Maria Plaias Nutrition & Functional Medicine

23/07/2025

🎯 3. INSULIN RESISTANCE & ATHEROSCLEROSIS
✨
It wasn't planning on writing about cardiovascular issues in the context of my insulin resistance series as I believe it's a well known fact that the two are connected and cardiologists usually check for metabolic issues (although I believe they look more at different cholesterol levels and ratios, and not as much at fasting insulin), but I found this study from 2023 whose title is exactly spot on on the topic of the relevance of hyperinsulinemia in chronic health issues.
✨
It's called "Early insulin resistance in normoglycemic low-risk individuals is associated with subclinical atherosclerosis" and it states that the HOMA-IR test can provide valuable information for identifying individuals at a higher risk of developing advanced atherosclerosis. It's an early indicator marker, but yet very valuable in preventive medicine for those people with low-to-moderate cardiovascular disease risk and who could benefit from early implementation of prevention strategies.
✨
Just to clarify, HOMA-IR is defined as fasting insulin (mU/L) x fasting plasma glucose (mg/dL). Yes, it's just a mathematical calculation, but the two separate markers (insulin and glucose) are always taken into consideration separately as well, as it's also about the relationship between the two, how high is that insulin to be able to keep glucose levels within the reference range. I don't even think there are labs that give you the HOMA-IR result without detailing it, so without giving you the fasting insulin and glucose levels at the same time. Or they just give you these two markers, and you can calculate the HOMA-IR yourself (put "HOMA-IR calculator" in your search engine and you'll find your answer).
✨
These were people who had normal glucose levels and normal HbA1c, who had no diagnosis of pre-diabetes, nor diabetes yet, and yet they developed subclinical atherosclerosis.
✨
I liked also how they defined early insulin resistance as "the slow progressive need for higher fasting insulin to maintain normal fasting glucose concentrations", and which "can be seen years or decades before the appearance of increased fasting glucose, glucose intolerance, and elevated glycated hemoglobin that are characteristic of the insulin resistance–prediabetes–type 2 diabetes spectrum.", definition that I see as very accurate.

They also say " Insulin is rarely measured in routine clinical practice, precluding identification of early insulin resistance until later, more advanced stages of the type 2 diabetes disease spectrum. Similarly, subclinical atherosclerosis frequently goes undetected until the first clinical event." Which, differently put, means that if we'd check hyperinsulinemia, we might be able to anticipate and prevent atherosclerosis way before it shows its ugly head.
✨
That's it, that's the whole post. I think the title of the study really speaks for itself.
✨
And here's the study for you:
Early insulin resistance in normoglycemic low-risk individuals is associated with subclinical atherosclerosis - https://cardiab.biomedcentral.com/articles/10.1186/s12933-023-02090-1

21/07/2025

Echipa celor de la Zenyth a structurat frumos webinarul meu despre abordarea integrativa in ADHD pe care l-am tinut la sfarsitul lui martie.
Pentru cine l-a urmarit dar si l-ar dori si structurat in forma scrisa, dar si pentru cine nu a reusit inca sa-l urmareasca si versiunea de text il ajuta mai mult, las aici mai jos linkul.

In versiunea video (pe care o atasez din nou in comentarii) sunt explicatii mai detaliate, asa ca - pentru cei interesati - ideal ar fi sa vizionati inregistrarea si apoi sa va folositi de text pentru a nu pierde nimic din toate punctele importante.

ADHD-ul este adesea perceput ca o tulburare a copilăriei, definită prin neatenție, impulsivitate și hiperactivitate. Însă realitatea este mult mai complexă. De la factori genetici și dezechilibre ale neurotransmițătorilor, până la influența nutriției, a microbiomului intestinal și a s...

20/07/2025

Am intrebat-o pe d.na Dr. Ciurea Naomi-Adina - Medic specialist gastroenterolog acum cateva zile cm a ajuns la medicina functionala, caci fiecare din noi trecem printr-un parcurs de dezvoltare personala si profesionala pana ajungem la o asemenea alegere.
Gasiti mai jos raspunsul ei 😊 💚.

