September 24, 2015

ITIS -- It's the Insulin, Stupid (pt 2/8)

Warning: This is a ridiculously long post. I was going to break it up into two, but I figured, what’s the difference between one really long post, and two semi-long ones? You can always read a couple paragraphs and then come back later if you don’t have time to read it all at once.

Also: My blog has a very eclectic audience. I have physicians, PhDs, and others well-educated in biochem and A&P reading this, but I think the bulk of my readers are interested laypeople. I try to tailor my posts to the laypeople, keeping in mind that they are of above-average intelligence, and certainly above-average knowledge about all this low-carb, high-fat, Paleo, and ancestral health "stuff." Just wanted to remind everyone of the diverse audience here, because this post, in particular, contains simplified explanations of complex processes, and I apologize if any of the pros find themselves bored. :-/ 

OKAY! Now we come to the next part of why all of this insulin stuff is so important. (Missed the first part? Click here. And you’ll notice Ive changed the title of this post to say it’s part 2 of I-don’t-know-how-many. In starting to write part 3, I realized this is going to be more like 5 or 6. I am learning new things about this every day that I feel are important enough to write about, and the number of posts it will take to include them keeps rising.) 

Here we go...

Insulin is elevated, and it’s elevated for a prolonged amount of time. I wouldn’t be devoting so much (unpaid!) time to writing about this if elevated insulin, in itself, weren’t such a big threat to good health. It’s even worse when coupled with elevated glucose, but it’s got some pretty nasty effects all on its own. So let’s break this down. Some of this you’ll be familiar with, but some of it might surprise you. Make no mistake, though, what Dr. Tim Noakes said is true:

The only point on which I disagree with Dr. Noakes is that insulin resistance (IR) is a “medical condition.” I would say it’s a pathological physiological state, for sure, but I don’t know if I’d call it a medical condition, as in, something that needs to be treated with medication. Insulin resistance is a medical condition in the same way a broken leg is a medical condition: it can come about due to forces beyond someone’s control, or it can come about because of misguided lifestyle practices. A broken leg, for example, can result from a freak car accident (forces beyond one’s control), or it can be the result of running with the bulls in Pamplona and getting trampled (misguided lifestyle practice). Insulin resistance can result from being born with very strong genetic and epigenetic propensities toward IR almost no matter what someone eats or how they live (forces beyond one’s control), and we currently hypothesize that it can result from a long time of overconsuming carbohydrates (and potentially all food), being sedentary, being chronically stressed, and not getting adequate sleep (misguided lifestyle practices).

But I’m no zealot. I’ll give a little and acknowledge that there are, indeed, individuals who need medication to help decrease their insulin resistance. There are plenty of people out there for whom a LCHF diet, exercise, better sleep, less stress, and the whole rest of the package just doesn’t take them all the way. Maybe these people really do need metformin, or, on the non-prescription side, maybe berberine, chromium, and alpha-lipoic acid. (And let’s not underestimate the power of vinegar!) But I still don’t know if I’d call IR a “medical condition.”

But that is neither here nor there. I am usually a stickler for semantics, but let’s not get hung up on the details this time. Whether it’s a medical condition, metabolism gone awry, or just one heck of a problem, insulin resistance is no joke. 

And I don’t think we can say with certainty what actually causes IR. I suspect it’s multifactorial. There are probably many factors in diet and lifestyle that combine in a “perfect storm” to wreck physiology and metabolism. So I don’t think it’s just excess carbohydrates. If it were, then a low-carb diet, by itself, would help everyone who’s insulin resistant, and while it is that simple for many people, I have clients who can confirm it’s often more complex than that. 

It probably looks something like both of these cascades:

(In fact, I have written extensively about the role of mitochondrial dysfunction in cancer. See here and here.)

But back to insulin.

When it comes to the role of increased small intestinal permeability (a.k.a. “leaky gut”), the scientific literature indicates that a leaky gut might be the driving force for health effects far and wide in the rest of the body. At the very least, there’s a gut-skin axis; a gut-brain axis, and a gut-joint axis. And I am hereby proclaiming that we can make a case for a glucose-insulin-every-system-in-the-body-axis.

