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Hey everyone, it's Mikki here. You're listening to Mini Mikkipedia and today I want to chat about visceral fat. Now, this is a conversation that has come up countless times probably in the interviews that I've done and other Mini Micropedia episodes. I believe I did one specifically on visceral fat and targeting it back in 24. Now the reason or the genesis I guess for this podcast episode

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It's because I want to unpack the difference between visceral fat and what people call stubborn fat or belly fat because I continue to hear these interchangeably being used out there in the social media space and in the questions that I get. People have this belief that visceral fat is hard to get rid of, that it's the last fat to leave, that it is real struggle street. And the thing is,

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They're two different things and they respond to different strategies. So I think that first of all, putting them together is problematic because people can get disheartened or frustrated by what appears to be a lack of progress. And I think this is particularly relevant if you are

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women in your 40s or 50s because what's happening hormonally during perimenopause directly changes where your body stores fat. And understanding that you can really shift it and how you think about your midsection, your scale weight and what's actually going on under the surface can be really empowering. So first of all, what is visceral fat? Visceral fat, to remind you, it's fat that's stored deep in your abdominal cavity, around your internal organs, your liver, your intestines, your pancreas.

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You can't pinch it. It sits behind the abdominal wall. And it's the fat most strongly associated with metabolic disease, insulin resistance, cardiovascular disease, type two diabetes, and systemic inflammation. Probably a whole lot more too. Now here's the thing that people get wrong. Visceral fat is actually quite metabolically active. And I have said this before. I probably said this a couple of weeks ago. It has a high density of

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what is known as beta adrenergic receptors. And these are receptors that burn fat, that has good blood supply, and it responds relatively well to an energy deficit. It tends to be mobilized early during weight loss, not late. So whilst it is the more dangerous fat, and we do need to be mindful of it, it's actually easier fat to shift. I'll come back to that. Importantly, you don't have to be overweight to have too much visceral fat. There's a phenomenon in the literature called

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coffee, thin outside fat inside, or metabolically obese normal weight. These people with a normal body mass index who carry a disproportionate amount of visceral fat. They can present with insulin resistance, dyslipidemia, fatty liver, and elevated markers despite looking fairly lean. They fly under the radar because they don't get flagged on BMI-based screening. And this is something that I do see clinically as well, and you might know yourself.

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is particularly relevant for perimenopausal women. I would say that the main group that you think about with visceral fat and belly fat tend to be men up until the perimenopausal of menopause transition. Then that does shift to including a lot more women in the cohort more at risk of visceral fat. And at this time, you can stay the same weight.

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You can stay the same dress size, but your fat distribution is shifting viscerally. Your waist circumference creeps up without the scale moving. So that's something to be mindful of. Not that I need to tell you that. So things that drive visceral fat accumulation specifically. It's a combination of energy surplus and hormonal factors that preferentially direct fat into the visceral compartment.

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First of all, and this is known in the literature, it's probably the single biggest hormonal driver of visceral fat, and that is cortisol. And the accumulation of chronic stress, poor sleep, HPA, that's your hypothalamic pituitary and adrenal axis dysregulation, cortisol upregulates lipoprotein lipase activity, and visceral adipocytes specifically. So that just means

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that it is directing fat in and around that area. Second of all, declining estrogen. Premenopausally, this is what I was referring to before, estrogen does favor subcutaneous fat storage in the glutathumeral region, like your hips and your thighs. Not all women, but that's a very typical shape. It's very favorable from a reproductive perspective. But as estrogen drops through perimenopause, there's a redistribution towards visceral

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and trunk fat. Critically, this can happen independently of total body fat changes, so you don't necessarily have to gain weight for this shift to occur. The evidence for this is fairly strong. Lovejoy and colleagues published this landmark longitudinal study back in 2008 in the International Journal of Obesity, and they followed 156 healthy pre-menopausal women over four years using both DEXA and CT scanning. So they were directly measuring visceral fat and not just estimating it.