Coincidenta face ca dr. Ciurea are si un doctorat exact pe tema permeabilitatii intestinale și implicațiile ei în dezechilibrele metabolice, legatura pe care am mentionat-o si eu in aceasta dimineata in postarea despre rezistenta la insulina si autoimunitate. 😊

20/07/2025

🎯 2. INSULIN RESISTANCE & AUTOIMMUNITY
✨
My second post in the insulin resistance series is about insulin resistance in the context of autoimmunity.
✨
Autoimmunity can be promoted via different mechanisms and one of them is connected, again, to the vagus nerve. Please check the previous post, if you haven't read it already, as it connects to this one. I explained there how high insulin ends up downregulating the dorsal motor nucleus of the vagus nerve and diminishing the extent to which the vagus nerve stimulates the downstream organs:
⸻
✨
🔴 One mechanism is that the downregulation of the vagal motor outflow mentioned is itself a promoter of inflammation.

🔴 The first downstream effect happens in the spleen.

During normal activity, the vagus nerve sends signals that inhibit the macrophages in the spleen, a a key organ in the immune system.
What are macrophages? They are cells of the immune system responsible, among other things, for the production of inflammatory cytokines (chemical messengers).

🔹So if you have adequate vagal motor outflow, the macrophages in the spleen are influenced away from production of inflammatory cytokines.

🔹Antibody production to circulating antigens by B cells is also directly influenced by spleen macrophages and is likewise inhibited by adequacy of vagal motor outflow.

⏩When we lower the vagal motor outflow (via hyperinsulinemia, but also other inflammatory mechanisms), we also lose its anti-inflammatory effect in the spleen so we get antibody production and production of inflammatory cytokines.
⸻

🔴A similar mechanism involving the vagus nerve happens in the liver.

The Kupffer cells mentioned in the study below are simply localised macrophages in the liver, and here we have central insulin action activating hepatic IL-6 and STAT3 signalling (so, again, inflammatory messengers).

⏩So, as the insulin level goes up, vagal motor outflow goes down and you’ll lose the inhibition of Kupffer cell production of IL-6 and STAT3.

⏩Loss of IL-6 inhibition means you're going to have more of a tendency toward autoimmunity.

⏩The more insulin you have, the less vagal motor outflow you have and, potentially, the more inflamed your liver gets, again it's a loop mechanism that pushes you on the autoimmune path.
(A few aspects about STAT3 here below.)
⸻

🔴 Another mechanism is through the co-activation of inflammation and autoimmunity.

We know from the immunology studies that there's a bidirectional relation between inflammation and the autoimmune process, and at the center of this connection is the fact that NF-kappa B, essential chemical actor in inflammation, drives the activation of STAT3, essential chemical actor in the tissue destructive process in autoimmunity.

⏩Each factor that drives inflammation, IR included, is going to have the added effect of potentially sparking up a flare of a person’s autoimmunity process.

⏩So IR might be both a trigger and a mediator of autoimmune disease.
⸻

🔴 Another mechanism is through a more complex connection between IR, subsequent SIBO (which we've already talked about in my previous post) and chronic inflammation which can feed the autoimmunity.

🔹 I already mentioned last time how SIBO is a driver of chronic inflammation, as the epithelial lining cells are producers of NF-kappa B when the balance of the microbiome is off in the intestine.

⏩NF-kappa B can drive the activation of STAT3, as just stated above, so autoimmune flare-ups are just around the corner.

⏩Same goes for dysbiosis by extension of course - both are expressions of a dysregulated microbiome.

🔹 On the other hand, the too many bacteria in the small intestine, in the context of SIBO, can influence the immune system at the gut lining towards not recognising particles of food as food, but more as food antigens, with consequent loss of tolerance, which again promotes inflammation.

⏩Loss of oral tolerance is one of the highways towards autoimmunity.

⏩So there can be a complex connection between IR leading to low vagal outflow, leading to SIBO, leading to loss of oral tolerance, leading to autoimmunity.
⸻

🔴 Last but not least, there's a bidirectional connection between IR and dysbiosis.

