance, that's a great way for us to reframe metabolism, and be a little bit more holistic around metabolism.
But you mentioned metabolic flexibility, and this concept fascinates me. I mean, how do we achieve it?
Jade: Well, one of the things that you don't do with a system that you want to be flexible, is force it into rigid patterns, I think. So in other words, doing the same thing, day in and day out, week in and week out, month in and month out, year in and year out, may not be the best approach. Because when you think about a flexible, reactive, and adaptive system, it will have reacted to anything you do on a regular basis.
And so one rule here is that if you cut calories sharply, and you start exercising a lot, and that is your only approach, and it is the continuous approach and it's the only thing you ever do, and you keep trying to force your will on metabolism, it's going to essentially adapt and react. And we can talk about the ways that it adapts and reacts, but it's going to adapt. And if you keep doing the same thing, it's going to be laughing at you saying “Look, I adapted weeks and months ago. You keep trying to do the same thing. I'm not going to respond.”
And so I do think we need to look at this as taking an approach that is not a continuous, static, predictable, linear approach. That this might be a better way to look at this and by the way, if you look at this from the standpoint of stress, one hint here is the following:
If you study stress, you know that the body responds to stress in different ways. It does not like prolonged extreme stress. If you're going to have an extreme stress, it has to be very short and the body will react to extreme stress that is short, it tends to adapt to that stuff, it tends to have an adaptation response from extreme, short periods of stress.
And it also responds fairly well to very gentle, long stresses. And so if we are going to diet, I think the best approach might be and of course, this needs to be worked out in science. But we do have some hints that this is the case and we can talk about it. The best approach might be either very short, extreme calorie reductions that then return back to maintenance, and/or a very gentle, a prolonged calorie reduction. And that we might want to be rethinking this very long duration, extreme calorie reduction. And by the way, let's give numbers to this.
Emma: Yeah, good.
Jade: Most of the time when you look at the research, we're talking 30% to 50%, reductions in caloric intake, over the long run.
Jade: Those are extreme levels, right? So 20% to 30%, maybe. Maybe, if we can do 10%, 15%. But right now I operate, if we can do 20% or less reduction in calories, maybe that's not going to be as intense as the 30% many studies use. And if we are going to go above that 30%, then maybe we need to have those diets last for a shorter period of time.
And so if we want to work with a flexible adaptive system, we have to understand the way that the metabolism reacts to stress. Extreme continuous chronic diets probably aren't going to be the approach that we need to use. And we have the data to show us this, by the way. People who try these approaches, only about 5% lose the weight. Which in research, by the way, just so we can all know what we're talking about, success is defined as 10% loss in body weight sustained over a year.
Jade: So only 5% of people are able to do that, which means 95% of people either can't lose the weight, and/or can't sustain that 10% weight loss over the course of the year. That number drops to 97% at year two, and drops to basically 99% at year three. So obviously the model we are using is not working.
Emma: Yeah, agreed. And as clinicians, we all see this in our clinical practices that patients struggle because of this rebound situation. And for us as clinicians to understand metabolism better, so that we can have more effective conversations with our patients, is absolutely critical.
I'm curious Jade, what are the best ways to actually assess metabolism? I mean, I love using a two-hour glucose tolerance test to assess insulin and glucose sensitivity. But what markers do you actually use to both assess and then monitor your patients?
Jade: Well, this is a really, really good question. And I think that for me, the best way is the same way we learn and assess about other diseases when we begin to diagnose, and that comes from signs and symptoms. So the metabolism is getting biofeedback all of the time, it is releasing signs and symptoms. Most of these things are either directly impacted by or directly caused by hormonal situations in the body.
So things like sleep. Is the sleep fragmented, and difficult? If it is, this tells us that the metabolism is probably less flexible and more rigid. Is hunger insatiable, and constant? If it is, this tells us the metabolism is probably more rigid. Are cravings unrelenting and continuous? What about energy levels? Is it unpredictable, low, and unstable? And this to me is a little funny term I've become famous for, I call it SHMEC, S-H-M-E-C. It's an acronym. Pronounced SHMEC. It stands for sleep, hunger, mood, energy, and cravings.
