181. How to reverse high blood pressure

You do not have high blood pressure or high cholesterol because you are getting older. You have high blood pressure and high cholesterol because you are living in an evolutionarily inconsistent way and Western medicine fails to realize this. This is the first hope I've had in 30 years. Check out this review on gut and digestion from heart and soil supplements from Francis L. She says, "I'm two weeks into animal based with heart and soil supplements and it's difficult to articulate just how excited and relieved I am to have finally found a healthy lifestyle of eating and movement. An animal based diet coupled with heart and soil supplements and gut and digestion has drastically improved the quality of my life. Overall inflammation is decreasing, energy is increasing, cognition and sleep are improving. As a sufferer of Crohn's disease for almost 30 years, this is the first hope I've had of existing without discomfort or pharmaceuticals. Thank you, Dr. Paul and the heart and soil team. Please don't stop what you are doing. We will not stop what we are doing. If you have GI issues, Crohn's, anything, I would recommend checking out an animal based diet. You can find all sorts of resources about how to do that at my website, carnivoremd.com, at heartandsoil.co. You can find gut and digestion from heart and soil supplements, desiccated organs, which include stomach and intestines, which many people with GI issues find to be massively helpful for their conditions. Our mission at heart and soil is to help you reclaim your birthrights, optimal health. Find us at heartandsoil.co. We have a whole host of different types of desiccated organ supplements so you can get more organs in your life and start thriving, get back to your real life. I'm so proud of what they're doing at heart and soil. So proud to be a part of this company. Also want to let you guys know the Kailas bullshit shirts are live. They are live. You can go to kailasbullshit.shop to get Kailas bullshit shirts to rep the movement. We also have sea oils or bullshit shirts. We have the old school stay radical shirts. There's a carnivoremd shirt. There's all kinds of good stuff there. There's hats. There's a hoodie. We're going to be expanding the merch because I want to see you guys on Whole Foods. I can't wait till I go to Austin or Miami or somewhere in the United States and I see somebody else wearing a Kailas bullshit shirt. I'm going to walk up, give you a big fist bump, maybe a hug and buy you a tomahawk. I can't wait to see how your friends, people in the grocery store react. But the world needs to know Kailas bullshit, sea oils are bullshit. You can find it all at kailasbullshit.shop. On this week's podcast, I wanted to talk about hypertension. Such a big deal. Millions, 116 million Americans with hypertension. Billions of people in the world with hypertension. What causes it? How do we reverse it? What about the drugs? Are they useful or not? Are they harmful? What are the side effects? I go into all of that in this week's podcast. Talk about how medical education is flawed, what we need to do to train doctors better so we can actually improve the health of our population. I know that you guys know someone with hypertension. Maybe you have hypertension. Maybe you have insulin resistance or you know somebody. Please share this podcast with someone who will benefit. There is so much to be said about this. It was a really fascinating podcast to dive into. Also want to give a shout out to my sponsors. They make the podcast possible. I want to start with White Oak Pastures, this sixth generation regenerative farm in Bluffton, Georgia. They've got a new thing going guys. You can get 5% off your recurring orders with the code Carnivore 5. Just for listeners of this podcast, Carnivore 5 gets you 5% off your order there. Carnivore MD gets you 10% off your order if you are a first-time customer. And I think you should consider becoming a first-time customer. They have grass-fed, grass-finished beef. They have lamb. They have Iberico pork. They have soy and corn-free chicken. They have amazing eggs. All kinds of organs. Like I said, it's a regenerative farm. Will and Jenny Harris are leading the charge in this movement. 120 years, six generations in the family. They're good people and this stuff is great. It's how we support the movement. Check them out. WhiteOakPastures.com. Also want to give a shout out to 8sleep.com. You can go to 8sleep.com/carnivoremd. The podcast is brought to you by 8sleep. You guys know Good Sleep is the ultimate game changer. I really think that, as I've heard other people say, if sleep were not something that we have to do every night, it would be banned as the single best performance enhancing substance on the planet, second only perhaps to liver or testicles, maybe some intestines and tripe in there. But getting to sleep is crucial. And more than 30% of Americans struggle with sleep. Temperature isn't one of the main causes of poor sleep. Your mattress is probably too hot. That's why I love 8sleep. I got a pod pro cover for my mattress in Austin. This thing is amazing. Each side cools and heats individually. Your bed partner can have a different temperature than you. It goes as low as 55 or as hot as 110. It has AI in the bed, not really, but it does biometric tracking, does HRV. It tells you all about your sleep. This thing is amazing. Super comfortable. They have the pod pro cover. They also have the whole mattress. It's the most advanced sleeping technology in the world. I think it's the best way to really cool yourself while you are sleeping. 8sleep users fall asleep 32% faster. They reduce sleep interruptions by 40%. It's incredible. I mean, I love sleeping on that thing in the States. And when I go to Airbnb, I hate it because I always sleep too hot, but you can get an 8sleep pod pro. Go to 8sleep.com. That's E-I-G-H-T-S-L-E-E-P.com/carnivore-M-D. Check out the pod pro cover. Save $150 to check out. They currently shipped to the USA, Canada, and the United Kingdom. Also want to give a shout out to another amazing regenerative farm, primopastures.com. New customers received 10% off their first order with the code carnivore-M-D. They were founded in 2012. Sole purpose was to promote better health through diet for themselves and their family. They were fed up with misleading labels found in supermarkets. They respect nature. None of their food has any antibiotics, hormones, or growth supplements. It's non-GMO, soy-free, certified organic feed in the chickens that receive feed. The cows are grass-fed and grass-finished. Always pasture-raised, no exceptions. Chickens never have supplemental feed with corn, and they deliver to your doorstep nation wide. They have chicken, pork, beef, lamb, wild caught fish, raw honey, pastured bone broth. Buy the name of coffee. I'm not a fan of that. They mention it here, but they sell it if you like it. If you're thriving, okay. If you're not, maybe get rid of the coffee. Go to primalpastures.com. New customers received 10% off their first order with the code carnivore-M-D. Another farm doing amazing regenerative work. People always ask me, "Where can I get good meat?" Primalpastures.com. White Oak Pastures.com. You heard it here on the Fundamental Health podcast. Last but not least, I want to give a shout out to the friends, folks at HireDose. You can use the promo code "Paul" at checkout and save 15% off. That's HireDose.com. They sent me a PEMF mat, and I love it. It's on the floor of my bedroom. It pulsed electromagnetic field, works by sending electromagnetic waves to your body at different frequencies to help promote your body's own recovery processes. Did you know that the earth has its own EMF field? You can recreate that with a PEMF mat. 