🔹On one hand, IR can worsen dysbiosis by compromising the integrity of the gut barrier, making it more susceptible to damage and permeability.
And IR can also affect the gut's immune response, potentially impacting the composition and function of the gut microbiota.

🔹 On the other hand, dysbiosis can lead to IR as, by making the intestinal barrier more permeable and thus allowing bacterial toxins, like lipopolysaccharides, to enter the bloodstream, causing endotoxemia and triggering systemic inflammation.

🔹Chronic inflammation by itself can also lead to IR, as we've mentioned before.

🔹Likewise, dysbiosis can alter the production of butyrate and other short chain fatty acids which play a role in regulating glucose metabolism and insulin sensitivity.

⏩A decrease in butyrate production can definitely worsen IR.

🔹And gut microbes can also cause metabolic changes by influencing various metabolic pathways, so there's even some research in using prebiotics & probiotics as a strategy for managing IR.

💯And we definitely know at this stage that there's is a very tight connection between dysbiosis, leaky gut and autoimmunity, therefore there's definitely an element of insulin resistance influencing the gut microbiome, influencing the gut lining and thus the autoimmune process.
⸻
✨
🔴 Obviously, just like before with SIBO, the more pronounced the IR is, the worse it is.
The systemic insulin resistance together with the chronic hyperglycemia that characterise diabetes are also going to trigger the inflammatory NF-kappa B response and other pathways associated with autoimmune flareups.
But that doesn't mean that insulin resistance by itself as just blood sugar dysregulation accompanied by insulin surges, without all the other complications, is not inflammatory.
⸻
✨
😇Most of this is pure functional immunology and it's not an easy one, so kudos to you for reading and trying to understand this far.
✨
🧯So do I check for insulin resistance in my autoimmune clients? You bet I am!
✨
👩‍⚕️🧑‍⚕️If for IR & SIBO I mentioned a multidisciplinary approach, as gastroenterologists and diabetologists could work together, here, in the autoimmunity field, things are less promising.

🤌Despite the enormous importance of the vagus nerve in immunology, as a bidirectional bridge between the nervous system function and the immune system function, it's being taken into consideration mostly in psychotherapy with the polyvagal theory, the somatic approaches, breathwork, yoga and all those practices which are stimulating the vagus, and much less in the medical field.

🤌As for autoimmunity, the only conventional approaches are hormonal substitution and/or immune suppression, there's zero interest in looking for triggers or mediators.

👌So the functional approach is where it's at. Or finding doctors who treat autoimmunity in an integrative way.
⸻
✨
And here're some of the studies, this time I mentioned too many to post them all here, but just ask if you need specific referencing:
Central Insulin Action Activates Kupffer Cells by Suppressing Hepatic Vagal Activation - https://www.sciencedirect.com/science/article/pii/S2211124716301358
Mechanisms of inflammatory responses and development of insulin resistance: how are they interlinked? - https://pmc.ncbi.nlm.nih.gov/articles/PMC5135788/
Neural reflexes in inflammation and immunity - https://pmc.ncbi.nlm.nih.gov/articles/PMC3371736/
IL-6: A cytokine at the crossroads of autoimmunity - https://pmc.ncbi.nlm.nih.gov/articles/PMC6286200/

17/07/2025

Nici ca putea sa vina mai bine postarea asta!
Personal, trimit foarte des clienti catre Clinica Medclinique, (ultima clienta am trimis-o alaltaieri si ieri mi-a confirmat deja ca s-a programat), spre mainile de aur ale dr.-ei Gabriela Mathieu, medicul cardiolog care mi-a restaurat increderea ca exista si cardiologie facuta bine, d**a toata trauma medicala prin care am trecut timp de-un deceniu. Si nu e singurul medic cardiolog bun, mai sunt, dar ea a fost prima despre care am aflat 🥰.
Si, absolut deloc intamplator, are si pregatire functionala caci exact asta o face un medic exceptional 🤩💪.