Jade: But to me the first sign and the first way to assess metabolic flexibility, or metabolic rigidity is your SHMEC, sleep, hunger, mood, energy, craving in check, or is it out of check? Now, by the way, sleep, hunger, mood, energy, and cravings, SHMEC, is really a catch all phrase for all biofeedback, so it also includes things like exercise performance and exercise recovery, menses, libido, erectile function, digestive function, joint pain, headache, signs and symptoms, immune reactivity, how likely you are to get a cold and a flu every season, those kinds of things.
So to me, the first way to assess metabolism, and its ability to be flexible or not, is that when you go on a diet is SHMEC in check? Or does it quickly go out of check.
Jade: So that's the first thing. The second thing would be, how likely and how effective is this approach, changing body composition. Not just weight, but body composition, is the person losing fat?
Emma: Yeah, critical.
Jade: That in my opinion, easiest way to set that is look at inches and weight, rather than just weight. If the weight is going down slowly or not changing at all, but you're losing inches, this is a great indication you are losing fat.
And then finally, we can get a little faster with continuous glucose monitors, things like hemoglobin A1C, fasting insulin, thyroid panels, heart rate variability, these kinds of things, right? So we tend to, I think, as clinicians, we tend to jump to labs and vitals first. But the truth of the matter is, those things aren't really necessarily going to be showing up until the dysfunction becomes disease. Right?
So what we want to do is catch this early, and if we're talking about just weight loss, most of these people aren't going to have dysfunction, necessarily, or disease, they're going to just be having signs and symptoms of being unwell. And most of us who are functional medicine practitioners know very well that long before you start seeing blood laboratory derangement, that there's going to be dysfunction showing up in the way the person looks and feels and functions in our everyday lives. And this is why I think SHMEC and body composition is probably the best place to go. But all three matter. So we should be using all three the way the person looks, functions, and feels, as well as vitals and blood labs. If that makes sense.
Emma: Yeah, and those signs and symptoms are primarily what drive patients in to see us. They'll have disturbed sleep. They'll have unpredictable energy, insatiable hunger, and cravings. I mean, these are the things that people deal with daily that actually, make them pick up the phone and come in to see us.
And I love, Jade, that you said look at inches as well as weight because people do tend to get fixated with a number which is inappropriate. And I think there is something to be said for the concept of body recomposition where we aim to replace fat with muscle.
And looking at those labs where you can, the HbA1C the fasting insulin, the thyroid panel, and I do love continuous glucose monitoring myself, both personally and with my patients to help assess their response in real-time, to food. Some great points there, Jade.
I wanted to just have a quick chat around leptin. We know it's released by fat cells in white adipose tissue and it signals to your brain that you're full and you have enough fat stored and leptin helps regular long-term weight control.
Now leptin resistance is something that is not discussed enough, in my opinion. I see it a lot in clinic. Can you explain what leptin resistance is? And I'm actually really curious because I was reading a 2021 review showing that giving leptin as an intervention doesn't work for weight loss, as the leptin receptor sensitivity has been so blunted. So if we have a patient that comes in and we do test their leptin, and it's elevated, what do we do for these patients?
Jade: Yeah, well, so first of all, I mean, just to make sure I'm sure everyone knows, so I'll just do a brief review for people who may have forgotten about leptin. But leptin is released from fat cells, it essentially goes to the brain. And it tells the brain “Hey, look, here's how much fat you have on the body. Here's how many calories you have stored away.” And the brain in response when the brain is functioning normally, should say, “Oh, okay, we got plenty of fat on the body. So let's stop being so hungry.” So typically when leptin goes up, the brain says “Shut down hunger.” It also has some degree, it looks like, effect on craving to more highly palatable foods. So cravings also should decrease.
The little other known things that leptin does is leptin will go to the adrenal glands and essentially to our thyroid gland and say, “Hey, you know what, maybe we need to bump up metabolic rate a little bit.” And it probably has some effects on mitochondrial function, perhaps. There's some indication it might be having some impact when it binds to other cells, on speedy fat burning. But it mainly works, so far as we know, through adrenal function and thyroid function to up-regulate basal metabolic rate, thyroid mainly binds and then begins to burn fat. So those are all well-known sort of aspects of burning fat.