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Hiredose.com, promo code PALL. Save 15% off. That is it, my friends. On to the podcast. Enjoy this one. Many of you may not have high blood pressure, but I am betting that you know someone who has high blood pressure, whether this is a parent, a grandparent, a brother, a sister, someone you know likely has high blood pressure. The epidemiology of high blood pressure is astounding. There are millions, millions of people who have high blood pressure in the world, in the United States, and I will show you, there are really hundreds of millions of people who have high blood pressure even in the United States. I will show you some graphics that discuss the actual profound burden of this condition in Americans and in the world. And so in today's podcast, I want to talk about what causes high blood pressure, connections with other medical illnesses like heart disease, otherwise known as atherosclerosis or kidney disease, and how to reverse. I'll talk about how Western medicine treats high blood pressure, why I think that that's actually not addressing the root cause, clearly not addressing the root cause, how we can address the root cause of high blood pressure with medications, though I'm not a fan of those medications. That will come later in the podcast and how we can actually address and reverse hypertension with dietary and lifestyle changes. Many of the themes in this podcast will be familiar to regular listeners of fundamental health podcasts in general, but it's interesting to see how it all ties together. As I've discussed in the past, I don't believe that there are 30,000, I think there's actually 10,000 diagnoses that medical students are tasked with learning in medical school. I don't believe there are 10,000 illnesses. I believe there are four or five things that cause the majority of issues for humans. And it's interesting for me to go down the rabbit holes of different conditions like hypertension or atherosclerosis and often find that the same cause lies at the root of so many of these things. So if that is the case, that is something I hope to advance within medicine, that's something I hope to allow more physicians, medical students, nurses, medical educators to become aware of with my work. When we realize that is the case, we realize we must focus on those root causes in a much more aggressive fashion than Western medicine is today. So look at the current burden of hypertension. You can see here, this is according to a 2017 paper which looked at the NHANES from 2015 to 2018. And there were 116 million people in the US with hypertension, 47.3% of the population, almost half of the United States population has hypertension. This is the true pandemic. This is an epidemic. If you look at how they break this down, this will foreshadow things I'll talk about later in the podcast, they say, okay, for part of it, for part of this group, lifestyle modifications are recommended. And for part of the group, lifestyle modifications plus medication are recommended. You can see here, if you go further down this pyramid that I'm showing on the video, all of the people for whom lifestyle modification was recommended remain uncontrolled. Essentially, all of them remained uncontrolled. The majority of people for whom lifestyle modifications plus medications were recommended still remain uncontrolled. Some of them become controlled according to the guidelines of what we think of as controlled blood pressure. Usually it's 120 over 80 millimeters of mercury. But I find it interesting that basically according to this graphic that I'm showing, no one within Western medicine for whom lifestyle modifications are recommended becomes controlled with their hypertension. I'll talk about why a little later in this podcast. But according to this graphic from the NHANES data, a very small percentage of people who have hypertension, 47.3% of the US population actually get that under control or less than 140 over 90 according to these guidelines. I would say it's even more rare that people get their blood pressure below 120 over 80. But even if they do get their blood pressure that low with medications that I'll talk about in this podcast, very few of them, if any, are treating the root cause, are treating the root cause of their hypertension, which will certainly manifest in other problems for them as you will see later in this podcast. Here's another paper from Nature Reviews and Nephrology from 2020 talking about the global epidemiology of hypertension. This is the leading cause of cardiovascular disease and premature death worldwide, hypertension. Owing to the widespread use of anti-hypertensive medications, the global mean blood pressure has remained constant or decreased slightly over the past four decades. But the prevalence of hypertension has increased, especially in low and middle income countries. 31.1% of adults worldwide have hypertension in 2010. That is 1.39 billion people. These numbers exceed even diabetes, but I will say later they are connected. Prevalence of hypertension among adults was higher in low and middle income countries with 31.5%, 1.04 billion people than in high income countries, 28.5%, 349 million people. So variations in the levels of risk factors for hypertension, such as high sodium intake, so here in the abstract, they go on to detail what Western medicine considers to be the risk factors for hypertension. I disagree with these risk factors, and I will talk about what I believe causes hypertension later in the podcast. But this Nature Reviews and Nephrology article says risk factors include high sodium intake, low potassium intake, obesity, I would agree with that one, alcohol consumption, I would agree with that one, physical inactivity, probably agree with that one, unhealthy diet, I agree with that. But what I consider to be an unhealthy diet is probably different than the authors of this study. But they say that those risk factors may explain some of the regional heterogeneity in the hypertension prevalence. Nevertheless, the point that I am making here is that the burden of hypertension in this country and in the world are enormous. You know someone with hypertension. Before we get into what we are taught about hypertension in medical school, I want to share with you guys a distinction that is made in the medical literature regarding hypertension, which is the causes of hypertension secondary versus primary. So when we think about hypertension, we are thinking of primarily primary hypertension, something that Western medicine says is age-related. Western medicine teaches medical students that as people age, for every decade they age, the systolic blood pressure, which is the top number, diastolic number being the bottom number, the systolic number increases for every decade that people age. Is this true for all humans? I say no, and I'll show you data to corroborate that in one moment, looking at a hunter-gatherer tribe, specifically the Hadza, who I like to talk about. But Western medicine teaches us doctors, teaches medical students that hypertension happens as we age. This is primary hypertension. In medicine, we also wrestle with something called secondary hypertension. Secondary hypertension is different. I'm not really talking about secondary hypertension this podcast, but many people do suffer with secondary hypertension. The numbers are much, much lower than primary hypertension. And the causes of secondary hypertension are things like kidney inflammation at the level of the glomerulus, the filtering apparatus, called acute glomerulonephritis, chronic renal disease, which is chronic kidney disease, polycystic kidney disease, renal artery stenosis. If the arteries that supply the kidneys or leave from the kidneys becomes stenotic, that is, narrowed, that can cause hypertension. Inflammation in the arteries supplying the kidneys, renal vasculitis, can produce hypertension, renin-producing tumors, which are going to activate the renin angiotensin aldosterone axis, something that I'll talk about later in this podcast, or aldosterone-producing tumors can also do this. So then there are endocrine causes of secondary hypertension, adrenocortical hyperfunction, Cushing syndrome, primary aldosteronism, that is a tumor-producing aldosterone, which is also part of the renin-renin-angiotensin aldosterone axis. In general, adrenal hyperplasia, exogenous hormones, glucocorticoids, or estrogens, birth control can definitely do this. Theochromositomo, which is the tumor that everyone loves to think about in medical school, is the prime zebra, but it's very rare. Acromegaly, which is related to excess production of growth hormone. Hypo or hyperthyroidism, these have to be very severe abnormalities in the thyroid, or pregnancy can also change blood pressure. Now, as I said, people with secondary causes of hypertension are much more rare than primary hypertension. The majority, I would say 97, 98% of what we see in medicine is primary hypertension, but I wanted to point out that secondary hypertension does occur, and there are causes for secondary hypertension that can be corrected if you remove the tumor, or you correct the endocrine abnormalities. I remember one time when I was a PA, I worked in cardiology before I went back to medical school, actually had a patient with severe hypertension, and many doctors had tried to put him on multiple medications. He was on all kinds of things, minoxidil, second, third-line medications for high blood pressure, and this was because no one could get his blood pressure under control, so I decided to check an aldosterone level on him, and his aldosterone level was through the roof. He ended up having an aldosterone-secreting tumor in his adrenal gland, so he had primary hyperaldosteronism caused by a tumor is in his adrenal gland, and when that was removed, his blood pressure got significantly better. We later found out that he also had a prolactin-secreting adenoma in his brain, in his pituitary gland, so he probably had some derivative of a multiple endocrine neoplasia, another zebra thing that medical students like, but this gentleman's blood pressure was never going to get better, no matter what we did, unless we removed the tumor that was secreting excess aldosterone into his blood. I'll talk about the