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They found that all women gained subcutaneous abdominal fat over time that was an aging effect. Now just to remind you, subcutaneous is the fat that's stored directly under the skin that you can pick up and pinch. That subcutaneous fat that's not from a health perspective overly worrying or concerning. So all women gained that subcutaneous abdominal fat over time, but only the woman who became postmenopause during that study has significant increase in visceral fat.

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this increased tract with declining estradiol, which is an estrogen metabolite, and rising follicle stimulating hormone or FSH. They also found fat oxidation dropped by 32 % in the woman who went through menopause, but didn't change in those who stayed pre-menopausal.

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Physical activity also halved in the four years leading up to menopause. you know, there's a bit going on there in terms of not just fat redistribution and fat storage. You've got a shift in that substrate use with less fat oxidation, so less fat actually being burnt for fuel. And then, of course, you've got that behavioral component with physical activity. Now, interesting, the SWAN cohort, and I've mentioned this before in a few podcasts. This is one of the largest longitudinal menopause studies.

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It did confirm this broader pattern. Greendal and colleagues found that the rate of fat gain doubled at the start of the menopause transition, while lean mass simultaneously declined. A couple of things with the SWAN study. The Greendal analysis used DEXA without separating visceral from subcutaneous fat. So you can't really determine which is just subcutaneous and which is visceral. But it is showing that central redistribution, but it's not actually looking at visceral fat.

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The other thing to be mindful of with the SWAN study is the doubling of fat gain sounds pretty dramatic, but the numbers will be relatively small. So do bear that in mind, the absolute values, which is in fact what we care about most more than just this relative value, which is pretty meaningless in the big scheme of uh clinical relevance, that the actual values are relatively small.

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When you look at causal evidence, is there any cause? When you look at studies which experimentally suppress estrogen, you do see that visceral fat gain, not overall fat gain, but visceral specifically. And then when get estradiol is added back in, visceral fat gain reverses. So this is super interesting in terms of human clinical trials showing this direct link between estrogen and visceral fat accumulation.

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Other drivers of visceral fat include insulin resistance and hyperinsulinemia. That's high insulin levels and this becomes both cause and consequence because visceral fat drains free fatty acids via the portal vein directly to the liver which worsens your liver insulin resistance and it becomes a self-reinforcing loop. Now alcohol is also a significant contributor, partly through its cortisol and liver metabolism effects.

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Alcohol pretty much shuts down all fat burning because it becomes preferentially oxidized. As soon as you drink, this is what your body is burning for fuel and it is completely uninterested in burning fat. Poor sleep. Physical inactivity. Independent of calorie balance is associated with visceral fat. There's no causal relationship there, but there's this association. And poor sleep, even short term sleep restriction of four to five hours has been shown to increase visceral fat deposition.

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preferentially. And this was demonstrated in a Mayo Clinic study published in 2022. Now, of course, restriction at that level will impact that hormone environment by increasing cortisol and increasing insulin. So it's indirect, but that's the loop there. Now, all of that being said, yes, we know that visceral fat is dangerous. Yes, we know that visceral fat occurs through the shifting

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hormone phases of perimenopause into the menopause transition. Yes, we know lifestyle contributes to this gain in visceral fat, but it is not hard to shift. And that is the whole purpose of me putting together this episode was just to remind you that there are things that you can do. Let's talk about then what does actually work. I would say one of the first things which has some of the strongest, most consistent evidence is aerobic exercise.

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I literally was listening to a podcast, a very uh popular, large podcast platform. He had on a guest who also has another podcast themselves. I'm not quite sure of his background, but he's, you know, I like a lot of his stuff, but he said his number one thing for visceral fat was resistance training. Yet if you go into the literature and look.

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it is aerobic training and specifically that moderate to vigorous aerobic training. Multiple randomized controlled trials and meta-analyses show that this reduces visceral fat even in the absence of weight loss. The effect is dose dependent. So the higher the intensity or the more volume you're going to produce greater reductions. And crucially, I think this is important, aerobic exercise reduces visceral fat.