And one thing I do want to say here just briefly because I even think clinicians get confused on this. Let's all remember the difference between lypolosis, the release of fat, and the burning of fat, they're not the same thing, right? When fat is burned, first thing that has to happen is it gets released from a fat cell, and then has to travel to the cell that's going to burn it, it's a muscle cell that needs to be taken into that muscle cell. And then it's essentially burned through beta-oxidation. Now, a lot of people that if fat is released, that that automatically means fat is going to be burned. But in a very rigid non-flexible metabolism like metabolic syndrome or insulin resistance or leptin resistance, oftentimes, you have no problem releasing the fat or you'll release the fat, but then it just gets restored because it can't be burned.
Now, leptin's job is to essentially say, "Brain, stop eating so much, and body, start burning fat."
Jade: Now, what happens when leptin is around for very high amounts for a long period of time, it's the same thing that happens with insulin — which by the way, we're starting to see this happens with lots of different hormones, including hormones like oestrogen and other hormones — hormone resistance begins to occur, the body regulates those hormonal signals by downregulating leptin receptors. So you become leptin resistant. And when that happens at the level of the brain, the brain never gets the signal that it has a lot of fat stores and therefore, rather than shutting hunger down, it doesn't change hunger, or maybe even increases it.
And so leptin resistance causes increased hunger. Leptin resistance causes less thyroid function. Leptin resistance causes less adrenal output. And by the way, leptin also speaks to the gonads, testicles and ovaries and has effects on reproduction, as well. So leptin resistance has far ranging sort of issues that come up for it.
Now, you ask the question, how do we begin to reverse leptin resistance? And this is the catch-22. Because obviously, if you've become leptin resistant from eating too much, so you might think that, “Okay, now all I need to do is the reverse, I'll just eat less and exercise more.” And what will happen is leptin will begin to drop, but oftentimes that's going from one stressful state, very high leptin, to also now very low leptin. So dieting typically causes leptin levels to plummet, especially if it is a very strict diet.
Jade: And so what we're perhaps doing wrong is we're perhaps going too extreme on the dieting. And the best way to reverse leptin resistance is to begin to go into a diet that is either very short and extreme or very long and gentle.
And also a diet, that controls hunger, because here's what's going to happen, there'll be excess hunger will occur and cravings when you're leptin resistant. But then when you go on an extreme diet and start burning a lot of fat rather than storing it, leptin levels fall, which is basically the same thing, right, now you're also not getting the leptin signal that you want and hunger goes up. Both issues, leptin resistance where leptin is very high, and falling leptin where leptin is very low, cause hunger and craving. And so whatever diet you use, needs to control for hunger and cravings. So not only do you need to take either an extreme, short approach or a gentle, long approach, but you need to do something to control hunger.
Jade: That hopefully doesn't have a whole lot of calories and all, with it. And we do have some tools here. Fibre, protein, and water seems to be the best things to help with hunger.
Now, this is somewhat individual, depending on the patient in front of us. Most people respond very well to higher protein diets to shut down hunger. Some people are vegans and vegetarians, so we can't get the protein on board, so maybe we have to use more fibre. But fat also can be, especially if we can get people into a ketogenic state where we're producing ketones, ketones also seem to be pretty hunger suppressing. And so the way to reverse leptin resistance in my mind is threefold. One, begin to control the stress of dieting, don't do extreme dieting for long periods of time.
Jade: And also control hunger by ramping up the percent of food in the form of protein, fibre, and water. And we also could potentially use a ketogenic diet for those that is appropriate for to help with this. And this will begin to address some of this leptin resistance.
Right now, to your point, Emma, we can't just give people leptin injections and expect for it to work with dieting, because hormones work in a symphony. They behave differently, depending on the other hormones they're socialising with. It is virtually impossible for us every time we try to isolate a hormone, and give it in isolation and expect for those effects to be isolated, it all falls apart because it depends on the other hormonal environment that is around, if that makes sense.
Emma: Yeah, it makes complete sense. And I think that that shows the nuances of hormones and the interconnectiveness of hormones.
But I also think, from a clinical perspective, if we understand fundamentally that the stress of dieting is a big factor, and patients will have come in, and they've already done those extreme diets, and they've rebounded their weight, and it's not working. And I really like that concept of trying either a long and gentle approach, or we do a short extreme approach, and that that concept of diet breaks and pulsing as well can be really helpful. But always controlling that hunger. I mean, we know fundamentally that our patients are not eating enough fibre or water, having enough water or enough protein, and getting their diets more aligned with that is going to be really helpful on that side of things.