aldosterone pathway within the retinal angiotentin-aldosterone cascade later in this podcast, but essentially, aldosterone is a hormone that works on the kidney to conserve sodium and causes the excretion of potassium. Now, if your hormones are overacting and you're conserving tons of sodium, you will have hypertension, not because of excess sodium in the diet, but simply because you are increasing your absorption of sodium at the level of the kidney. So let's turn our attention back to primary hypertension. The rest of this podcast will be focused on primary hypertension because I think of primary hypertension, colloquial hypertension, as a chronic reversible illness with diet and lifestyle. Now, what does the Mayo Clinic say about primary hypertension? I'm showing you this to illustrate what mainstream Western medicine does for this condition. There is a top number of systolic pressure, a diastolic pressure. They talk about what is hypertension. Anything over 120 over 80 is really hypertension. At this point, you should not have blood pressure of 120 over 80. And if you look at the Mayo Clinic, they do break this down into primary and secondary hypertension, where secondary hypertension having the potential causes that I mentioned earlier, though they do add obstructive sleep apnea, which I think is a good thing to be aware of. But risk factors for primary hypertension, according to the Mayo Clinic include age. I'll comment on that in a moment, race. There is some predilection of certain races to develop hypertension earlier than it does in Caucasian, specifically African Americans, develop hypertension more severely and at an earlier age than Caucasians. Family history is a risk factor for high blood pressure. Again, I'm going to comment on that in a moment. Being overweight or obese. Yeah, I would agree with that. Not being physically active. Probably, though, I think that as I've spoken about in the past, if you correct your diet and it is evolutionally appropriate, you will want to be physically active because you will feel good. Tobacco can do it. Yes, too much salt in your diet. I disagree with this one. I don't think salt is a root cause of hypertension, though excess salt in the diet can worsen hypertension once you have it. But I'll talk about sodium. Why I don't think removing salt corrects the root cause and hypertension later in this podcast. Too little potassium in your diet. Again, I doubt this is a root cause for many people, though in conditions that I will talk about later, specifically insulin resistance that are at the root of hypertension, there is a hormonal milieu that can lead to excess sodium and lower amounts of potassium in the diet. People always ask about potassium on a carnivore diet. Something I've spoken about in the past is that meat has a good amount of potassium and it's not about how much potassium you get in your diet alone. It's also about how much potassium you retain. There's plenty of potassium in fruit. Anyone on an animal based diet, which is what I am more a fan of, will be getting plenty of fruit and plenty of potassium in their diet. You don't need vegetables to get enough potassium, nor does excess potassium correct hypertension. You must correct the root cause. Mayo Clinic says drinking too much alcohol. Yes, that can do it. Stress can do it, but it's only temporary and the blood pressure should return to normal. Certain chronic conditions, they say kidney disease, diabetes, and sleep apnea. Those are really correctable conditions. Those are considered mostly secondary hypertensive conditions. What about age and family history? To me, this is really a cop out within Western medicine. This is the type of thing that we are taught in medical school. As I said, we are taught that as you age for every decade that you age, blood pressure increases, systolic blood pressure specifically, and many people will say, "I have a family history of high blood pressure. I was told by my doctor there's nothing I can do." Bullshit, bullshit, bullshit. I believe both of those are cop outs by Western medicine. In many people who have a history of high blood pressure, high blood pressure will develop, but this is not because of the family history. The family history is perhaps a predisposition that can manifest if these individuals are not living in an evolutionarily consistent way, but a family history of hypertension, cardiovascular disease, that is atherosclerosis, heart disease, dementia, stroke, cancers. These are not for sure in humans. These are simply predispositions that we have that are then manifest by the way that we live our lives. Western medicine fails to teach medical students this, and all too often, I have heard from patients in the past that there's nothing I can do about my high blood pressure because it's in my family history. There's nothing I can do about my high cholesterol. I have a family history, or I have high cholesterol. I have high blood pressure because I'm getting older. No, no, no. You do not have high blood pressure or high cholesterol because you are getting older. You have high blood pressure and high cholesterol because you are living in an evolutionarily inconsistent way, and Western medicine fails to realize this. Western medicine fails to counsel patients that this is actually a correctable, reversible condition. When patients go to their doctors and they are diagnosed with primary hypertension, 99% of the time, I believe they are told there is no cure for this. We don't know what causes it. There is nothing you can do about this. Take this medication. 1% of the time, perhaps, maybe 5% of the time, if we're generous, physicians will say cut down on certain foods in your diet. They will often recommend lower salt, but as I've mentioned, and as I will elaborate on later in this podcast, that doesn't correct the root cause, and it causes more problems for many of these individuals. This paper should be shown to every single medical student across the United States, across the world. The title is the physical activity patterns and biomarkers of cardiovascular disease, risk, and hunter-gatherers. Herman Ponser is one of the authors on this paper. He was on the podcast previously, and they say in the abstract, we found no evidence of risk factors for cardiovascular disease in this population of hodds of hunter-gatherers. There was a low prevalence of hypertension across the lifespan, optimal levels for biomarkers of cardiovascular health. I've spoken about this paper in the past when I've illustrated the notion that hunter-gatherers do not get chronic illness. They do not have risk factors for cardiovascular disease as they age, as do people in the Western world. But the most important point I will make about this paper in this podcast is this graphic, which shows the systolic blood pressure in men and women and the diastolic blood pressure in men and women across the lifespan. You can see here that on the x-axis is age in years, and it goes up to 80 plus years old. Yes, hunter-gatherers live long, ripe, vital lives, and our notion that they die early is confounded by higher rates of infant mortality in wild human populations. And as you can see, the systolic blood pressure does not rise in any significant amount as they age. Even into their eighth decade of life, the average systolic blood pressure was only slightly above 120 millimeters of mercury for the hodds of hunter gatherers. Diastolic blood pressure remains between 60 and 80 millimeters of mercury across the lifespan well into the eighth decade of life for these hodds of hunter-gatherers. There is no age-related increase in systolic or diastolic blood pressure in wild living humans. That is hunter-gatherers, the hodza. I visited the hodza in February of 2021. I spent time with them. I've spoken about my experiences there and their diets at length in the past on this podcast. In summary, animals are what they dream about. It is what they think about all the time. They are hunters. They celebrate meat and organs like nothing else. They don't give a shit about vegetables. They really won't eat vegetables unless they're starving. They do not eat the Baobab seeds unless they're starving. They will eat occasional tubers, but they get excited about honey and fruit. But even more so, they get excited about meat and organs. They have no seed oils in their diet from their natural state. They are being influenced by local missionaries who provide them with cornmeal, unfortunately, and some seed oils. Trappings of Western civilization are creeping into their diets, but they are not a significant part of their diet. I believe they were even less a part of their diet when Herman Poncer and his associates did this research on their systolic and diastolic blood pressure. So, systolic and diastolic blood pressure do not rise with age in free-living wild human populations. This notion should be taught to all medical students as should the notion that free-living humans do not suffer rates of diabetes, obesity, chronic age-related illness, cardiovascular