Cand voi termina seria asta despre rezistenta la insulina, am sa fac o postare separata cu toti medicii cu specializare sau deschidere spre medicina functionala pe care ii stiu in Romania, cu siguranta e o informatie ce poate fi de mare ajutor. Nu sunt foarte multi, dar sunt mana cereasca. ☺️
Evident exista si dieticieni, nutritionisti, health coaches, tehnicieni si poate si alte figuri profesionale pe care nu le stiu, dar postarea va fi doar despre medici. Medicina e una singura, studiile medicale de specialitate sunt aceleasi pentru toata lumea, abordarea face toata diferenta.

p.s. Cu dr. Gabriela Mathieu am inregistrat acum cativa ani doua podcasturi, am sa le las in comentarii pentru cine doreste sa asculte 😊.

❓ Știai că în Cristian, jud. Sibiu, există o clinică medicală care pune pe primul loc tratarea afecțiunilor pornind de la cauzele bolii?
👩‍⚕️ La Medclinique Therapy Center nu ne limităm doar la tratarea simptomelor, ci prioritizăm în tratament înțelegerea întregului organism, de la factorii genetici, la mediul înconjurător și stilul de viață.

🩺Urmărim să dezvoltăm planuri de tratament personalizate deoarece fiecare pacient este unic. Prin abordarea medicinei funcționale înțelegem întreg organismul și interacțiunile care au loc, pentru a trata cauzele afecțiunilor.

Programări la 📞 0369 419 111
📍 Cristian, str. VII, nr. 13, jud. Sibiu

16/07/2025

🎯 1. INSULIN RESISTANCE & SIBO (Small Intestinal Bacterial Overgrowth)
✨
I've decided to start a series on insulin resistance (IR), and detailing what I was already alluding to in my previous post about IR, as it seems there's a bit of disagreement about what hyperinsulinemia does to the body and all the chronic health problems it can cause, besides the metabolic issues connected to obesity, fatty liver, pre-diabetes and diabetes that we've all heard about.
✨
Before I start, a definition maybe is required.
In simple words, hyperinsulinemia means higher levels of insulin in the blood and, whilst it's often associated with type 2 diabetes, it's not the same as diabetes itself. We can have excess insulin in the body, but glucose levels still below the pre-diabetes threshold, years (often even more than a decade) before our cells fail to respond to our increasing circulating insulin and we start also seeing high glucose levels in the blood and high HbA1c, since this marker provides an average of our blood sugar levels over the past 3 months. And while there are always patterns of hypoglycemia with insulin resistance because of all the blood sugar rollercoaster that the IR causes (hence the importance of monitoring insulin levels even when blood sugar levels are low), it does take a while till we'll also see constant hyperglycemia.
High insulin is the consequence of the resistance of the target cells to open and uptake the glucose circulating in the blood so the pancreas is secreting more and more in order to force the process and to obtain the same result, as having high glucose levels in the bloodstream is very inflammatory, hence the term of insulin resistance.
✨
In terms of symptoms, IR is not that obvious. People will search for medical advice for the most varied signs and symptoms. From my clinical experience, nobody will come and tell the medical professionals: "Hey, I have insulin resistance" or "Hey, I have dysglycemia".
Instead they'll complain about generalised fatigue, about feeling completely wiped out after meals, about struggling to fall asleep or to stay asleep during the night, about depression or anxiety, about gastrointestinal issues, about joint pain, about irregular menstrual cycles, about not being able to get pregnant, about hirsutism, loss of hair on top of their head, or acne on the jawline if they're women, about growing b***s or having low s*x drive if they're men. About feeling completely inflamed. And yes, about weight gain, but not always.
As you can see there's a big variety of symptoms! So these people will search for help from different specialists and it would be our responsibility, as healthcare professionals, to connect the dots and fix the underlying imbalance. And people do develop many of these symptoms way before things go south and they might also receive a pre-diabetes or diabetes diagnosis.
✨
Today I'll talk about how hyperinsulinemia can trigger or maintain SIBO.
It goes without saying that it gets worse, the more pronounced the dysglycemia is, so everything mentioned here is relevant for diabetes and the other metabolic issues as well.
✨
There is a very important mechanism through the vagus nerve:

🔴 Higher insulin is going to downregulate the dorsal motor nucleus of the vagus nerve and is going to diminish the extent to which the vagus nerve is stimulating the downstream organs

🔹The dorsal motor nucleus of the vagus nerve's role is to regulate the gastrointestinal function by sending parasympathetic signals to the enteric nervous system.