I wanted to just shift gears a little, Jade, and discuss cortisol because I know you've done a lot of work in this space. And as part of our fight-flight response, cortisol is naturally anti-inflammatory, which sounds super helpful from a metabolic perspective. But with chronic stress, cortisol is consistently elevated, which causes the hypothalamus to become less responsive. Once again, this receptor side of things comes up. And this can shift cortisol into having a net pro-inflammatory effect. Can you comment on this? I mean, cortisol can be both fat burning and fat storing. So talk to us a little bit more about this.
Jade: Yeah, well, I call cortisol the “Jekyll and Hyde hormone.” And so Dr. Jekyll was this very gentle, introverted man who drank this potion that brought out his evil side, right, Mr. Hyde. And so hormone cortisol can be either the Dr. Jekyll, very helpful and beneficial for us, or the Mr. Hyde. And it works on the Goldilocks principle, too much cortisol or too little cortisol brings out Mr. Hyde. So we need it, but we need it in just the right amount. And the way to think about what it does, is if you think about the metabolism as a sensing and responding apparatus... You said it just right, Emma, that the hypothalamus and pituitary is the command and control centre. It is the satellite dish that is pointing into the body and also outside of the body. So imagine a satellite that is taking signals from outside. It's got two dishes, let's say. One dish pointed inside the body and taking signals from inside the body. And another dish looking outside the body.
Jade: Cortisol causes this sensing apparatus to become scrambled. It basically puts earmuffs on the satellite, so to speak. And now the hypothalamus can no longer release its other hormones appropriately. So signalling to the pituitary can be disrupted and then downstream signalling to the adrenals, the gonad, and the thyroid hormone can be impacted from there. And this is why when we give adaptogens and we reduce stress, we oftentimes see that we get multiple effects. So people go “Well, is this an adrenal effect?” We used to think back in the day that adrenals fatigue.
Jade: Adrenals really don't fatigue and adaptogens don't really work on the adrenal system. They're working on the brain and the adrenals are being impacted by the downstream effects of hypothalamus-pituitary-adrenal, hypothalamus-pituitary-thyroid, and hypothalamus-pituitary-gonadal function. So that's the first thing cortisol does, is scramble that system. Now we all know how important that is.
The other thing cortisol does that a lot of people don't realise, is cortisol is incredibly antagonistic to insulin and the insulin receptors. And so the more cortisol there is, the more insulin resistant you become. Now, a lot of people don't understand this because we tend to think about insulin resistance as being something that happens when you eat too much. But you can also stress too much because cortisol is antagonistic to insulin.
The other thing that's interesting about cortisol is you get a cortisol-release impulses. One of the things that happens is when you eat, cortisol is released because it acts as an anti-inflammatory. You've got all this foreign substance that we have to translate into sort of friend-food, and cortisol will be reactive during that time. Cortisol also is reactive when we fast, because cortisol...remember, glucocorticoid, it's in the name, it manages glucose, and so it will raise glucose levels and antagonise insulin.
And so cortisol is doing a ton. And yes, it has pretty profound impacts on our immune system, mainly reducing our first line of defence of secretory IGA, the immunoglobulin A, and it does a ton more. So what we want to do is we want to get cortisol reacting appropriately again. And so to get it reacting appropriately again, cortisol is pretty diurnal in the way it functions. And so we can use our circadian clock to help cortisol and we also can use our food timing to help cortisol, cortisol is meant to rise in the morning, basically, as soon as you get up, and it's meant to fall at night. And so by waking up with the light, exposing ourselves to light, getting outside, and getting our eyes exposed, we help that cortisol response at night.
Jade: And by dimming our lights and preparing for nighttime and reducing our food intake at night, we can begin to lower cortisol. So rule number one with getting cortisol to be in the Goldilocks zone, once again, is to start paying attention to our circadian rhythm. Glucose intake mainly in the morning, less carbohydrates at night. More light exposure in the morning, less at night, these kinds of things. And of course, with many of our patients, we can begin to use adaptogens. But I think the biggest way to begin to address what's going on with cortisol is to help people get back into alignment with their circadian rhythms, and also get the stress load off the system. So many people “I got to do this, I got to do that, I got to avoid this, I got to avoid that.” Actually, our functional medicine sort of environment sometimes adds to the stress when we start telling people there's toxins on every corner and you shouldn't eat this and you shouldn't eat that and avoid this and avoid that. We need to get people to woosah a little bit, to relax, to om, move into... And that's the other second way. Get them into really paying attention to rest and recovery when it comes to cortisol.