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disproportionately relative to total fat loss. So it preferentially can target that visceral component. And this is because exercise increases the catecholamine output and visceral adipocytes are highly responsive to catecholamine driven lipolysis through those beta adrenergic receptors. So just to add some clarity around that, when you exercise, your sympathetic nervous system activates and releases catecholamines, primarily that's adrenaline,

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your adrenal medulla into the bloodstream and noradrenaline from sympathetic nerve terminals in adipose tissue directly. So these catecholamines are the primary signal that tells fat cells to mobilize stored triglycerides into free fatty acids and glycerol and this is the process of lipolysis. The catecholamines bind to these

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adrenergic receptors on the surface of the adipocytes. These are the little receptors on the surface of your fat cells basically. And there are two families that matter here. The beta receptors, which are stimulatory, they're going to activate that hormone sensitive lipase and promote this breakdown of...

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fat tissue and then there's the alpha two receptors which are inhibitory. They suppress enzymes and put the brakes on that fat burning. So the net lipolytic response of any given fat depot does depend on the ratio and density of these receptors. The more beta receptors you've got, the higher the likelihood of fat being burnt, the higher the ratio of alpha two receptors, the less fat burning you're going to get.

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Visceral uh adipocytes have a higher density of those beta receptors relative to the alpha-2 receptors. So when those catecholamines flood in during exercise, that dominant signal is mobilized. That fat breaks down, free fatty acids are released into the portal circulation, and they're delivered to the liver for oxidation. This is why visceral fat is so responsive to exercise. The receptor profile is set up to respond to exactly that signal that exercise provides.

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Now stubborn subcutaneous depots like in the lower abdomen where a lot of people struggle with, the hips and the thighs subcutaneously, these all have the opposite profile. They're alpha-2 receptor dominant. So when the same catecholamines arrive, the inhibitory signal competes with or overrides the stimulatory one. The net effect is blunted fat loss or blunted lipolysis.

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the fat stays put or at least it mobilizes much more slowly. This is where it can get nuanced because the catecholamine output scales with intensity of exercise. So low to moderate intensity exercise produces this modest catecholamine response. At these concentrations, the beta receptors, which have a higher affinity for the catecholamines, they preferentially activated. The alpha two receptors

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aren't maximally stimulated. So even at these lower intensities, you get a relatively favorable beta to alpha activation ratio, even in that stubborn area. As the intensity increases, catecholamine concentrations rise substantially. So now you're flooding both receptor types, both beta and alpha. In visceral fat, which is a larger amount of those beta receptors, that's great.

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But in that stubborn fat area which has a higher affinity or higher amount of those alpha-2 receptors, that's going to still blunt that fat oxidation. So this is why very high intensity exercise can be pretty ineffective at mobilizing stubborn fat compared to say modern intensity because the alpha-2 inhibition can catch up.

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Now, this is the mechanism, the proposed mechanism, I will say. So most of the receptor biology and catecholamine kinetics that I've just described, these do come from in-vitro and micro dialysis studies. just translating this cleanly to whole body fat loss in free living humans is a bit harder. And the intervention studies that specifically measure regional subcutaneous fat mobilization in response to different exercise protocols are quite limited.

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The physiology is sound though. So that's why there's this recommendation for that moderate vigorous exercise for visceral fat specifically. so the physiology is sound. And in addition to that, even in light of no direct studies comparing the information I've just shared, we do have those multiple randomized controlled trials and meta-analyses.

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showing that moderate to vigorous aerobic exercise does reduce visceral fat. I think that we can be, you know, have some confidence in that. Interestingly, before we get on to the calorie deficit piece, which obviously I think is important, you can lose visceral fat without being in a calorie deficit actually. There is a series of studies

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known as STRIDE, and this is from out of Duke University. And it showed that aerobic exercise reduced visceral fat even when participants went dieting and even when total body weight didn't change. Conversely, they found that inactivity led to rapid visceral fat gain. So even a modest amount of activity equivalent to walking about 19 kilometers per week was enough to prevent accumulation with higher amounts actually reducing it.