🔹The ENS controls functions like peristalsis (muscle contractions that move food through the gut), secretion of digestive enzymes, and blood flow in the GI tract.

🔹What we know is that insulin receptors are expressed in the dorsal motor nucleus of the vagus and insulin crosses the blood-brain barrier and is transported into the brainstem.

🔹Here, higher insulin significantly reduces the frequency of the electrical signals of the vagus nerve, essentially downregulating the vagal motor outflow

🔹The reduced vagal motor outflow will directly affect the ENS and thus the stomach, the enzymes secretion and it will affect also the downgoing peristalsis. The stomach will lose its capacity to properly secrete hydrochloric acid and thus to kill the bacteria coming from food and this will cause a migration of the flora from the stomach towards the small intestine. Likewise, the inhibited downgoing peristalsis will cause a migration of the flora from the large intestine towards the small intestine.

🔹This is a very known mechanism of SIBO, as the small intestine is mostly sterile so, whichever way the bacteria is moving, upwards from the large intestine or downwards from the stomach, we get more bacteria in the small intestine which will then feed on the fermentable food aimed for us. And we develop SIBO.

🔹Moreover, the epithelial cells of the intestine will get inflamed because of SIBO and will produce NFkB (a protein that induces the expression of various pro-inflammatory genes), which will lead to systemic inflammation

🔹The systemic inflammation will lead to brain inflammation and we're back again to losing even more the vagal motor outflow.

⛔️This is one of those feedback loop mechanisms which, under normal circumstances, is just fine, but when you’ve got insulin resistance and your level of insulin in the body and brain is ramping up, you’re going to have excessive inhibition of vagal motor outflow, you’re going to become systemically inflamed, it’s going to worsen the insulin resistance even more and, with it, the gastrointestinal issues impacted by the enteric nervous system not functioning.
✨
These two imbalances influencing each other need a multidisciplinary approach in order to improve's someone's health. Or, better yet, a functional approach.😉
✨
Here's also the study describing in detail and in more technical terms all of the above, for the nerdy ones among you 🤓:
Insulin reduces excitation in gastric-related neurons of the dorsal motor nucleus of the vagus - https://pmc.ncbi.nlm.nih.gov/articles/PMC3469664/