disease, dementia, or cancer that are even a fraction of what we do in the West. Freedom from all of these things is completely possible if we align our diet and lifestyle with what our human body is expecting. That's the work that I do. That's how I frame all of the work I do. Let's return back to the conversation of hypertension. How many patients who go to their doctors receive counseling about dietary and lifestyle changes for hypertension? I would say very few, some perhaps. Again, the majority of this is limited to salt restriction, which I am not a fan of. Furthermore, we must be honest with ourselves about the health of our doctors. From a 2007 study, 50% of male physicians in the United States, this is the Physicians Health Study, were obese and overweight. Those are two different BMI categories that I'm combining, but obesity and overweight were 50% of U.S. male physicians. In the Nurses Health Study, 39% of nurses were obese and overweight. And we know that in an obese physician and likely in an obese or overweight nurse, counseling regarding dietary and lifestyle changes will be very different, if present at all. There is good research to corroborate this notion. You can see here a very sad study that is unfortunately true from 2012, the impact of Physician Body Mass Index on Obesity Care and Beliefs. This is using a national cross-country survey of 500 primary care physicians from 2011. We found that physicians with normal BMI were more likely to engage their obese patients in weight loss discussions as compared to overweight and obese physicians, 30% versus 18% with a p-value of .01. Physicians with a normal BMI had greater confidence in their ability to provide dietary and exercise counseling to their obese patients. A higher percentage of normal BMI physicians believed that overweight and obese patients would be less likely to trust weight loss advice from overweight and obese doctors. And physicians in the normal BMI category were more likely to believe that physicians should model healthy weight-related behaviors, maintaining a healthy weight, exercising regularly. The probability of a physician recording an obesity diagnosis or initiating a weight loss conversation with their obese patients was higher when the perception of the patient's body weight met or exceeded their own personal bodymate. And those numbers are substantial. So the probability of a physician recording an obesity diagnosis was 93% versus 7% and 89% versus 11% for the probability of initiating a weight loss conversation when the obese patient's body mass index was greater than the physicians. So if the patient was not fatter than the physician, the doctors didn't talk to them about weight loss and why would they even if the patient was overweight clearly. These results suggest that more normal weight physicians recommended obesity care to their patients and felt confident doing so. Yeah, no surprise there. But interestingly, I have had conversations with many friends from medical school, from residency, and friends who are currently residents. And this is just my observation, but they will often tell me, dependent on specialties, most of their colleagues, even in residency are drinking, they're overweight, not eating healthfully, we're not creating a future cadre of physicians who value health. We're creating physicians who value work, who value money, and who value getting the heck out of the hospital most of the time. So I believe the medical system is massively broken and statistics suggesting that half of all male physicians are obese and overweight. I can't even imagine how many male physicians or female physicians for that matter have elevated levels of fasting insulin. We are not creating a group of healthy doctors. So how could we be expected to counsel patients properly regarding the most important things that they can do for their health, dietary changes aligning their diet with what is evolutionary consistent for humans and lifestyle changes, exercising more sunlight, avoidance of toxins in the environment, clean drinking water, etc. So now that we've talked about the background of hypertension, the differences between primary and secondary hypertension, how Western medicine thinks about primary hypertension, age related family history, irreversible. Let's talk about how Western medicine addresses hypertension, mostly medications. Salt restriction is part of it. I'll talk about that in a moment, but the medications that Western medicine uses for hypertension include angiotensin converting enzyme inhibitors, angiotensin receptor blockers, direct renenin inhibitors, calcium channel blockers, beta blockers, diuretics like thiazides or loop diuretics. I'll talk about the ACE, ARB, and direct renenin inhibitors in the context of the renenin angiotensin aldosterone axis, which I'll detail in a moment. But none of those medications correct the root cause of hypertension, which I believe most of medicine agrees on and we know very clearly. Do we have a medication that treats the root cause of hypertension? We do actually. I'm not a fan of using it and I'll talk about that later in the podcast. I'm going to keep you guys in suspense for a little bit longer, but that medication doesn't do great things for humans as it's correcting the root cause, but we have a medication that corrects the root cause of hypertension. I'm not advocating that we use it. I only will bring it up later in the podcast to illustrate the cause of hypertension, how correcting the cause of hypertension can reverse other issues and be beneficial and how insulin resistance can be fixed. So stay tuned for all of that. So what are the side effects of the medications we use to treat hypertension? Well, if you're on a beta blocker, it's going to slow your pulse. It causes erectile dysfunction. It can cause depression. Calcium channel blockers cause peripheral edema. We're sitting of swelling in the limbs and that can cause orthostasis or lightheadedness when people stand up leading to falls and orthopedic injuries. Diuretics, whether they're loop diuretics or thiazide diuretics, cause loss of critical electrolytes for humans and nutrients that are not intended to be lost. Look at the list of nutrient deficiencies associated with a loop diuretic like lacyx or ferrosomide. It is long. B vitamins, magnesium, other minerals, massive deficiencies follow when we cause diuresis in humans to treat hypertension without treating the root cause. Thiazide diuretics can also cause problems in terms of electrolyte deficiencies and nutrient deficiencies. These are a nightmare for our human long-term health. This is the problem with western medicine. It's myopic. It looks at a symptom, treats the symptom, and then ignores the side effects of the medication or must use other medications to treat the side effects of the medication it uses. Why not just treat the root cause? Angiotensin receptor blockers, ACE inhibitors, direct random inhibitors, all can cause electrolyte issues. Many of them can cause angioedema. ACE inhibitors specifically cause a dry cough associated with bradykinin. None of these medications are ideal for humans. No medication that we give to humans is ideal in general. They all have utility. Have I prescribed all of them in the past? Yes, absolutely I have. I was once a physician assistant who worked in cardiology who did not understand the root cause of hypertension. And so I've prescribed all these medications. I have also prescribed statins to patients in the past. Would I do this now? No. I would strongly counsel patients regarding the root causes of hypertension, which I believe are insulin resistance, and I'll get to that in a moment. And how to change that, I will definitely talk about that in this podcast. For the sake of completeness, I've spoken about the renin-angiotensin aldosterone system a number of times in this podcast. I will do a little bit of education about what this is. In the liver, there is a substance produced called angiotensinogen that is converted to angiotensin 1 by a substance called renin, which is produced by the kidneys. Renin will be released from the kidneys if the kidneys sense that blood pressure is low in a number of ways, at the level of arterioles, at the level of something called the JGA or the juxtaglomerular apparatus. Angiotensin 1 is converted to a more active form. Angiotensin 2 by an enzyme called ACE. Angiotensin converting enzyme found in the pulmonary and renal endothelium. Angiotensin 2 has many effects on the human body that are necessary for our survival in the setting of massive blood loss or dehydration, including increasing sympathetic activity. That is the fight or flight nervous system, something that causes our blood pressure to be stable because our blood vessels will contract. Tubular, sodium and chloride reabsorption, potassium excretion, water retention, that is primarily through the actions of aldosterone. And that is at the level of the kidney. You can see angiotensin 2 increases aldosterone secretion at the level of the adrenal