The Arrow #223

Hello everyone.

Greetings from Dallas where the weather is quite beautiful but windy.

Comments from Readers

I received a vaccine comment from a lady that I thought was extremely pertinent. Here it is in part.

I don't care about the MMR, but I am interested in knowing how unsafe the vaccines targeted to my elderly generation are. I am referring to the shingles, the pneumovax pneumonia, and even the dTap, because you can't get just a tetanus shot anymore.

I’ve spent most of my time writing and researching on childhood vaccines and mRNA Covid vaccines. No one taking the former would be reading this newsletters (thought their parents might), and I doubt many (with good sense at least) are taking the later.

So this lady’s suggestion is a terrific one. Let’s start out with shingles.

Shingrix for Shingles

For those who don’t know, shingles is a disorder fairly common to elderly people who have had chicken pox in their youth (which means almost everybody). After their spots fade, the chicken pox virus migrates up the nerves and hides out in the nerve roots and ganglia. The virus hangs out there held in check by the immune system.

As our patient ages, he/she has a fall off in immune function that, sadly, is a part of aging. Everything functions a little less well over time, the immune system included. Sickness, stress, aging itself, cancer, and any number of stresses can allow the virus to migrate back up the nerve and cause a breakout.

The pattern of the blisters runs from the center of the body toward the side, which is the distribution of the nerve. If the blisters stretch across the centerline of the body, it probably isn’t shingles.

I did a pretty deep dive on the Shingrix, the shingles vaccine available now. The first thing I wanted to know about it was, of course, was it tested under placebo-controlled conditions. As it turned out, the test was placebo controlled with a real placebo. According to the paper describing the study

Shingrix 0.5 mL or placebo (saline 0.9% solution) at month 0 and month 2.

The vaccine does have an adjuvant.

Along with the Recombinant Varicella Zoster Virus Glycoprotein E (gE) Antigen (the active ingredient), the injection contains the AS01B Adjuvant System. Here’s what it says about it.

This adjuvant enhances the immune response to the gE antigen. It contains Monophosphoryl Lipid A (MPL): A detoxified derivative of lipopolysaccharide from Salmonella minnesota, which activates innate immunity through Toll-like receptor 4 (TLR4) signaling. QS-21: A saponin extracted from the bark of the Quillaja saponaria tree, which boosts both humoral and cellular immune responses by stimulating antigen-presenting cells. And liposomes: Composed of dioleoyl phosphatidylcholine (DOPC) and cholesterol, these serve as a delivery system for MPL and QS-21, ensuring their stability and effectiveness.

The adjuvant more or less fires up the immune system to react against the antigen, the Varicella Zoster (chicken pox) virus.

How safe is Shingrix?

Within the first few days after the vaccine, recipients experience the following mild reactions:

  • Local reactions: Pain (78%), redness (38%), and swelling (26%) at the injection site.

  • Systemic reactions: Fatigue (44%), muscle pain (45%), headache (38%), shivering (27%), fever (21%), and gastrointestinal symptoms like nausea (14%).

Some had worse side effects.

  • Grade 3 reactions: About 17% of recipients experienced severe side effects that temporarily interfered with daily activities, such as intense fatigue or muscle pain.

  • Guillain-Barré Syndrome (GBS): Post-marketing studies identified an increased but rare risk of GBS, with an estimated 3–6 excess cases per million doses administered.

  • Severe allergic reactions: Rare but possible, including hives, facial swelling, difficulty breathing, or dizziness.

According to the literature, subjects taking Shingrix or placebo suffered the same degree of Serious Adverse Effects.

  • 2.3% for Shingrix vs. 2.2% for placebo within 30 days of vaccination.

  • Over one year, SAEs occurred in 10.1% of Shingrix recipients compared to 10.4% in placebo recipients, consistent with the general population's health conditions.

I couldn’t find the specific serious adverse events in the paper containing the above, so I went to the package insert.

Serious Adverse Events (SAEs): In the 2 studies, SAEs were reported at similar rates in subjects who received SHINGRIX (2.3%) or placebo (2.2%) from the first administered dose up to 30 days post-last vaccination. SAEs were reported for 10.1% of subjects who received SHINGRIX and for 10.4% of subjects who received placebo from the first administered dose up to 1 year post-last vaccination. One subject (<0.01%) reported lymphadenitis and 1 subject (<0.01%) reported fever greater than 39°C; there was a basis for a causal relationship with SHINGRIX. Optic ischemic neuropathy was reported in 3 subjects (0.02%) who received SHINGRIX (all within 50 days after vaccination) and 0 subjects who received placebo; available information is insufficient to determine a causal relationship with SHINGRIX.