13/07/2025

Because it's Sunday, I'd like to do a different post today and tell you a few things about me and the why of my functional approach ☺️.
✨
I'm the daughter of two brilliant teachers, my mom was a teacher of Romanian language & literature at the best highschool in Cluj, and my father was the head of the marketing department at the University of Economic Sciences, PhD coordinator and one of the first winners of the Fulbright grant for professionals.
Who our parents are might not be relevant for everyone, it's usually not, but it's very relevant for me. I was educated not only to appreciate the patient skill of studying, but also to develop the not-so-common critical thinking which is often frowned upon.
✨
Not sure if it was because I grew up seeing teachers first and foremost as human beings, but I've never respected my teachers simply because they were teachers. It was the quality of their knowledge and skills and not their label & title that got my admiration and my openness to learn from them. This made me an unruly teen, I still remember - barely 14 years old - getting up from the back of the class and loudly contradicting my teacher of Romanian who struggled to understand and thus explain the difference between a subject clause and a relative clause. I would correct him, he would tell me to keep quiet and sit down as he was right, and I would come back the next day with the Academy's Book of Grammar and Punctuation to prove to him I was right and he was wrong 🙂.
This didn't change much the following years, I just got a bit smoother, luckily the ratio of bad teachers vs good teachers improved greatly. And I've definitely known a few: I spent 4 years studying for my first degree and 5 years studying for my second degree and my masters. I was the student of or won scholarships to 4 different universities on different continents: Babes-Bolyai in Cluj, University of Padua in Italy, University of New South Wales in Australia, and Boston University in the US. The Australian scholarship was the only one available for my entire university, thousands of students. And I won it. Twice in two consecutive years. I probably am, to this day, more than 20 years later, the only Romanian non-resident to ever study at an Australian university. They were also the ones to remind me, once again, just how important critical thinking is.
Just to make things clear, I'm not a nepo baby, quite the opposite, everything I had achieved was through a high work ethic and very hard work, I had been a working student all throughout my scholar years while also being a brilliant student.
✨
That's why it's not at all surprising that I got sick and met, for the first time as a chronic patient, another type of professional: the doctors.
I wasn't there to question their work, God forbid I wasn't there to do their work, all I wanted was for them to help me heal so that I could continue doing what I loved and what I had dedicated my life thus far to. I wanted to put my entire trust in their work, just like I had done in my good teachers.
And yet, they failed. Not once, not twice, not three times. They failed even if they were also university teachers, they failed even if they were the director of a hospital, they failed even if they were Romanian or Italian or American. They failed and I continued being medicated for 8 long years just to keep my symptoms under control.
✨
So what was I to do? Just suck it up and take that medication till I died? I started first reading and then studying medicine to understand what was happening with my body and to hopefully try and fix it myself. And in the process I found out there's an entire medical world, outside of "a pill for every ill", a medical approach that looks for and treats the underlying cause. So logical, so simple and yet so rare! A medical approach that addresses the root cause instead of the symptoms. So obvious!
If you have a light bulb blinking in your car telling you you're low on petrol, you go ahead and put some petrol in your car, right? You don't take a piece of cloth and cover that light so you don't see it blinking anymore. You fix the problem, not cover it up till it's too late. And yet, what we don't do to cars, we do to humans.🤯
✨
Did I end up getting another university degree in medicine? No, I didn't see the point. I did not care about the label if that meant just learning which pill to give for which supposed diagnosis. And yet, 90% of my colleagues are doctors and ALL of my mentors & teachers are doctors too. I have the utmost admiration for those doctors who, after completing a conventional education, realised its limits in addressing chronic diseases and continued to train in the integrative, functional approach. I have friends doctors and I have doctors who love or like all of my posts on social media and whose work I appreciate in return. Just like I have doctors who have asked for my advice or who have been my clients or sent their family members to me as clients.
✨
On the other hand, I haven't chosen the easy way into the medical world just to "influence" people, there was nothing easy about this choice considering all I had to sacrifice from my previous career, the mere thought is ludicrous. If anything, I'm barely present online, I preferred to spend the last 11 years studying and researching rather than aggressively selling my services.
And, again, just to make things clear, every single medical course I've done and got certified for, and I've done loads in these 11 years, has been carefully chosen - as was its teacher - and studied out of deep interest: not for the grades, not just to pass the exam and forget about it, but to understand.
✨
I don't think I'm anyone's first therapist choice: my services are expensive, the functional testing I provide is even more expensive, I'm not covered by insurance, and yet I have a neverending waiting list and people are asking for my help daily. I guess I must be doing something right, outside of social media, for this to happen.
So I'm just thinking, functionally: instead of attacking the end result, i.e. my own professional figure, and calling it names, why don't we fix the underlying cause, the very one which would make my role redundant and completely unnecessary? 🤔
And yes, that would be the conventional approach to chronic health issues.
I'm not holding my breath.

P.s. here's, for the algorithm, just an old photo of me the day I turned 30 and with already a heart disease diagnosis and having already taken a daily medication for the past 3 years.