gland. There is arteriolar basal constriction, increase in blood pressure, that is small arteries. And at the level of the pituitary gland, specifically the posterior pituitary, antidiuretic hormone or vasopressin is released, which causes water retention at the level of the kidneys. All of these are part of an in extremist situation for humans for blood loss and dehydration. We will leverage this system in hypertension, but we are definitely cranking on levers that are not meant to be cranked on in this situation. We are pushing the gears and levers much past what they are meant to when we are not correcting the root cause of this problem. Some medications for hypertension in Western medicine direct renin inhibitors like tecturna will block the actions of renin converting angiotensinogen to angiotensin 1. ACE inhibitors will inhibit this enzyme, angiotensin converting enzyme so that angiotensin 1 doesn't become angiotensin 2. They have a significant side effect involving a dry cough due to decreased breakdown of bradykinin without the ACE enzyme. And there are angiotensin 2 receptor blockers, which will mitigate many of these downstream side effects, at least in terms of sympathetic activity and other functions of angiotensin 2. So that is how these things work. The problem, as I've mentioned, is that they come with many side effects, angioedema, swelling of the lips, which can be massively bad for people dry cough, hyperkalemia, increased potassium. None of these medications are perfect, but it's what we use in Western medicine. My problem here is that we are not addressing the root cause, which I believe is insulin resistance. And there is a large amount of literature to illustrate very clearly that insulin resistance and resultant hyperinsulinemia, elevated levels of insulin result in hypertension. I would say something very strong at this point in the podcast. Hypertension is insulin resistance until proven otherwise. If you have hypertension, you have insulin resistance, unless you have a secondary cause of your hypertension, all of those things I discussed earlier. But if you have primary hypertension, you have insulin resistance. And that is correctable with dietary changes. I'll talk about all of that as we finish the podcast up. But Paul, doesn't salt cause hypertension? No. In a healthy individual who is insulin sensitive, eating sodium does not cause high blood pressure. Though my body would rebel and tell me not to do this, I could eat 20 plus grams of sodium per day and not develop chronic hypertension. Would I have an increased blood volume for a day before my kidneys did something called natrioresis and got rid of that sodium? Yeah, my blood volume might be slightly high. I might actually have temporary hypertension if I eat a massive amount of sodium, but my body is going to tell me to get rid of it. It's not going to be pleasant to do that. And the kidneys will adjust. The kidneys will get rid of that excess sodium and my blood pressure will return to normal. So sodium itself is not the cause of high blood pressure. And in individuals who have insulin resistance, there will be excess resorption, excess holding on to sodium at the level of the kidney. So what can we do if we don't correct the root cause of hypertension, which is insulin resistance, we must get rid of the sodium. The problem is that sodium is critical for so many functions in the human body. We know that in individuals who are insulin resistant, who limit their sodium, they will have more orthostatic hypotension, meaning they get up, they get lightheaded, and they can fall over or blackout. They will have more erectile dysfunction. They will have lower blood volume, lower energy. Low sodium diets are a nightmare for humans. It is no way to live as a human to be a low sodium individual. Limiting your sodium too much will cause you to feel miserable, cause all of the issues I've talked about, orthostatic hypotension, potentially erectile dysfunction, and you will activate your renin angiotensin aldosterone system. One of the things that system is primed to do is to conserve sodium if you don't get enough. So the renin to aldosterone ratio is a critical thing you can look at in humans. If you limit your sodium too much, you will see aldosterone and renin rise because your body is trying to conserve the sodium. What is an ideal amount of sodium for humans? See what works for you. I would say that on a daily basis, I probably have six to eight grams of salt in my diet. I use a low microplastic sea salt. I'm very intentional about that, which translates to about three and a half or four grams of sodium per day. Sodium chloride is of course a salt, so half of the weight of the sodium chloride will be the sodium. That's what works for me. Ketogenic dieters often need more than that because remember that the actions of insulin at the level of the kidney are critical for the maintenance of proper electrolyte levels. I did a podcast previously where I talked about why I no longer think a ketogenic diet is ideal for humans, why I stopped a ketogenic diet in the past. And one of the things I talked about in that podcast was that a postprandial after eating spike in your insulin is a healthy, good thing. It affects hormones positively. It allows you to retain the sodium that you eat so your electrolytes can be balanced. When sodium becomes disordered, all of the electrolytes become disordered. Chloride, potassium, magnesium, it's a nightmare. People on ketogenic diets often must chase electrolytes round and round like a dog chasing its tail. Don't fear carbohydrates. I believe that fruit is the least toxic source of carbohydrates, but getting some carbohydrates in your meat-based diet will improve your electrolyte maintenance. And conversely, excess insulin in a state of hyperinsulinemia will lead to excess resorption of sodium. So if you have high blood pressure and you have hyperinsulinemia, if your fasting insulin is high, you're holding onto too much sodium. How do you fix that? You fix the insulin resistance. You fix the insulin resistance. What else does too much insulin do? It causes increased sympathetic tone. It causes that fight-or-flight nervous system to go up. It increases the production of angiotensin-2. And it appears, and I'll speak about this at the end of the podcast, that in hypertensive individuals, angiotensin-2 may be increased independent of insulin as well. Hyperinsulinemia decreases the formation of nitric oxide through many of the second messenger cascades. Hyperinsulinemia also appears to raise LDL, lower HDL, and raise triglycerides. Oh, now we're back to lipids. Yeah, it's all connected. And perhaps most importantly, hyperinsulinemia leads to disordered wound healing. We know very clearly that in diabetic individuals, there is immune compromise and delayed wound healing. Why is that important for hypertension? Well, I want to link hypertension and cardiovascular disease now. We know that high blood pressure is a risk factor for cardiovascular disease. Why is that? Let's return to something that I've spoken about in the past. Humans do not get atherosclerosis. We do not get heart disease in our veins. In a normal intensive individual, there is no atherosclerosis that will occur in the veins, no matter what, because they are a low pressure system. We only get atherosclerosis in our arteries, really no matter what our systemic blood pressure is. Now, these blood vessels are contiguous. The same amount of LDL particles, the same amount of ApoB-containing particles are circulating through the veins in the arteries. And the endothelium looks exactly the same on the inside. Why do we only get atherosclerosis in the arteries? Because the arteries are a higher pressure system, and that high pressure damages the arteries. And that damage to the arteries is where the beginnings of atherosclerosis lie. So, what happens with insulin resistance? Why is insulin resistance so critical for the development of atherosclerosis? Because insulin resistance impairs the wound healing of the damage in the arteries that is done from a higher pressure system. I believe that even in normal intensive individuals, there is probably some damage being done in arteries at pressures of 120 millimeters of mercury or higher than that when you exercise, especially at bifurcations, the branch points of the arteries. But in an individual who's insulin sensitive, I believe that your immune system, your repair system in your body will fix the damage in your arteries. In an insulin-resistant individual, that damage goes on way too long, and that is the beginning of an atherosclerotic plaque. That is why a hypertensive individual who also has insulin resistance, that is my premise, because there is no hypertension without insulin resistance in primary hypertension, will have delayed wound healing in the damage caused in the arteries from the hypertension, and that leads to accelerated atherosclerosis. So, that is why hypertension is so bad for your blood vessels. You must repair those blood