Deaths: From the first administered dose up to 30 days post-last vaccination, deaths were reported for 0.04% of subjects who received SHINGRIX and 0.05% of subjects who received placebo in the 2 studies. From the first administered dose up to 1 year post-last vaccination, deaths were reported for 0.8% of subjects who received SHINGRIX and for 0.9% of subjects who received placebo. Causes of death among subjects were consistent with those generally reported in adult and elderly populations.

Potential Immune-Mediated Diseases: In the 2 studies, new onset potential immune-mediated diseases (pIMDs) or exacerbation of existing pIMDs were reported for 0.6% of subjects who received SHINGRIX and 0.7% of subjects who received placebo from the first administered dose up to 1 year post-last vaccination. The most frequently reported pIMDs occurred with comparable frequencies in the group receiving SHINGRIX and the placebo group.

Other Medically Relevant Events: In the auHSCT study (NCT01610414), relapse or progression was reported by 315 of 922 subjects (34%) who received at least one dose of SHINGRIX and 331 of 924 subjects (36%) who received placebo from the first vaccination to study end.

In the auHSCT study (NCT00920218), relapse or progression was reported by 17 of 59 subjects (29%) who received at least one dose of SHINGRIX and 8 of 30 subjects (27%) who received placebo from the first vaccination to study end. In the hematologic malignancy study, relapse or progression was reported by 45 of 283 subjects (16%) who received at least one dose of SHINGRIX and 58 of 279 subjects (21%) who received placebo from the first vaccination to study end.

In the renal transplant study, biopsy-confirmed allograft rejection was reported by 4 of 132 (3%) of subjects who received SHINGRIX and by 7 of 132 (5%) of subjects who received placebo from the first vaccination to study end (approximately 13 months later). Creatinine as a measure of graft function and changes in alloimmunity post-vaccination were not systematically evaluated.

In the HIV study, at least 1 event of worsening HIV condition was reported by 9 of 74 (12%) of subjects who received SHINGRIX and by 5 of 49 (10%) of subjects who received placebo from the first vaccination to study end.

I looked up the effectiveness of the vaccine, and based on the numbers I found, I figured they were listing the relative risk and not the absolute risk. But, have no fear, I found the absolute risk.

Here is what they want you to see.

Effectiveness in Healthy Adults:

  • Ages 50–69: Shingrix is 97% effective in preventing shingles and 91% effective in preventing PHN.

  • Ages 70 and older: It remains 91% effective in preventing shingles and 89% effective in preventing PHN

    (PHN is postherpatic neuralgia, which is pain after the blisters are gone.)

The numbers above are relative rates of effectiveness. I looked up the absolute rates in the paper linked above.

The overall incidence of herpes zoster per 1000 person-years was 0.3 in the Shingrix group and 9.1 in the placebo group, for an overall vaccine efficacy of 97.2% (95% confidence interval [CI], 93.7%-99%; P < .001) among participants.

What this means is that of each 1,000 people getting the vaccine, 0.3 ended up with shingles whereas in each 1,000 receiving the placebo, 9.1 ended up with shingles. What it really means is out of every 1,000 people, 9.1 are going to get shingles. That’s what you’re odds are of getting the disease. That’s the figure you should use to determine whether or not you want to take the jabs. Your odds are ~991 out of a thousand of not getting shingles if you don’t take the vaccine.

Long-Term Effectiveness Shingrix maintains high efficacy over time:

  • It remains 73% effective after four years, based on real-world studies.

  • Long-term data show that its efficacy can stay above 79.7% for up to 11 years after vaccination.

Single vs. Two Doses

  • A single dose is less effective, providing only 64–76% protection, with significant waning over time.

  • Completing the recommended two-dose series ensures maximum and prolonged protection.

Now there is a new twist to the Shingrix story.

Yet another study has been done which is a clever take on a randomized-controlled trial. It’s about as close as you can come. The study was done at Stanford and the researchers looked at how many people developed dementia after taking the Shingrix shots compared to those who don’t.

As it turned out, fewer of those who took the Shingrix vaccine developed dementia than those who didn’t. A fifth more, in fact. The researchers involved made an nice video about the research.

Much more needs to be done to figure out where this effect comes from. One thing the researchers do know, is that is it much stronger in women than men. Given the strength of the showing, I’m positive much more will be coming forth on this in due course. Here is the Nature paper on the study for your review.

You may ask whether I’m going to take the vaccine or not. My vote right now is no. I’ve got a zillion elderly relatives and none, as far as I know, have come down with shingles. So I think my odds are pretty good.

But if this dementia prevention work turns out to be as good as it’s looking, I may take the shots just for that.

Let’s take a look at another adult vaccine. This one will be short and sweet.

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The Latest Flu Shot

This year’s flu vaccine should be avoided, unless it’s a case of the flu you want. Then, by all means, take the shot.

The Cleveland Clinic volunteered its many employees to determine the effectiveness of this year’s flu vaccine.