11/07/2025

Is testing for insulin resistance relevant?
✨
I'm writing this because it's close to impossible to test for fasting insulin in Ireland, and in Romania I can see doctors (mostly diabetologists) on social media insisting on the uselessness of such a test. So let's break it down:
✨
Insulin resistance is a pre-syndrome if you like, it's a condition which indicates sugar imbalances in your body and which precedes other diagnoses like metabolic syndrome, fatty liver, pre-diabetes or diabetes. There's a downward spiral of dysglycemia which starts with postprandial dysglycemia and which can, years later, turn into diabetes with all its complications.
✨
But insulin resistance is not only relevant in the dysglycemia realm. It's relevant in any chronic disease as it's almost impossible to recover from any chronic issues if you suffer from a chronic blood sugar disorder.
👉 if you suffer from IR and you complain of fatigue, this can be because insulin resistance leads to decreased cellular glucose with then leads to decreased ATP, the energy currency of your cells. And all biochemical pathways require ATP!
👉 IR can make males produce more estrogen and females more testosterone with subsequent potential consequences of gynecomastia, PCOS, hair thinning and even infertility.
👉 IR can lead to brain dopamine disruption, so it can show up as mood swings, anxiety and depression
👉 IR may appear as insomnia, some people can struggle to stay asleep, while others struggle to fall asleep
👉 IR can change the microbiome and can lead to dysbiosis which, in turn, can lead to intestinal permeability. And dysbiosis and intestinal permeability together are bad news as you can get endotoxemia, i.e. leaking toxins (lipopolysaccharides) into your body which cause plenty of systemic inflammation with all its consequences
👉 systemic inflammation, whichever way it comes, but especially in the context of intestinal permeability is the straight highway to autoimmunity. And you can't fix that leaky gut, no matter how much glutamine you ingest, if you don't first fix that insulin resistance. There's even a very fancy term, immunometabolomics, which really is a study of the way that issues about cellular metabolism have a very direct and potentially profound relevance for cellular immunology
👉 if you have IR, since your brain has receptors for insulin in the brainstem, IR will ramp up the level of insulin in the brain as well and you’re going to have excessive inhibition of vagal motor outflow. That translates to issues with your digestion, with reflux, with a higher risk for SIBO and with an increase of inflammation
👉 inflammation can lead by itself to more gluconeogenesis, so you get more insulin resistant and more chronically inflamed. It has become a loop.
✨
These imbalances are definitely worse the more you go down that dysglycemia spiral, but they are already an issue even if you're insulin resistant. So do you think it's relevant to know if you have it or not? HELL YEAH!
✨
Why is it irrelevant in the diabetologist world?
Well, if you work with patients with diabetes, those patients have already climbed down that dysglycemia ladder so yeah, of course, figuring out if those patients also have insulin resistance is unnecessary. Of course they do! Been there, done that. Or more accurately: been there, ignored that...
But saying it's irrelevant tout court is unprofessional. Is as if I'd work with only bald clients (let's say people with alopecia) and I'd scream on all social media platforms that washing your hair is pointless. It might be pointless if you don't have any hair left, but it can be very important if you still want to keep the hair you have. I'm exaggerating of course, but you get the gist.
✨
And why is it irrelevant in the conventional medical world generally?
Well, because in the conventional medical world there's hardly any prevention. There's no time for it and dare I say there's little to no interest for it. The treatment to everything is medication or surgery. If you don't fill the criteria to get medicated, continue what you're doing and just wait a while. Sooner or later there will be enough damage or enough organ destruction to justify either the medication or the surgery.
Am I wrong? How many times you've been sent away by a doctor because you weren't sick enough YET, without any recommendation about what to do not to get sicker than you already were? I personally heard countless of stories like this from my clients.
✨
I've also read that making people aware they're insulin resistant is a scare tactic and why would you want to do that? I have to laugh at this. And yes, there's plenty of people who don't care about anything other than their comfort, who have no interest in changing anything in their diet or lifestyle. Who don't want to understand there's a responsibility in taking care of their health. "Give me a pill and send me on my way." There's a lot to say here about why this type of attitude, and trauma comes to mind.
All I want to say here though is: why you, as a medical professional, think applying the ostrich approach is the right strategy? Encouraging people to bury their head in the sand can mean avoiding preventive screening, can encourage women to avoid getting annual mammograms, can even push people with diabetes to avoid monitoring their blood sugar levels.
✨
So let people who do preventive medicine continue doing preventive medicine, even if (or especially because?) that means fewer people who will become diabetic later on in life. Make that insulin marker more available in Ireland. And if you're one who doesn't test for it, that's fine, just let everyone else do their job without throwing any judgment. Thank you.