vessels. In order to repair those blood vessels, you must be insulin sensitive. I've talked about this at length in the past. How do you know if you're insulin sensitive? You can either wear a continuous glucose monitor from a company like NeutroSense or whoever. I've had the folks from NeutroSense on the podcast who talk about my continuous glucose monitor readings. The easiest way is to get a fasting insulin checked, and a fasting insulin should be less than five, ideally less than three microIU per ml. I shared my recent blood work from both July and August previously on the podcast, if you want to go back and see what my fasting insulin levels were. Hint, very low. One was 3.3, and one was less than three. I believe it was 2.9 microIU per ml. So, I've made a couple assertions in the podcast that I want to back up with a little bit of literature. The first is that nutrition is not taught in medical schools. Here's a nutritional education in the U.S. Medical School's latest update of a national survey. This is depressing. It's from 2010. The basic gist is that medical schools don't freaking teach nutrition, which needs to change. Fasting insulin, insulin resistance, and the risk of hypertension in the general population. A meta-analysis from 2017. The conclusions, elevated fasting insulin concentrations, or insulin resistance, as estimated by the HOMA IR model, which is calculated by multiplying your fasting insulin and your fasting glucose, is independently associated with an exacerbated risk of hypertension in the general population. Early intervention of hyperinsulinemia or insulin resistance may help clinicians identify high risk of hypertensive population. Yeah, but what does Western medicine do for hyperinsulinemia or insulin resistance? They don't know what to do. They might give metformin. You might give drugs for diabetes. Sort of corrects the root cause. Not really. This has got to be diet and lifestyle change. We know very clearly that you can change diabetes with diet and lifestyle. High blood pressure, bone mineral loss, and insulin resistance in women. This is yet another thing that hyperinsulinemia can do in humans. And they show that women with hypertension had worsening indices of bone mineral loss. You do not want hypertension. You do not want osteoporosis. There's a 1990 article. We have known since 1990 that insulin resistance and hypertension were corrected, and yet we still fail to treat hypertension as an insulin-resistant process. The effects of diabetes mellitus on wound healing. This is from a plastic surgery journal. In 1991, they talk about limitation of neutrophil functioning, worsening of malnutrition, increasing hormones that cause catabolism, leading to impairments of wound healing. Perhaps the best paper on this topic, the impact of obesity and the metabolic syndrome on immunity. This is from 2016. The authors say that obese individuals are at a greater risk for chronic disease, often present with clinical parameters of metabolic syndrome, insulin resistance, and systemic markers of chronic low-grade inflammation. It has been well established that the cells of the immune system play an important role in the pathogenesis of obesity and metabolic syndrome-related diseases evidenced by leukocyte activation and dysfunction in metabolic tissues, such as adipose tissue, liver pancreas, and the vasculature. Recent findings have highlighted the substantial impact that obesity and metabolic syndrome parameters have on immunity and pathogen defense, including the disruption of lymphoid tissue integrity, alterations in leukocyte development, phenotypes, activity, and the coordination of the innate and adaptive immune system, those two immune system branches. Basically, being diabetic or prediabetic, having insulin resistance wreaks havoc on your immune system, and you know that your immune system is critical for the repair of parts of your body. You must repair your skin, your arteries, whatever, with your immune system. That is how your immune system works to repair tissues. So, diabetics have delayed wound healing. When I was a PA, I saw this constantly in patients in the cardiology practice. They would come in with horrible injuries. That were the result of nothing more than a simple nick on the foot. A diabetic can stub their toe and get a cut, and if they don't pay attention to it, they will possibly need an amputation. The immune system, the healing of arteries, the healing of soft tissues of the human body in diabetics is abysmal because of these issues related to insulin resistance, the effects on the immune system. So, do not doubt that, and this is happening in the arteries of diabetics as well. This is happening in the arteries of people with hypertension as well. So, how do we treat hypertension? How should we treat hypertension? We should focus on insulin resistance. I believe that in human physiology, it is very clear that broken fat cells are the cause of insulin resistance, and I'll talk about that in more in a moment, but at this point in the podcast, I want to talk about one class of medications we have in medicine that improve insulin resistance. They do other bad things, but they do improve insulin resistance. These are called thiazolidine diones. It's a mouthful. We'll just say TZDs from now on, but TZD medications improve insulin resistance. How do they do this? Well, they do this through signaling of a couple of pathways connected with P-PAR, peroxazone, proliferator, gamma, and alpha, and increasing signaling in those pathways means that fat tissue gets bigger. So, TZDs make you fatter, and making you fatter improves insulin resistance, it turns out. I'm not saying we should have more fat people, so there's less insulin resistant people, but expansion of fat mass improves insulin resistance, at least in the short term. And that will make sense in a moment when I show you literature illustrating that the reason people get insulin resistant is because of broken fat cells that can't expand. Fat cells need to do one of two things in their life. They need to either grow, which is hypertrophy, or they need to divide, that is hyperplasia. There's very good evidence that in individuals who are insulin resistant, fat cells are broken. I'll talk about why later in this podcast, but fat cells are broken, and they cannot divide. They cannot do hyperplasia. They can only hypertrophy, so the fat cells get bigger, and bigger, and bigger, and they balloon, and they get inflamed, and there's infiltration of macrophages and other immune cells. They release lipokines, they release inflammatory mediators, they release non-esterified fatty acids, and all of human physiology goes into the toilet because you become insulin resistant when your fat cells can't divide. When your fat cells can only grow, can only hypertrophy, they essentially start to leak and break, and that causes inflammation. Well, TZDs, like pyoglutazone, also known as actose, help the fat cells start dividing again, but people get fatter. So increasing the adipose tissue mass can improve insulin resistance. We can give people pyoglutazone, for instance, and that will improve insulin resistance, but it makes them fatter. It's not a good medication long-term, but it illustrates a point, and that point is that if you give someone pyoglutazone, it also improves their blood pressure. Reversing insulin resistance, even with a medication, improves blood pressure. Check out this paper. The effects of pyoglutazone on metabolic control and blood pressure are randomized study in patients with type 2 diabetes mellitus. Inclusions, the study demonstrates the efficacy of pyoglutazone 30 milligrams a day and 45 milligrams a day, and the treatment of type 2 diabetes with an improved lipid profile, because we know that improving insulin resistance improves the lipid profile. LDL goes down, HDL goes up, triglycerides go down, and decreased blood pressure in addition to improved glycemic control. So yes, Western medicine has a medication that improves insulin resistance. In fact, a number of medications in this TZD class that improve insulin resistance. We don't use them for blood pressure, probably because they make people fat, because you're expanding the fat mass. If your fat cells are broken and they can't expand, increasing the number of fat cells will improve your insulin resistance, but then you get fatter, which isn't a good thing long-term either. Look at this paper from 2007. Obesity-associated improvements in the metabolic profile through expansion of the adipose tissue. Yes, broken fat cells cause insulin resistance. If you fix the fat cells and people are still eating the same garbage, they'll get fatter. This is really part of the body's innate adaptive response. It's a protective measure to say, "Hey, I'm already too fat. I don't need anything else. I don't want to expand my fat tissue. I don't want to be 500 pounds. I don't want to be 700 pounds." But you can do it with medications, and it will improve insulin resistance temporarily until the fat mass again reaches