Among 53402 employees, 43857 (82.1%) had received the influenza vaccine by the end of the study. Influenza occurred in 1079 (2.02%) during the study. The cumulative incidence of influenza was similar for the vaccinated and unvaccinated states early, but over the course of the study the cumulative incidence of influenza increased more rapidly among the vaccinated than the unvaccinated. In an analysis adjusted for age, sex, clinical nursing job, and employment location, the risk of influenza was significantly higher for the vaccinated compared to the unvaccinated state (HR, 1.27; 95% C.I., 1.07 – 1.51; P = 0.007), yielding a calculated vaccine effectiveness of −26.9% (95% C.I., −55.0 to −6.6%). [My bold]

A vaccine effectiveness of -26.9 percent, means that 26.9 percent of those vaccinated ended up with the flu. In my view, it would best be avoided.

More on Dr. Peter Marks

I have a reader who has worked (or tried to work) with Dr Peter Marks, whom RFK, Jr. just canned. I’ve read multiple articles recently about how Dr. Marks refused to let RFK, Jr. look at the Vaccine Adverse Events Reporting System (VAERS) records. I would have fired him on the spot, too.

Although I don’t know Dr. Peter Marks, one of your fellow readers does. Here is the comment he posted about having to work with him:

Peter Marks is a giant pile of lying human excrement. I have seen and read his false testimony in multiple court cases for which he submitted declarations in support of the Covid-19 vaccines. Another war criminal who deserves the same as the Nazi doctors got at Nuremberg. If he is lucky, he should be thanking god almighty that all he gets is fired. If he had an ounce of sense he would crawl back into whatever dank, darkened hole spawned his ilk and shut his mouth - BUT, like most of the criminals who were at FDA and NIH and CDC and profited handsomely off of Covid-19, they can never shut their cakeholes or stop justifying their crimes. Amen, Halleluah, and pass the gravy that he's gone.

Dale, the author of this comment is an ex-marine helicopter pilot who shifted careers in the military from flying helicopters to being a lawyer. He’s since retired from the Marines, but is suing the military on behalf of many personnel from all the services who were issued the vaccine mandate and refused to comply. They were all discharged and lost considerable in terms of retirement and other benefits.

Based on Dale’s work with soldiers forced to take the experimental anthrax vaccine from years before, he was sought out for Covid.

Marks appeared as an expert for the government in most of the cases filed against the military (and other) vaccine mandates. In each case, he would file a declaration that would spin facts, reinterpret what he had previously said when caught in a contradiction, attack experts (like McCullough or other doctors), or just flat out lie. Anyone who disagreed with him was (obviously) not qualified like he is; his declarations just drip with that special smugness available only to the government expert.

I told him I thought Trump had executed TROs to give all those folks their bennies back. But apparently that wasn’t the case.

We got a partial win in our Coast Guard case (Harkins v. United States, 23-cv-1238), in which the judge has ordered the case to be remanded so that the Coast Guard can (1) notify the 1352 members who filed religious accommodations (all denied) that they may have a claim; (2) Coast Guard must determine if there was any licensed vaccine available at the time of their order to take it, and (3) if not, they win, if there was, the USCG has to properly adjudicate their RAs. In our other two class actions for the other service branches and the national guard, the govt has no asked for a voluntary remand in light of Trump's EO. We're arguing about that now in motions in those two (Bassen v. US, 23-cv-211 and Botello v US, 23-cv-174).

He ended up our back-and-forth with this.

And for whatever it's worth, lest my comments seem hyperbolic, I just got an email that there have been criminal referrals requested for Fauci and seven state Covid officials. https://x.com/NicHulscher/status/1910042589648081132

That's not really anything concrete, but it's the first crack in the wall. We may very well see people prosecuted over what they did in regards to Covid-19.

I’m fervently hope we’ll be seeing people prosecuted over all this. It will have taken a while, but revenge is a dish served best cold.

Years ago when Dale was working as a lawyer for the military he was assigned a case in which a handful of military from the various services were either in the brig or headed for the brig for refusing to take an experimental anthrax vaccine. He ended up defending these guys against Uncle Sam.

He wrote a book about it that I loved. He gets into all the chicanery involved in suing the government—I’m surprised more people don’t off themselves when they get stuck so deeply in that tar baby. Give his book a read. It is really good.

I also put a link down by my recommended newsletters for Dale’s Substack, which is wonderful. Please take a look.

Thyroid and Low-Carb, Ketogenic Diet

I’ve gotten a bunch of emails over the past few weeks about thyroid and thought I would write a bit about it. A year or so ago, I got a flurry of emails on the same subject and intended to write on it then, but had other things on my mind. Then the thyroid emails dried up, so I kind of forgot about it until this new bunch of emails came in.