After digging through this stuff for a while, I have come to the following conclusion:


Just off the top of my head, here are six body systems that take a very gnarly hit from chronic hyperglycemia and/or hyperinsulinemia:

Reproductive system

It is fairly well established that polycystic ovarian syndrome (PCOS) is related to hyperinsulinemia. Not in every case, but in a great many. Additionally, hyperinsulinemia, hyper- and hypoglycemia may cause PMS to be darn near unbearable, partly because of insulin’s effects on sex hormones, but also for the much more obvious reason of wild blood sugar ups and downs causing mood swings and irritability. But it’s not all about the women. Oh, no, fellas, you’re not immune to the effects of elevated insulin on your precious gonads. Y’know all those commercials pushing pills and potions for “low T”—i.e., low testosterone? Well, there are lots of reasons your “T” could be low, but one of the biggies is hyperinsulinemia. See, insulin upregulates an enzyme called aromatase, and aromatase converts androgens into estrogens. The more aromatase activity a man’s body has, the less testosterone and the more estrogen he probably has floating around in his bloodstream. Elevated estrogen—and, really, just messed up hormones in general—in men can lead to all sorts of nasty stuff, including gynecomastia, benign prostatic hypertrophy (BPH), prostate cancer, and infertility. Elevated PSA (prostate-specific antigen) levels? Is it cancer, or hyperinsulinemia? “Man boobs?” Maybe that guy needs a low-carb diet. Shooting blanks? Maybe that calls for some insulin-lowering lifestyle interventions. “The up-regulation of aromatase produces increased intracellular oestradiol […] in combination with insulin, to cause aberrant downstream transduction signaling, and thus induce metabolic syndrome and mitogenic prostate growth.” Right. “Mitogenic prostate growth.” That’s science-speak for enlarged prostate, which it seems like tons of older men are being “diagnosed” with. Is there something wrong with the prostate gland, itself, or is it hyperinsulinemia? The author of this paper concludes that these conditions are a result of excess insulin & estrogen, rather than “low T.” 

Bottom line: High insulin is bad sexual health & fertility juju for both sexes.  (Know someone struggling to get pregnant? Tell them to contact me!)

Cardiovascular system

According to Dr. Kraft, “Those with cardiovascular disease not identified with diabetes are simply undiagnosed.” Can you imagine? This sh*t has nothing to do with cholesterol. Cholesterol is accumulating in the blood vessel walls in order to repair the microdamage inflicted by all the glucose & insulin! Sure, arteries being “blocked” by a buildup of plaque can lead to ischemia (reduced blood flow) and infarction (total lack of blood flow and resultant tissue death), but rather than getting rid of the cholesterol by any and all means possible, the question should be, WHAT is CAUSING the plaques to form in the first place?

Okay, now that I’ve gotten the rant out of the way, let’s look at some of the ways in which hyperglycemia and insulin resistance affect the cardiovascular system:

Glycation:  I sprinkled the term “hemoglobin A1c,” or just A1c, throughout part 1 of this series. A1c is “glycated hemoglobin,” and it’s an approximate measure of your average blood glucose during the past 3-4 months. Glycation happens when a sugar (such as glucose) gloms onto a protein (such as hemoglobin in the blood) and doesn’t let go. It’s an irreversible process. Think of it like an unwrapped lollipop accidentally left on a car dashboard in a closed-up car in the dead of summer. That sugar is going to melt and get sticky, hard, and brittle, and it’s going to be darn near impossible to remove it. I am simplifying here for the sake of explanation, but if your A1c is elevated, think of it like your blood being sticky and gunky. Its consistency/viscosity has gone from watery to more like maple syrup or molasses. But hemoglobin isn’t the only protein that can become glycated. Any protein—including structural ones in blood vessels—can also get glycated. The result is, they become hard and brittle. They go from soft-ish, rubbery hoses that are quite accommodating (meaning they can expand and contract easily), into something more like glass tubes. They’re brittle and fragile. So when you have chronically elevated BG, and your A1c is high, instead of water flowing through a nice, rubbery hose, we have thick, dense molasses being forced through a brittle glass tube at a high pressure (due to hypertension…more on that in a sec). The extremely logical and semi-inevitable effect of this is the high incidence of all the cardiovascular complications so many diabetics experience, many of which are the results of compromised blood vessels: stroke, heart attack, burst blood vessels in the eyes, poor circulation, kidney failure, loss of feeling in the extremities (diabetic neuropathy)—particularly in the feet, and more. So I have to agree with Dr. Kraft: people with cardiovascular disease not seemingly related to diabetes are probably the exact people I talked about in part 1: people with diabetes in-situ. Undiagnosed diabetics, who remain undiagnosed because the only things their doctors are looking at are A1c and fasting glucose.  