And then the other final thing is, exercise is really interesting, right? Because exercise, all exercise, will increase cortisol and we do not want not to have that. That is a beneficial effect. Intense exercise, long duration exercise should raise cortisol, and that's a really good thing. But then we want cortisol to fall pretty quickly after that. And so we have to realise that if we exercise too hard, too often, or too long, too often we're possibly disrupting this cortisol rhythm as well. And so we want to balance our intense and prolonged activity with relaxing activities. Things like creative pursuits. Things like meditation and massage. Things like sex and orgasm. Things like time with pets, relaxing music, time in nature, and all the things that can lower cortisol. Perhaps the best thing to balance cortisol is walking. And not power walking because that might raise cortisol but nice, relaxing nature walking, has the effect to lower cortisol.
The Japanese researchers have shown that it is actually more pronounced when it's done sort of slower and in a more meditative way in a nature setting. And walking also, not only does it lower cortisol but it also sensitises the body to insulin. It's one of the few types of activities that does both. It's also incompatible with eating for most people unless you live in the United States, and I don't know how it is in Australia, but yes, in the United States you will see certainly people out walking and eating, but for most people, that's not the case.
Jade: So that's the story on cortisol. It is really important. And it does speak to our current environment of go, go, go, stay up late with bright light on our faces that kind of thing. We have to begin to pay attention to this stuff.
Emma: Yeah. And look, one thing that you said which I think is such a good reminder for myself and our listeners, is not to sort of overwhelm patients and go back to the basics, those tips that you spoke about, food timings that work with the cortisol-circadian rhythm, eat more in the morning and less at night and reduce your light exposure at night, get up with the sun. Reduce your stress load, ensure there's rest and recovery happening, that involves relaxing activities, and walking, especially walking in a green environment. Those things can really work synergistically to reduce our cortisol levels, and then have it more the Dr. Jekyll, the helpful form of cortisol in our bodies, I've really liked those reminders. So important.
Jade: Yeah, and one other thing I'll say here, Emma, that is kind of cool. One of the other things you can do to help with cortisol and stress, in general, is temperature regulation, and temperature exposure. So very short exposure to cold, and/or hot, can help with cortisol. For example, we know that cold exposure first thing in the morning can increase norepinephrine, epinephrine, and cortisol. And warmth at night can begin to lower cortisol.
One of the interesting things about temperature exposure at night too, is that you've got to kind of think about the way that heat has an acute effect on you and cold has an acute effect on you, but then heat and cold also have an adaptive response. So obviously, if you heat yourself up at night, with a hot shower or hot bath or hot sauna, what happens is all the blood vessels dilate, they start to dissipate heat and to cool the body down. Well, we all know that that cooling sensation of cooling the cooler down is a natural signal for bedtime.
Jade: And regular sauna bathers have been shown to reduce cortisol levels. And so cold might be something we can use to raise cortisol when we want it high. And heat might be something we can use to lower cortisol levels. And these temperature effects also can have very beneficial effects in helping us do better with this rest and recovery activity.
The final thing I'll say here is that when it comes to alternating hot and cold, so-called contrast hydrotherapy, where you go from hot to cold, back to hot, back to cold, over and over again, this is a great way to exercise the hypothalamus.
Jade: And to get it to be a little bit more sensitive because remember the hypothalamus, one of the things it also does is regulate temperature. Now of course this would need to be studied, but I have a theory and a hypothesis that one of the reasons contrast hydrotherapy has been shown to be so effective in things like immune function and reduction of Alzheimer's risk and cardiovascular benefits, reducing risk of cardiovascular disease, is that it really is helping manage cortisol and making the hypothalamus-pituitary axes, adrenal thyroid, gonadal, more functional. So those are all things I think we as clinicians can be looking for to help the system.
Emma: Yeah, yeah, some really great pointers there. And it is about working upstream and downstream, coming from both angles is always going to be a good thing.
I’ve wanted to pick your brains on oestrogen. Now a decline in oestrogen can cause changes in fat distribution and an increased storage of abdominal fat. And you have written oestrogen is insulin-sensitising, making it less likely that excess calories are stored as belly fat, and more likely a calorie deficit results in fat loss rather than muscle loss. So can you share with us how oestrogen levels affect metabolism and a woman's weight?