its threshold, and people become massively sick, obese, corpulent, all sorts of complications from being even fatter. The idea is not that people should become fatter, but that the medications do work, and that insulin resistance is at the core of hypertension. You can see this study has done in mice. The mice displayed increased expression of P par gamma target genes, and a reduction in macrophage infiltration and adipose tissue and systemic inflammation. The transgenic mice were morbidly obese with significantly higher levels of adipose tissue than their OB-OB littermates. OB-OB mice have a deficiency of leptin. They're leptin knockout mice, so they have no satiety, and they eat to become massively obese. But these mice, they made even fatter than the OB-OB mice, but unlike the OB-OB mice, they didn't have insulin resistance. So if you activate P par gamma, you can sort of fix what's wrong with the fat cells, but you'll get massively fat. Again, this is all meant to illustrate the fact that insulin resistance causes hypertension. If you fix insulin resistance with a medication like pyoglitazone or you improve it temporarily while somebody gets fatter, their hypertension will get better. But that's not the way you should do it. You should actually fix what causes the insulin resistance. As I've shown, and I'll continue to show, broken fat cells are the cause of insulin resistance, and then I'll talk about how to fix the broken fat cells. It's also important or interesting to point out that when you fix insulin resistance with pyoglitazone, depression seems to get better too. Imagine that. Insulin resistance is at the root of so many of our issues. Remember at the beginning of the podcast when I said I thought there were four or five things that cause problems in Western medicine? Insulin resistance is one of the biggest. If you fix it with diet or with a medication, a lot of things will get better temporarily. Remember, if you're giving someone pyoglitazone, they're getting fatter. You're not fixing this person long term. You're kicking the can down the road, but it illustrates the mechanism. Conclusion here, pyoglitazone alone or an add-on therapy to conventional treatments could induce remission of major depressive episodes, suggesting that drugs with P-PAR gamma agonist properties may be true and clinically relevant antidepressants, even in patients without metabolic comorbidities. I'm going to disagree with that. If you're using a drug in someone that has a P-PAR gamma agonist activity, they have metabolic comorbidities. You just don't know about it because this is such an important issue. One more article, insulin resistance in atherosclerosis, implications for insulin sensitizing agents, again, TZDs. They say considerable evidence review to hear in suggests that insulin resistance and the insulin resistance syndrome contribute to this unexplained cardiovascular risk in patients with type 2 diabetes. Accordingly, cardiovascular outcome trials with pyoglitazone have demonstrated this insulin sensitizing thiazolidine dione, TZD, reduces CV events in high-risk patients with type 2 diabetes. In this review, the roles of insulin resistance and the insulin resistance syndrome in the development of atherosclerotic CV disease and the impact of insulin sensitizing agents and of other anti-hyperglycemic medications in CV outcomes are discussed. Improving someone's insulin resistance with pyoglitazone improves atherosclerosis and cardiovascular outcomes. Insulin resistance causes hypertension, it causes atherosclerosis, it causes depression. I'm not saying we should use this medication to do these things. This is merely to illustrate the mechanism. Fix the insulin resistance at its root. Don't use the medication that makes people fatter. Don't kick the can down the road, but this is an illustration of the fact that the insulin resistance syndrome is at the root of all of these things. So look at this paper, thiazolidine diones, TZDs, regulate adipose, lineage dynamics. Combining in vivo lineage marking and BRDU lineage labeling strategies, they use a different TZD called rhodozaglitazone, a member of the TZD class, markedly increases the evolution of adipose progenitors into adipocytes. The TZDs will allow adipose tissue to do hyperplasia, they affect fat cell lineages, they allow the body to expand the fat mass. Furthermore, here's a paper, insulin resistance and impaired adipogenesis. What I've been talking about. Insulin resistance is impaired adipogenesis, impaired hyperplasia of fat cells. You can look at these articles if you want. This one is from 2015. One more article, adipocyte dysfunctions, linking obesity to insulin resistance and type 2 diabetes, and skeletal muscle. Insulin resistance can result from high levels of circulating fatty acids. Those are coming from fat cells that are leaking, that disrupt insulin signaling pathways. The severity of insulin resistance varies greatly among individuals. Here we postulate this variability may reflect differences in the level of lipid droplet proteins that promote sequestration of fatty acids within adipocytes in the form of triglycerides, thereby lowering exposure of skeletal muscle to the inhibitory effects of fatty acids. But adipocyte dysfunctions are what cause insulin resistance and then type 2 diabetes. The way it works is essentially that the fat cells get broken. We'll talk about why. They can't do hyperplasia. They can't divide. You can fix it with TZDs, but then they get really fat. If they can't divide, they become hypertrophic. They release all sorts of inflammatory mediators, and they have macrophage infiltration, inflammation in the adipocyte depots, adipose macrophage infiltration is associated with insulin resistance and vascular endothelial dysfunction in obese subjects. They have broken fat cells. Insulin resistance is broken fat cells unquestionably. These findings suggest that adipose tissue inflammation may be linked to vascular injury and increased cardiovascular risk in obese subjects. I want to pause there for one moment, take a slight detour into something that is very fascinating with regard to atherosclerosis. I've spoken about this condition before. It's called familial lipidistrophy, specifically a dunnegan type. There is premature atherosclerosis associated with monogenic insulin resistance. There are very few cases of this in the medical literature, but this is a condition known as dunnegan familial partial lipidistrophy where there is one gene, specifically the LMNA gene at codon 482 that is mutated that causes atherosclerosis and causes insulin resistance. These people cannot expand their fat depots. This is called dunnegan type familial partial lipidistrophy. It's a rare autosomal dominant form of insulin resistance. Patients are born with a normal fat distribution but lose fat from their extremities and gluteal region after the onset of puberty. This results in prominent well-defined musculature, flebectasia in these areas, and central accumulation of fat because facial, truncal, and visceral adipose depots because facial, truncal, and visceral adipose depots are not dystrophic. These patients cannot expand their subcutaneous adipose tissue depots, so they must stuff all of the fat they can into the face, the truncal area, and the visceral adipose depots. They have massive visceral adiposity. Visceral adipose tissue is not something I've spoken about in this podcast. I did a YouTube video about my concerns for Elon Musk and what looks like visceral adiposity for him. Visceral adiposity is a problem because when the visceral adipose tissue expands, you get inflammation, you get all sorts of lipokines going straight to the liver, it's a topic for a separate podcast. But patients with partial lipidistrophy like these Dunningan types, these individuals have one gene that's mutated and the subcutaneous adipose tissue cannot expand. They can't be like the mice who are given TZDs, who are given P-par gamma agonists to expand the fat mass. They can't get any fatter in the subcutaneous adipose tissue depot, so they must stuff fat into the visceral, the face, and the truncal regions. Those fat cells get overexpanded, they leak fatty acids, they get non-acerified fatty acids in the blood, and they become insulin resistant. They also release lipokines, inflammatory mediators. They also release lipokines and inflammatory mediators. But what's also interesting about these people with familial, partial lipidistrophy is they do not have elevated LDL. As you can see here, their LDL is lower than their familial control subjects, but their fasting insulin is massively higher. And many more of them have hypertension because insulin resistance also causes hypertension. So this is an illustration of how all of this works. If you cannot expand your fat mass, if your fat cells are broken, either because of a mutation in the LMNA gene, like the monogenic form of familial, hyperlipidistrophy, denigrant type, or because you've broken your fat cells by what you eat, and I'll get to that