Okay, now that we’ve covered the cardiovascular system, let’s go one step further and connect this back to reproductive function. With what we just discussed about the effects of hyperglycemia on the blood vessels, another very common problem among men of all ages, but particularly older ones, emerges: erectile dysfunction. Informed doctors will confirm that erectile dysfunction is, for many men, the first sign of heart/cardiovascular problems. Why? What does the southern brain have to do with heart function? Easy-peasy. Erectile dysfunction isn’t typically caused by lack of desire. The man wants to perform; it’s that damn little soldier who’s not following orders, right? Well, failure to get and/or maintain an erection may well be due to impaired blood flow to the penis. If blood circulation is compromised, and the body has to do triage, despite what men might think, the penis is not his body’s most important organ. In fact, the penis is probably one of the first places the body would stop sending adequate blood to if it had to prioritize. (So you can see why ED really can be an early sign of heart trouble, particularly in the absence of other indicators.)

Check out this post from Dr. Gerber for a closer look at the cardiovascular connection to hyperinsulinemia, and why the traditional way of measuring heart disease risk is way off the mark.

Bottom line: High glucose & high insulin are bad cardiovascular juju.


I hate to start sentences with “everybody knows,” but really, everybody knows poorly managed type 2 diabetes can cause complications with vision, the most serious of which is straight-up blindness. The retina contains teeny, tiny blood vessels, and we just reviewed what happens to blood vessels in the sustained presence of lots of glucose. It’s bad enough when large, strong, hardy and usually accommodating blood vessels, such as arteries, are glycated. Imagine what happens when itty bitty ones in the eyes become brittle and unforgiving. Burst vessels all over the place. (My mother had poorly managed type 2 diabetes, and she experienced these all the time.) Hence the term “diabetic retinopathy.” There are people whose diabetes was initially diagnosed not by a family doctor or endocrinologist, but by an ophthalmologist! Eye doctors can look directly at your retina, and they might be the first person to notice that you’ve got a problem with blood glucose.

Bottom line: Hyperglycemia is bad eyesight juju.

Kidney Function

As well-known as eye problems are among individuals with poorly managed T2D, it is equally acknowledged that poorly managed T2D has horrible, fatal implications for kidney function. There are two main reasons for this:
  1. The renal tubules, which are the parts of the kidneys responsible for filtering the blood, contain teeny, tiny blood vessels, just like the retinas do. And at the risk of beating you over the head with it at this point, you know what happens to blood vessels—particularly very small ones—when constantly exposed to high glucose. If these little blood vessels in your renal tubules go kaput, you will be in serious trouble. There’s a reason so many diabetics end up on dialysis. (But don’t forget the role of cholesterol-lowering drugs in statin-induced renal failure!) Hence the term “diabetic nephropathy.”
  2. Insulin has a huge influence on sodium dynamics in the body. More insulin ---> more sodium retention. And more sodium retention ---> higher blood pressure. (Note: this doesn’t mean you need to avoid salt. If anything, reducing sugar and other carbohydrates will be more effective for curing managing hypertension than cutting back on sodium. Hypertension has so little to do with salt in the diet, it’s not even funny. I keep saying I have a sodium series planned for after the series on the metabolic theory of cancer is done. Frankly, I think it’ll blow your mind.) How does increased sodium retention cause an elevation in blood pressure? Well, there’s a phrase in physiology that says “water follows sodium.” If the kidneys are holding onto more sodium, more water will naturally be drawn back into the body. More water means more water in the blood, raising the blood volumeSo we have a greater volume of blood flowing through the same amount of blood vessels, which will cause the pressure to increase. The increase will be even greater if the blood vessels are somewhat glycated, because then, instead of being able to expand/dilate easily to accommodate the increased blood flow, these vessels are hard and unforgiving. And remember: when it comes to diet-induced hypertension, it is insulin that is driving the train far more than it is sodium. 
Healthy kidneys should be able to reabsorb or filter out sodium as needed. But when some other, more powerful regulatory force—such as insulin—exerts its effects, this process can be overridden. “Hyperglycemia potentiates insulin antinatriuresis through an effect on the proximal tubule (sodium-glucose cotransport).” (“Antinatriuresis” is a fancy medical word for “preventing the excretion of sodium.” The Latin word for sodium is natrium, hence its symbol on the periodic table being Na.) And guess what else? “Insulin antinatriuresis is accompanied by a reduction in the urinary excretion of uric acid.” And, “In hypertensive patients, higher uric acid levels and lower renal urate clearance rates cluster with insulin resistance and dyslipidemia.” And y’know what reduced excretion of uric acid means, right? Yes: gout. Gout is likely not a result of too many dietary purines; it’s looking more and more like yet another of these conditions driven by hyperinsulinemia. (You may have heard that gout is strongly linked to fructose consumption. Indeed, this is probably due to the effects of fructose on insulin. See, fructose doesn't elevate blood glucose much, but it does raise insulin. Dr. Fung explains starting about 17 minutes into this video.)