Jade: Yes. And one of the things that we should do is that whenever we talk about oestrogen, we really need to talk about her twin sister progesterone because they really do work together. I say twin sister because I do think the best way to learn this is to think about oestrogen and progesterone as non-identical twin sisters. They're twin sisters because they are absolutely dependent on each other. They're non-identical twin sisters because they don't do exactly the same thing.
Now oestrogen is the sister who's the go-getter. She's the type A athlete, wants to go, go, go is very rambunctious, very adventurous. She is very strong. And progesterone is more sort of a nerdy sort of relaxing more painter, more writer, more like motherly, wants to stay home, more introverted of the two sisters. And you can imagine if oestrogen gets out of control, either oestrogen is not around and nothing gets done. But if oestrogen is too much, she gets in trouble. So progesterone is always trying to regulate and protect her sister oestrogen.
Now, oestrogen dominates most of the time, progesterone mainly plays a regulating role here. And oestrogen is insulin-sensitising to the body, which essentially means that when you are overeating, oestrogen makes it more likely that those calories will be stored as muscle. Certainly, you'll store some as fat but it will make it more likely that the woman stores fat as muscle. If the woman is dieting and stressing herself out with very low carbohydrate diets when oestrogen is around, she'll be more likely to lose fat and less likely to lose muscle. So oestrogen is a really, really good one to have around.
Also, oestrogen helps amplify dopamine and serotonin levels in the brain, which together, you know, people think of serotonin is relaxing, but it is but it's mainly a self-esteem oriented sort of feeling and makes you feel good about the world. And dopamine certainly is a neurotransmitter that allows us to fall in love with the process of achievement. So it's very driven and goal-oriented and likes that. So that's what oestrogen feels like. Now, when oestrogen begins to dominate, she begins to have negative effects on thyroid function, she begins to have negative impact in certain areas of the body. Tissues begin to overgrow, leiomyomas or fibroids, endometriosis, these kinds of things begin to dominate.
However, one of the things that she's really good at is she's really good at keeping fat off of the midsection, that hourglass shape is mainly driven by oestrogen and it has to do with oestrogen's dual impact on sensitising the body to insulin and reducing cortisol and keeping control of cortisol. And so oestrogen is really good at that.
Now progesterone her twin sister helps oestrogen's cortisol but antagonises oestrogen's impact on insulin. So progesterone is insulin desensitising. Progesterone causes more insulin resistance. And for those of you who are confused about that, think about it like this, that post ovulation, that's when progesterone start to make herself known. Post ovulation, there might be a baby coming along. So it makes sense to have increased triglycerides, blood fat and increased glucose around in case that egg gets fertilised and you have a baby that needs to be sort of taken care of. Because the progesterone is very smart. She's like, “We might have a kid. Let's make the body a little bit more insulin resistant so we have some extra blood fats and extra glucose around.” And so this is what oestrogen and progesterone are doing. This is how they're playing.
And another way to visualise this is think of Joan of Arc. Think of Joan of Arc out there on the battlefield. Oestrogen is the suit of armour. Progesterone is the shield and testosterone is the sword. Obviously, you don't want to lose your armour. That is going to be the biggest influence. But you could lose your shield and still be protected somewhat. So progesterone plays a slightly different role.
Now, when you understand this, now you understand that perimenopause when progesterone goes away, oestrogen gets incredibly volatile. Sometimes it's high sometimes it’s low. You can think about that as a sister losing her sister. She's distraught. Sometimes she's okay. And sometimes she's freaking out. And that's why oestrogen levels, are so volatile. And this is where you start to see some of the accumulation of weight around the middle. So what do we do about that? Well, if we don't have progesterone, progesterone is very relaxing in the brain. It has an impact on GABA. And that is very relaxing to the brain. So now women specifically, need to begin to be a little bit more sensitive to their own needs for rest and recovery, because progesterone isn't going to supply that. They need to be very aware that stress is going to have a negative impact.