now, you will become insulin resistant, you will become hypertensive, you will get atherosclerosis, you'll probably get depressed because they're all connected. Again, you can use TZDs to fix it, but you'll just get fatter. That doesn't solve the problem. It just illustrates that the mechanism is sound. So where have we come so far? Hypertension is a huge burden for the United States, not surprising because we know that the majority of people in the United States have at least one feature of the metabolic syndrome. I would say that according to this study from looking at the NHANES study from 2009 to 2016, 87.8% of the people surveyed had at least one feature of the metabolic syndrome. So if you have one feature of the metabolic syndrome, you're probably pre-diabetic, you're probably insulin resistant. Now features of the metabolic syndrome, as they detail here, are increased waist circumference, increased fasting glucose, increased hemoglobin A1C, increased blood pressure, systolic over 120, or a diastolic over 180, a diastolic over 80, triglycerides greater than 150, and HDL less than 40 or 50 for men and women, respectively, not taking any medication. So 87.8% of the population had one of those characteristics. Are we surprised that half of the population has hypertension? The only thing surprising to me is that more of the population doesn't have hypertension. Our population is massively sick. If we think we're doing good in Western medicine, we are diluting ourselves. Only 12.2% of people in the population surveyed in that study were metabolically healthy, did not have one of those metrics, and a friend sent me a study recently that showed that number has gotten even smaller. If you have low triglycerides, high HDL, a low fasting insulin, and you're not obese, count yourself an epic mutant X-Man or woman, because you are part of the metabolic elite, my friends. And I imagine there's a lot of those people listening to this podcast, but those of you who aren't can get there with what I'm going to tell you in this podcast. So hypertension is a huge burden to our society. It's a major problem. Medications control the symptoms, but don't fix the root cause, which is insulin resistance. Medications have bad side effects. Half of male physicians are obese and overweight. 39% of nurses are obese and overweight. We know that doctors aren't taught nutrition and that obese physicians and nurses are much less likely to counsel their patients or to even diagnose obesity. We have an epidemic of obese, unhealthy nurses and physicians. We have an epidemic of medical students who are overworked and overstressed and not taught nutrition and not taught to prioritize their own health. And we have an epidemic of pharmaceutical research that is the majority of what new medical students are learning. So why would things be any different? That's why I do what I do to give more of a holistic perspective. Of course, pharmaceuticals are valuable. We need them. They should not be first line. What should be first line? Diet and lifestyle. The lifestyle pieces are fairly straightforward, not the topic of this podcast in the end. Exercise, a moderate amount, lift some heavy things, get in the freaking sun, avoid toxins. That's a subject for a different podcast. Maybe they want to glyphosate that I did previously. Diet. What do I think is the ideal diet for humans? It's an animal-based diet of organs, meat, fruit, honey and raw dairy. The Hadza don't do raw dairy because they're not pastoralists, but their neighbors, the Masai do, but they do love honey and fruit. Like I said, they don't care about vegetables. They love organs. They eat them. They never waste them and they love meat. That is what they think about all the time. I believe that is the most evolutionary, really consistent way we can recreate the human diet. Why do I mention that? Because I believe what causes fat cells to get broken is excess linoleic acid, evolutionarily inconsistent consumption of an 18-carbon omega-6 fatty acid that gets into our cell membranes, changes some membrane signaling and breaks our fat cells. We don't have any direct evidence to prove this. It would be very hard to design a study to show that, but perhaps in the future, once we get some funding for the ABNRF, the Animal-Based Nutrition Research Foundation, ABNRF.org, we're working on a study right now with Stefan van Vleet at Utah State University. You can see that at our website, abnrf.org. But hopefully that'll be something we can study in the future. I would love to show that excess amounts of linoleic acid in the membrane of adipocytes lead to insulin resistance long-term. It's just hard to study in the short term, but we do know that linoleic acid breakdown products are associated with adipocyte dysfunction. This study is particularly interesting. The role of physiologic levels of 4-HNE for hydroxynoninol on adipocyte biology, implications for obesity, and the metabolic syndrome. This is from 2013. What they say here is that our studies demonstrate that acute and repeated exposures of adipocytes fat cells with physiologically low concentrations of HNE, a breakdown product of linoleic acid, is sufficient to promote oxidative stress, impaired adipogenesis, alter the expression of adipokines, and increase lipolytic gene expression that increases free fatty acid release. This is pretty close to getting us where we need to go and putting the nail in the coffin for linoleic acid and fat cell biology. We need to link this a little more carefully because many things can cause 4-HNE from linoleic acid, but we also have studies that show that the more linoleic acid you eat, the more of the linoleic acid breakdown products like 4-HNE, including the hodes, HODEs, these all have these horribly long names, are increased. So if you eat more linoleic acid, you get more linoleic acid breakdown products. More 4-HNE leads to impaired adipogenesis in animal and cell culture experiments. So I believe there's a real clear indication that we should do more research here. The hypothesis remains very strong that excess linoleic acid is what breaks your fat cells. You can do the experiment yourself. Cut out seed oils from your diet, get rid of excess linoleic acid, make linoleic acid 2% of your calories, which is why I'm not a fan of avocado oil because it has too much linoleic acid, not a fan of even olive oil, too much linoleic acid. I'm just a fan of animal fats, definitely not a fan of seed oils, corn, canola, safflower, sunflower, soybean, massive amounts of linoleic acid. I think that if you are hypertensive or you are insulin-resistant, your goal should be to reduce linoleic acid in your diet as much as possible. That means getting rid of avocado oil, getting rid of olive oil, getting rid of all the seed oils and focusing on tallow and butter. The things your doctor will tell you not to do, but will improve your obesity and will improve your insulin resistance and then will improve your hypertension. This is something we've seen happen over and over and over. We now have hundreds if not thousands of anecdotes. The medical system will eventually wake up to this. This is why we do the work we do. I also want to show you guys this paper, "Lowering Dietary Linoleic Acid Reduces Bioactive Oxidized Linoleic Acid Metabolites in Humans." You can see here these results show that lowering dietary linoleic acid can reduce the synthesis and/or accumulation of oxidized linoleic acid derivatives that have been implicated in a variety of pathological conditions. The study is from 2012. What do we know? We know that lowering the amount of linoleic acid in your diet lowers bioactive oxidized linoleic acid metabolites in humans. We know that a linoleic acid metabolite for HNE leads to impaired adipogenesis in animal and cell culture models. We know that broken fat cells that cannot do adipogenesis, that cannot hyperplasia, are the root cause of insulin resistance. I would say the case is getting stronger and stronger that excess linoleic acid and extremely evolutionarily inconsistent behavior by humans is at the root of insulin resistance. Getting rid of these seed oils, decreasing linoleic acid in the human diet, I believe, will be the single greatest change in our health moving forward. The Hadza, other hunter-gatherer groups, only about 2% of their calories from linoleic acid, there's probably a biological threshold for this. Lower your linoleic acid. If you have hypertension, insulin resistance, obesity, etc., lower your linoleic acid guys. So what else should you do? Eat an animal-based diet, organs, either fresh or desiccated like we make from heart and soil. Fruit is great. Don't fear fruit. Honey, raw dairy. I love it. Talking on Instagram a lot about differences between raw and pasteurized dairy. So hypertension, big problem. Medications don't fix it. It's not salt. That's the problem. Fix your insulin resistance. You know how to do it. Hope you guys enjoy this podcast. Hopefully it's helpful. If you know someone with hypertension, please send them this podcast.