Okay, so there’s hypertension, and there’s kidney function. What’s the connection? Well, hypertension is very hard on the kidneys. The kidneys are responsible for filtering the blood—every last drop. They filter out “toxins” as well as the harmful byproducts of normal metabolic processes, and they also decide how much of which minerals and electrolytes to get rid of, and how much to reabsorb. High blood pressure makes this harder to do. (So does dehydration. Remember: thick, sludgy blood forcing itself through tiny, brittle blood vessels.) 

Bottom line: Hyperglycemia & hyperinsulinemia are bad kidney juju.

Brain Health & Cognitive Function

Hello? I wrote a whole friggin’ book about the connection between elevated insulin and Alzheimer’s disease. I also talked about Alzheimer’s as “diabetes of the brain” or “type 3 diabetes” on podcasts I recorded with Jimmy Moore on the Livin’ la Vida Low Carb show, and Robb Wolf, on The Paleo Solution Podcast. In my conversation with Robb (still can’t believe I talked to him…squee!), I made a point to mention Kraft’s work (and Ivor’s), and that many people with cognitive impairment or Alzheimer’s disease have exactly what we’ve been talking about here: “normal” fasting BG, and “normal” A1c, but they are insulin resistant out the wazoo. (As I mentioned in both shows, the more insulin in the blood, the more the amyloid plaques accumulate.) These people are not type 2 diabetics, because they lack the elevated FBG and A1c that would trigger a diagnosis. What they do have is raging hyperinsulinemia, or what we can now call “diabetes ­in-situ.” 

Bottom line: Hyperinsulinemia is BAD brain juju.

Cochleovestibular disorders
(affecting inner ear & balance) 

After learning all this fascinating stuff about diabetes in-situ and hyperinsulinemia, I wrote a post about it for my freelance gig. I specifically looked at cochleovestibular disorders. (A handful of the many conditions that fall under this category are vertigo, tinnitus, Ménière's disease, and mal de debarquement syndrome.) In fact, medical doctors in the ear, nose, and throat (ENT) specialty were among the first people to note the connection between these seemingly “idiopathic” conditions and elevated insulin. (“Idiopathic” means no one knows what the hell causes it.)

Now, the thing is, I don’t know the mechanism at work here. But I’m sure there is one. (I’m not well-versed in inner ear anatomy & physiology, nor the mechanisms that underlie postural balance.) And unfortunately, I have recently lost easy access to the full-text of most articles on PubMed, so I will simply hypothesize here. (If anyone out there is well-informed on this stuff, and can explain this better, please email me privately, or chime in in the comments!)

Okay. We know insulin affects renal sodium retention, and, therefore, fluid dynamics throughout the whole body. Might there be a role for insulin in influencing fluid balance in the inner ear? Some healthcare practitioners have made the case that, for some individuals who are sensitive to gluten, the ONLY manifestations of the sensitivity will be outside the GI tract (i.e., non-celiac gluten sensitivity). For example, there’s “gluten ataxia” – a (supposedly) gluten-induced state of general clumsiness. And there seem to be other neurological, dermatological, and other systemic effects from gluten, wherein the affected parts of the body are the only indications that there’s a gluten sensitivity. So, what if some of these cochleovestibular conditions are the only manifestation of someone’s hyperinsulinemia? Because, remember, we are talking about individuals who have normal fasting blood glucose, normal A1c, and a normal response to an OGTT. (All of which look only at glucose.But if they are hyperinsulinemic, you’ve got to think the glut of insulin is wreaking havoc somewhere in the body, no? And maybe, just maybe, the only place it’s doing so is the inner ear. On the same theme, for individuals with normal BG and normal A1c, maybe hypertension, or infertility, or BPH, or reduced GFR [glomerular filtration rate -- an indicator of kidney function], is the only manifestation of insulin resistance.