And then, of course, at menopause when oestrogen falls away as well, and now the armour is lost, now, they really have to be extra diligent about not just stress reduction, but also perhaps, calorie intake. The same diet, and exercise that worked for a younger woman is probably not going to work for her in her older years, because oestrogen and progesterone are now reduced. And she's gonna have to take a more stress-reducing effect in a more calorie...start looking at calories and perhaps start looking at carbohydrate intake as a greater consideration than when she was young. When she was young, maybe she could just count calories and cut calories back a little bit. Maybe as she loses oestrogen, she needs to be a little bit more leery about carbohydrate intake.
Emma: Look, I really love that analogy, Jade, of the non-identical twin sisters with progesterone being the relaxing, creative, nurturing one and oestrogen being the type A, adventurous, goal orientated, dominating one. And when I think about this information through my clinical lens, I'm thinking of the women that come in to see me that are perimenopause or saying, “10 years ago, I used to just do X, Y, Z, and I would drop those three kilos really easily. Now, I can't do it at all.” But if we can reframe that, and explain to women, that they are no longer enjoying the benefits of as much progesterone, and therefore they need to make lifestyle choices and really help preserve that function of rest and recovery in order for them to drop that little bit of weight. I think that's critical from that clinical pearl perspective, and really just watching the carbohydrate intake, I do think we need to earn our carbs after a certain age. I think you're very right on that level.
Jade: Yeah, I think it's very, very well said. And of course, we have to remember as clinicians, one of the things that makes us clinicians and not researchers, is that we have to deal with individuals. Remember, research is a tool for averages, not individuals. We deal with individuals. And so each woman or each person we have to deal with, we have to take into account their unique physiology, psychology, preferences, and practical circumstances. And when it comes to oestrogen and progesterone, it's very good to know what their unique physiology is, because a young female has a very different physiology than a more mature female. And medicine and research certainly has not looked at that much in the lens of weight loss. But then of course, we have to say, “Okay, now we have to take into account psychology,” how some people are very resilient to stress psychologically, some are not. And we have to think about preferences. Some are vegetarians and vegans, and some aren't right, and some are, you know, omnivores. And nowadays, some are carnivores and paleo dieters, and so all of this, we have to take into account.
But obviously, if we miss the oestrogen progesterone story, and we're not even taking it into account, and we're doing one size fits all diet, we are potentially doing harm. And this comes into consideration where things like fasting or keto diet and things like that might be seen one way in a younger woman who has oestrogen and progesterone. Or one way, in a particular menstrual cycle, you know, like the first two weeks of the menstrual cycle when oestrogen is dominating. Maybe that's a time for more extreme dieting and exercise. But that's very different in someone in the second half of the menstrual cycle and very different than someone who's perimenopausal, menopausal or postmenopausal. And these are all things, I think, that we have ignored because what we do is we look at it in the clinical lens. Like for example, when we think of menopause clinically, oftentimes, we think of “Oh, this means that this woman is one year without menses and/or has an FSH of 30 or above,” right?
Jade: However, we also need to be thinking menopause. Oh, menopause usually means she's got very little oestrogen and progesterone floating around. Right? And perimenopause is low progesterone with volatile oestrogen, that's a little different than menopause. Volatile oestrogen with low progesterone is a little different than low progesterone and low oestrogen. So these distinctions matter. And I think they matter a lot.
Emma: Yeah, I would 100% agree because people do think one size fits all and as naturopaths and integrative clinicians we know that this individualised medicine approach is so important so that their patients do actually get the results that they're looking for.
Jade: Yeah, 100%.
Emma: It's amazing. Jade, thank you so much for joining us today. There's a few key points I've taken away. There's actually many and I'm trying to get my brain unscrambled. But the first one is that metabolism is complex and nuanced, making case-taking for the individual extremely important.
I love this new framework for metabolism, thinking of it as a sensing and responding apparatus that responds to the internal and external cues to regain balance and homeostasis. And the importance of educating our patients on the role that hormones play in their metabolism so they get a deeper understanding.
And really, hormone receptor responsiveness is where we need to be focusing our efforts, the things we spoke about: food timings, light exposure, the rest and recovery, the walking, the temperature regulation, all of those things can really help across all those fronts.
Jade: I think it's absolutely critical to be looking at all of that stuff. For sure.
Emma: Yeah, amazing. Thank you everyone today for listening. Don't forget you can find all the show notes, transcripts, and other resources from today's episode on the FX Medicine website, fxmedicine.com.au. I'm Emma Sutherland and thanks for joining us. We'll see you next time.