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know, any level of activity is going to be favorable in this area. And I do think this is important for perimenopausal clients or any lean individual who doesn't necessarily need to lose weight, but they're noticing that their waist is thickening and their metabolic markers are creeping up. So you do not have to be grinding through a deficit to shift that visceral fat. Consistent, moderate activity can do it.

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So I mentioned that a calorie deficit was also on the cards. Visceral fat is highly responsive to an energy deficit and it tends to come off early. So diet composition matters less than the deficit itself of visceral fat specifically. Of course though, you know that protein in a calorie deficit diet is so important and reducing refined carbohydrates that may contribute to this blood sugar balance issue with

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rising insulin and rising blood glucose and minimizing alcohol, is correlated with high visceral fat, that tends to be a smart move and it could have an additional benefit. So that's definitely worth noting there. So number three is resistance training. Of course, it's still important. It's just not got that same sort of level of evidence behind it that aerobic training does.

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The resistance training improves insulin sensitivity. It increases our lean mass and muscle mass specifically. So we're able to take that glucose, dispose of it into the muscle, which is really important from an insulin perspective and metabolic health perspective. And it does help address that sarcopenia profile that contributes to the TOEFI phenotype that I mentioned earlier. Clearly that combination of resistance training plus aerobic training is going to be optimal.

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And then you have reducing alcohol, optimizing sleep, stress management, and for some women, potentially menopause hormone therapy, all of which have supporting evidence for visceral fat reduction. Now, there is a reason that the scale might not move much even when visceral fat is dropping. So visceral fat loss may only represent maybe half a kilo to a kilo and a half, so not a ton of weight. And that can easily be offset by gains in muscle mass

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in changes in glycogen storage or even just how we store water, especially if someone is starting resistance training. And the scale measures everything. So unless you get like an MRI or an ultrasound or a DEXA or something like that, it's very difficult to see these shifts in visceral fat. But just know that someone who does lose a kilo of visceral fat and potentially even gains a kilo of muscle, that takes a long time if you're not a newbie.

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They've dramatically improved their metabolic health while the scale reads the same number. So do be mindful that the scale does have limitations when it comes to assessing these things, even your fancy four-compartment scales. Now, with visceral fat explained, I do want to have a little bit of...

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chat around this other stubborn fat. And this is what most people are actually pointing to when they grab the lower belly, their hips, their thighs and say that they can't lose it. And they just assume it's visceral fat because it's in the abdominal area, but it's subcutaneous fat. And I've already mentioned about that receptor biology and why fat depositions here are just far more resistant to fat loss. just

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To summarize what I've already said, they have a much higher ratio of these alpha-2 adrenergic receptors compared to the beta receptors. So when those catecholamines bind to those alpha-2 receptors, they inhibit fat loss. They don't promote it. So the normal catecholamine response to exercise or an energy deficit um is blunted in these areas. Because don't forget that being in a calorie deficit can create a catecholamine response

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because it's stressful to be in a calorie deficit. On top of that, stubborn fat does have poorer blood flow, which means even when fatty acids are liberated, the transport away from the tissue is slower and they can get re-esterified, so put back into the tissue before they leave. So this is why someone can lose eight kilos and see it come off their face, their upper body, their trunk.

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but their lower belly and hips look exactly the same. The body has a mobilization cue. It pulls from those easy depots first, visceral, upper body, subcutaneous, maybe the trunk for some as well, but those stubborn subcutaneous depots are at the back of the cue. So how to reduce that stubborn fat? What I would say is if you haven't already listened to my episode with Brandon de Cruz on spot reduction, I'll pop it in the show notes.

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Definitely go back and listen to that because he's got some advanced strategies that he has seen work with his clients. I will also say though that in general, you guys will know this anyway, a sustained calorie deficit over time. So you cannot meaningfully shift stubborn subcutaneous fat at energy balance through exercise alone. You do need a deficit and you need it for long enough that the body works through the easier deadpots and starts accessing the more resistant ones.