This is an area supremely ripe for research employing low-carb or ketogenic diets as therapy, for the same reason they are so desperately warranted for Alzheimer’s: these are conditions for which pharmaceutical drugs are either nonexistent or woefully ineffective. Millions of people have their quality of life crushed because of these weird, freakish-seeming conditions of “unknown origin.” It’s like Robb Wolf says every time someone asks him if a Paleo diet works for “x” rare autoimmune condition they have, and he says, “Couldn’t hurt to try!” For goodness' sake, people, TRY low-carb/keto!

To their credit, as I mentioned, some physicians in the ENT specialty were among the first to realize that Dr. Kraft might be onto something, and they started investigating hyperinsulinemia among their patients. And lookie, lookie, at what they found:

HOLY COW, right? Why have none of us ever heard of this before? (BTW: Dr. Naiman has mentioned that a patient of his was cured of tinnitus after adopting a LCHF diet. Just sayin’.) 

Bottom line: Hyperinsulinemia is BAD inner-ear and balance juju.

I mentioned a Dr. Kenneth Brookler in part 1, and I said we’d come back to him. Well, here he is. He’s an otolaryngologist, and was one of the first physicians to understand the importance of Kraft’s work. He made a lot of headway in uncovering the link between hyperinsulinemia and these “idiopathic” inner-ear disorders. Again, big thanks to Ivor Cummins, the Fat Emperor, for interviewing Dr. Brookler and making the video available to all of us: 

Here’s what’s coming next time:

You’ll note that, in all of this discussion about diabetes, glucose, and insulin, I have not said a single thing about obesity. The reason I wanted to address weight after all the other things we covered today, is that, frankly, a little bit of excess adipose around the ol’ hips and gut is the least of the issues that can come from elevated insulin and glucose.

Nevertheless, no blog series on insulin would be complete without a look at the role of insulin in fuel partitioning and the regulation of adipose tissue. So that’s where we’ll go next.

P.S. In case it wasn’t clear from our discussion of erectile dysfunction, heart disease, kidney failure, Alzheimer’s, loss of vision, and inner-ear disorders, BEING THIN DOES NOT AUTOMATICALLY MEAN YOU ARE HEALTHY!! For sure, millions of thin people have Alzheimers, tinnitus, vertigo, heart disease, kidney failure, infertility, and more. Having been LUCKY enough to not become obese does not imply you do not have rip-roaring problems with glucose & insulin. Obesity is simply one manifestation of insulin resistance, but because it’s the one we can see most easily, it’s the one that everybody thinks is causing everything else. If we could see someones serum triglycerides, someone’s renal tubules, someone’s arteries, or someone’s fasting insulin, all the fat-shamers out there would SHUT UP PDQ. (Sorry...this is a huge, huge sticking point for me, professionally and personally.)



  1. Replies
    1. Thanks! Now go enjoy a plate of liver, marrow, brains, nuts, greens, and vinegar. ;D You know I say that with love!

  2. I could not agree with you more about the importance of insulin! Have you seen the latest data about resistant starch? Resistant starch lowers insulin levels beginning an hour or two after you eat it - independent of exercise and weight loss. There are also 8 or 9 clinicals showing that resistant starch (delivered as a powder or baked into snacks) significantly improved insulin sensitivity in the muscles (but not the liver). The data really is extraordinary! The FDA is evaluating a qualified health claim petition right now with a decision expected next year.

    Resistant starch is a type of insoluble dietary fiber which is fully and slowly fermented in the large intestine. It changes the expression of hundreds of intestinal genes associated with lipid and glucose metabolism. I'm convinced that prediabetes is largely due to a lack of fermentable fiber and may have less to do with excess refined carbs!

    If we were eating unprocessed carbs, we'd be getting lots of resistant starch, but processing destroys the resistance. Beans, peas and under-ripe bananas are good food sources, but the vast majority of the 70+ clinical studies used relatively high quantities of an isolated but natural type of resistant starch.

    I've been blogging on it at, which also has links to all the scientific studies and FDA petition. A new review article published this week outlines animal studies showing anti-aging benefits - which ties into all of your points about insulin. Human clinicals have shown improved kidney function, changes in fatty acid metabolism within the adipose tissue, improved intestinal health and more.

    Keep up your promotion about the importance of insulin! It's hugely important.

    1. Thanks, Rhonda! I don't think a lack of RS is the major cause of all this metabolic dysregulation, but it certainly could be a contributing factor, and proper use of it could be part of a multi-pronged strategy for helping people recover their health. For sure, the refinement of carbohydrates -- the removal of them from their natural state and the stripping away of the fiber and full complement of nutrients -- has been a disaster for human health in the modern age.

  3. Great post. I am looking forward to more on this subject.

    Are you going to devote any time to systemic inflammation caused by hyperinsulemia?

    1. Hey Mark, I wasn't planning on it, if only because I really don't know much about that connection. But check out this comment by Alice Ottoboni, PhD, on Part 1. Looks like it's largely the result of insulin stimulating the enzyme delta-5-desaturase. Not a problem if the n-6/n-3 ratio is good, but when it's hugely skewed toward n-6, more insulin ---> more inflammatory prostaglandins.

    2. Thanks. I'll check it out.

  4. Wow, you are really nailing it!!!

    I have PCOS which I had when I was a thin young thing, and I blame the hyperinsulemia from PCOS for eventually (after monkeying around with my hormones to conceive through IVF) contributing to my obesity (yes, of course the knife and fork helped!). My 14 year old daughter has PCOS, too with significant insulin resistance, and her BMI is 18--thin as a rail. So clearly, the insulin resistance comes FIRST in the case of our hereditary form of PCOS (I suspect my mother had this as well). I suspect hereditary insulin resistance is MUCH more common than is currently recognized.

    Anyway, the point I wanted to make is that there are a good number of thin "cysters" (a solidarity term for women with PCOS). They often assume they are not insulin resistant and therefore an LCHF diet will be of no benefit for their fertility and other PCOS related health issues, but my take on it--as a formerly thin "cyster"--is that they aren't obese YET. It takes a good deal of time for the obesity to develop, but the diabetes in situ you identify is already present and they ignore hyperinsulemia to their peril. Most doctors, even reproductive endocrinologists who have huge practices of PCOS patients don't test for markers of hyperinsulemia--they should know better, but they don't have a clue. And often, when a "cyster" presents when already obese, she receives the worst possible advice--low fat, high carb diets are prescribed--along with a lot of blame that her overeating caused obesity that in turn caused the PCOS. In my experience, endocrinologists are among the worst fat shamers in the business.

    When will they ever learn???

    1. I COULD NOT AGREE MORE, JAN! Have you been able to steer your daughter toward a LCHF diet? (Even if only a little.)

    2. Unfortunately no. We eat relatively healthfully (kind of Paleo Mediterranean) at home (I limit my carbs) but she is not willing to go low carb, partly because my husband frowns upon it (even though she was conceived because of LCHF) and buys the junk food. But at least she knows about LCHF and when she's ready to take charge of troubling symptoms she'll know what to do. I don't want to push too hard because she's at an age where she's got to have some autonomy over her own body. I regret, deeply, I didn't insist on low carb when she was much younger so it would be the norm now.

    3. Well, at least she's seeing that it's possible to feel better, when she's ready. And it's a fine line...too many women grow up with lifelong "issues" around food, imparted by their mothers, grandmothers, sisters, etc. We need to break the cycle. I can't imagine how hard it is to raise a daughter in 21st C America.

  5. I used to have chronic vertigo. I could only sleep on one side for years, otherwise my head would spin sporadically. I was also fat with high triglycerides. I ended up reading GCBC and realized, dude you need to cut the junk food. So I went low carb, and although my vertigo had been steadily improving before I did LCHF, I'm now vertigo free.

    HOWEVER whenever I fall off the low carb wagon and binge carbs (yeah my body wants to gain that 60 lbs back) and it's not balanced with fat and protein, my ears feel congested shortly after eating, say, a bagel.