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And this is like a last mile problem. It requires patience and the rate of visible change slows significantly in these areas, even though the deficit is still working. And that's where it can get frustrating. And this is why progress photos are really helpful because you can assess change over time. In addition, patience and consistency over intensity. You are much better off going low and slow than trying for rapid and extreme methods because we know that stubborn fat

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doesn't respond to this. It's too stressful for that fat to be mobilized. So, and I do think this is especially relevant for perimenopausal woman whose cortisol may already be elevated through other hormone changes. So an aggressive cut can make the problem worse and not better. Now, I do think that there is a reasonable physiological rationale for low intensity fasted exercise. In the fasted state, insulin is low.

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So removing one of those breaks on those alpha two dominant depots. And low to moderate intensity exercise keeps catecholamines in a range that preferentially activates beta receptors without flooding the system enough to maximally stimulate those alpha two receptors as well. Higher intensity exercise drives those higher catecholamine output. And that activates both receptor types, including those inhibitory ones in those stubborn areas. So theoretically then,

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And this is all theoretical, easy cardio in a fasted state, walking, a light jog if you're a jogger, gentle cycling, swimming. And I will also just reiterate the randomized controlled evidence for this specifically targeting stubborn fat is limited, but the physiological rationale I do think is coherent. Number four for stubborn fat, managing insulin levels. Because stubborn fat is particularly sensitive to insulin's anti-lipolytic effect or its ability to shut down fat burning,

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Dietary strategies that keep insulin lower for long abortions of the day may help. It could be a lower carb approach. It may be a time restricted eating window, just not grazing and having meals, timing carbohydrate around after exercise. And remember, this does only work in or help in the context of that deficit. Lower insulin and energy balance won't liberate meaningful amounts of stubborn fat.

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Number five for stubborn fat, improving local blood flow through exercise involving the relevant muscle groups. And this is part of the Brandon D'Cruz episode that I was referring to. So, Storknet and colleagues showed that in 2007 that lipolysis was higher in subcutaneous fat adjacent to exercising muscle. So, increased regional blood flow does improve that fatty acid transport away from that adjacent adipose tissue. The evidence is preliminary.

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but the mechanism is sound. Tack a low intensity aerobic exercise onto that and that's putting that theory into practice. And then of course, sleep and stress management come in as supporting factors again. Elevated cortisol promotes insulin resistance as I mentioned and impairs catecholamine-driven lipolysis. Poor sleep disrupts that growth hormone pulse which supports lipolysis. And so for these reasons, we need to think about stress and sleep management.

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So in summary, visceral fat and stubborn fat are physiologically different. Visceral fat is metabolically active, responsive to exercise without a calorie deficit, and tends to be mobilized early. Stubborn subcutaneous fat is receptor resistant. It's poorly vascularized and requires a sustained deficit and time. So for visceral fat, the more dangerous one, the prescription is encouraging, of course.

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Regular aerobic exercise, everything we discuss, resistance training, sleep optimization, reducing alcohol and managing stress can all improve the picture, weight loss or not. So these exercise and lifestyle factors can meaningfully shift that visceral compartment. The stubborn fat, and this is the cosmetically frustrating type, the one that we're all pinching and going, what's going on? Honestly, it requires patience, time, a moderate sustained deficit.

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resistance training to preserve lean mass, adequate sleep, and maybe some of that blood flow exercise activity that I referred to earlier. The danger is when someone interprets the stall that is always inevitable when you are in a sustained deficit as failure and they either quit or they do something extreme like crashing your calories, which paradoxically makes the problem worse. You don't want to do that. And remember, if someone loses half a kilo of

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visceral fat and gains half a kilo of muscle, the scale hasn't moved because you're still the same weight, but your metabolic health, it's transformed. Your fasting glucose is better, your triglycerides are lower, your inflammatory markers have improved, your waste has come in, and that is one of the best outcomes you can achieve, but the scale just won't see it. So,

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That's my visceral fat versus stubborn fat mini episode. I'd love to hear what you think and what you believed with regards to the abdominal fat. uh Catch me over on Insta threads and X @mikkiwilliden Facebook @mikkiwillidennutrition, or head to my website, mikkiwilliden.com. Scroll down to the bottom, pop your name in the box and jump on my weekly email list. All right guys, you have the best week. See you later.