    1. Very cool that you've made this connection! I wonder how many people -- millions? -- are living with vertigo, tinnitus, and more, and have no clue it might be related to diet.

  6. Yay, AB came out swinging here.

    Sounds like it is all coming together, the gigantic ITIS conundrum (where the hell did this weird conundrum word come from?....)

    Health is all about ITIS, organized medicine appears to be as false and useless as organized religion (sorry for those that pray, but the analogy is too good)

    Ready for chapter #3!

  7. My daughter, Esmée, sent me your first 2 blogs on insulin. Fascinating! I look forward to blog #3 also as I am in the yoyo obese category. Good blood work numbers, but never tested for insulin resistance!!??

    1. Thank you! Esmee does a world of good, herself, in helping people find their way back to health. :)

  8. Do you think there is also a link to arthritis? I have had both knees replaced and haven't turned 60 yet. I was never obese, never played sports or had any type of injury, my cartilage just gradually disappeared. My 91 year old mother has never had any knee pain. At my first visit to the orthopedist, I was told all they had to offer me was a new knee. I asked what caused it and the only thing they could come up with was arthritis caused by inflammation. What caused the inflammation? They had no answer. I have long suspected it was diet related.

    1. Yes, there's a big link to inflammation. In a nutshell: insulin stimulates activity of one of the enzymes involved in generating inflammatory cell signaling molecules. This is compounded when the diet is high in omega-6 rich oils and low in omega-3 fats, so you want to make sure you're getting enough good marine fats and go easy or avoid altogether things like soybean, corn, and cottonseed oils. Joint pain, specifically, also sometimes has a big wheat (gluten) component, so a low-carb diet can help with that just be being low in wheat, by default, but some people find a totally grain-free diet to be even better. (Or gluten-free, if nothing else.) Traditionally made bone stock can help too -- with long-simmered bits of collagenous and cartilagenous bones & joints.

  9. High blood pressure, easy to get uric acid kidney stones (not gout), and BPPV....check, check, check. :o

  10. Just to add that insulin is probably related to tinnitus but far from the only factor. Mine was caused by aspirin. Ibuprofen caused it but at a much lower level, acetaminophen and codeine not at all.

    I had no need of NSAIDS for a long period and the tinnitus went away. Then I was conned into daily low dose aspirin, and after a while the tinnitus returned and is now permanent. Thanks, doc!

    Not usre how common this is but I know others who have had similar responses, especially to some of the prescription-only NSAIDS.

    Why was I taking painkillers in the first place? I used to suffer from not-quite-frozen shoulder and not-quite carpal tunnel. I suspect the high BG was glycating my connective tissue. So yes, insulin WAS involved but not directly.

    Tight BG control and reduced insulin levels/IR has permanently cured this.

    1. I know this is an old post, but what you have sounds exactly like me. The solution in my case is gluten free (totally)and starch free. Gluten causes reactive arthritis and starch causes tinnitus. The tinnitus comes on about half an hour after eating starch and lasts for a couple of days. Gluten-based arthritis can last for weeks. Both I suspect caused by leaky gut and inflammation, but presumably with some insulin reaction as well. BTW starch is in almost all drugs and supplements. I have had to throw away all my old ones�� Ali_r

  11. Amy, this is awesome. You just answered a question my A&P professor never managed to. Going through the textbook on kidneys, it stated that high blood glucose raised blood pressure. When he mentioned it in class, I asked if that was simply due to osmotic pressure or if there was another mechanism. His reaction was great, but I never managed to find out why until finally getting around to reading this.

    My prescription I administer to myself whenever I start to feel odd, whether sick, hungover, or suffer from issues scatological, is to fast until I feel normal. It's the poor man's ketogenic diet :p


  13. Amy, I was diagnosed pre-diabetic 6 months ago, and since then feel like I've been running around the woods with a blindfold on bumping into trees and tripping over shrubs. Your blog has enlightened me. Thank you so much for your wisdom and for the wisdom of others that you share. Just one other note... I love your writing style. At first I thought you were maybe just a little too cute, but after reading you a while, I see that you're just the perfect amount of cute. I think you just made another major positive change in some unknown stranger's life (mine).

    1. Well, Robert R, you're not some unknown stranger *anymore,* are you? ;-) Thanks for reading, and I'm very glad you've found something useful here. My own mother had disastrous complications from extremely poorly managed T2D (and very ignorant doctors). She was unable and/or unwilling to take my advice, so now, I guess I'll just help strangers on the internet. Seriously though, your comments really warm my heart. My first love is writing (undergrad degree in creative writing, in fact), and outside my nutrition practice, I'm an aspiring novelist, so any time someone compliments my writing, it really lifts me up.

      As for being "too cute," I'm not sure if you're referring to my writing or the pic on the website. It's a very old picture! I promise, I don't look *quite* that good anymore. :P

      Thanks again for reading!

  14. I was referring to your writing style... too much humor detracts, too little makes your writing like a tofu sandwich on stale white bread... you've got the perfect mix, don't change a thing. I would however be just as accurate if referring to your pic. Even though it's several years old I'm sure you've aged well because you've got a firm grip on your metabolism, which is what it's all about. I used to wonder why some people would age really well until they hit 50 or so and then overnight they'd seem to hit the wall and crash. That's about the time a person's pancreas starts wearing out from years of abusive carb spikes and insulin chasers... it's all downhill after that.

    On a related note, under the heading of "why I have so little faith in doctors... I saw mine yesterday. She told me my A1C of 5.7 is perfectly normal... didn't even tell me to exercise more and start limiting my carbs (both of which I already do). Were I to listen to her I'd probably have full blown diabetes in 2 or 3 years. Also, when asked to include an insulin level test in my blood work, her exact words (uttered through an exasperated somewhat irritated sigh) were "You're not insulin resistant. If you were you'd be diabetic by now." I thought to myself... can't really say here what I what I thought, other than I wished she would read your blog.

    Have you been published? Is there a link for that on your site?

    1. Yes, sadly, most medical and nutrition professionals are absolutely *clueless* when it comes to this stuff. not really sure why, as most of it is rooted in very basic anatomy, physiology, and biochemistry, all of which I know they study in medical/nutrition school.

      To answer your question, it depends on what you mean by "published." I haven't been published anywhere too official, but I've self-published an e-book regarding Alzheimer's disease as "type 3 diabetes," and you can find that here:

      Other than that, I've recorded a couple of podcasts and have had some guest posts on Robb Wolf's blog:

      I was also published in Wise Traditions, the quarterly journal of the Weston A. Price Foundation, and that article is what eventually expanded into the e-book:

  15. I'll check the podcast out. Robb's Blog is how I ended up stumbling in here by the way.

    Also... just wondering, will borderline bilirubin and Urea Nitrogen levels follow blood sugar levels down with LCHF? Kind of hard to limit protein with this diet. I'm only talking 1.2 on the Bilirubin but I don't feel comfortable with any numbers out of range, even slightly. If you've addressed this anywhere please direct me.

    1. I'm not sure. I'm not very familiar with the ins & outs of BUN & bilirubin, but I'd be surprised if they didn't improve, in time. They have a lot to do with kidney & liver function, both of which generally improve on low-carb, partly for reasons I discussed above -- at least, for the kidneys. I didn't say anything about the liver, specifically, but the truth is, a reduced glucose & insulin load is so helpful for the body *across the board* -- really no organ or system that *isn't* positively impacted by that. I'm not sure how long it might take before you'd see a change in anything, but also remember not to get overly alarmed by just *one* measurement on *one* blood draw. Could be higher or lower a week later..who knows.

  16. I would feel happier if there was a definition of insulin resistance in terms of a number. Many studies use the upper quintile as "insulin resistant" by either fasting insulin, HOMA-IR or some other measure. A recent Gardner study took the upper 50% by IR as "insulin resistant" leaving the other half as "insulin sensitive".

    So is there an insulin related statistic we can use to objectively define insulin resistance ?

    1. I don't think this is even that important. We need to be looking at insulin levels themselves. So we know what normal ones are and if you are higher, to the extent that you are, this is always pathogenic. Keep in mind that this is where the pointy end of the stick here, and it is never desirable or appropriate to be hyperinsulinemic.



  19. .it started with a tweet after dinner via interface which I've taken to using these days.
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  20. Interesting. I've never hear of 'medical condition' defined as a condition treated with medication. Is that a US definition?

  21. This comment has been removed by a blog administrator.

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