People are concerned when they go on a low-carb or ketogenic diet and discover their thyroid hormone levels have suddenly fallen off. There is a pretty simple explanation for it, but there is also a different variation on the typical explanation. I’ll go through both and also explain why you might find your thyroid stimulating hormone (TSH) level go up as you age. And I’ll clue you in to how my own doctor might have come close to doing me in on thyroid medications.

Before we get into how this all works, let’s review all the working parts of the hypothalamic-pituitary-thyroid (HPT) axis. I looked at innumerable graphics on the web trying to find a simple one to show what this axis looks like. Every one I found was either was way too complex or way too simplistic. All I wanted was one showing the basics. You would think that would be an easy find. Nope. Made me realize I should have been a medical illustrator.

I ended up buying an image. It isn’t perfect, but it’s better than any other I found online.

Okay, let’s walk trough this. At the very top you see the hypothalamus identified. Hanging right below it is another gland, the pituitary gland. There is a semi-circular blue arrow with a big bubble on it containing the letters TRH that goes from the hypothalamus to the pituitary gland. TRH stands for thyrotropin releasing hormone.

The graphic is a little inaccurate as the blue arrow implies the TRH travels outside the hypothalamus to get to the pituitary gland, when it really doesn’t. It goes directly from the hypothalamus to the pituitary gland without going through the blood.

When TRH enters the pituitary gland, it stimulates the release of thyroid stimulating hormone (TSH). TSH does travel through the blood to the thyroid gland and stimulates the thyroid cells to make and release the thyroid hormones T3 and T4.

T3 is the active thyroid hormone whereas T4 is basically a reservoir for T3. T4 can convert to T3 when needed. The thyroid under stimulation by TSH releases about 13 times more T4 than it does T3, but it can convert to T3 quickly, if needed.

When T3 levels begin to decline, a signal goes back through the blood to both the hypothalamus and the pituitary gland that T3 levels are getting low. When that message is received, the hypothalamus releases TRH and the pituitary releases TSH, which tells the thyroid to make and release more T3 and T4.

Since T3 and T4 are released into the blood, we can measure them. Same with TSH, but not so much with the THR, because it doesn’t really get into the circulation.

So, we’ve got T3, T4, and TSH to measure. And we can learn a lot about what’s going on with the thyroid from just those measures.

If everything is hunky dory, we find that T3, T4, and TSH are within normal limits.

But now let’s say something goes wrong with T3. Maybe the thyroid is having a problem of some sort and isn’t able to pump out enough T3. What happens then?

The hypothalamus and the pituitary would get feedback that T3 levels are low and that the body needs more T3. They would respond by cranking out more TSH to stimulate the thyroid to make and release more thyroid hormone. Increasing the TSH under these circumstances ends up driving the thyroid to make more thyroid hormone, but it requires more than the normal amount of TSH to drive the process.

If you were to have blood drawn at this point, your thyroid hormones T3 and T4 might look normal, but your TSH would be elevated. It would tell you your thyroid gland had a problem as it requires more than a normal amount of TSH to stimulate the thyroid into action.

Now let’s say we have a situation in which the T3 is low, but the TSH is normal or even a bit low itself. What does that mean? You might think it would indicate that something is wrong with the hypothalamus and/or pituitary, because these glands aren’t cranking out enough TSH to stimulate T3 production in the thyroid.

That could indeed be an issue.

But before we go that route, we would want to see if the body were experiencing any signs of thyroid dysfunction.

We haven’t talked about what T3 does, but it is an extremely important hormone that regulates in one way or another many processes in the body. I’ve heard my friend Professor Ben Bikman say that T3 makes everything work better. Whatever tissue it stimulates just works more intensely under its provocation.

I don’t have time to get into everything T3 does, but it does a lot. For one, it increases the basal metabolic rate and enhances oxygen uptake and energy consumption by tissues. T3 is essential for normal skeletal growth and maturation. It potentiates the effects of growth hormone and other hormones involved in bone development and closure of epiphyseal plates.

T3 increases heart rate and heart muscle contractility by upregulating certain receptors in cardiac tissue. It also increases or maintains systolic blood pressure and decreases diastolic blood pressure, which improves cardiac output.

T3 promotes lipolysis—the release of fat from fat cells. It also regulates protein synthesis and degradation. Too much can end up breaking down muscle tissue.

T3 is involved in the regulation of reproductive hormones in both men and women, affecting fertility and reproductive health. It increases gut motility and helps support good digestion.

I just touched the surface of everything thyroid hormone does. I could go on and on, but let’s leave it at T3 is an incredibly important hormone for countless bodily functions. And when T3 production is too low to perform its duties properly, health declines significantly.

So a low T3 and a high TSH means the hypothalamus and pituitary gland are whipping the thyroid to make it produce more T3, but it just isn’t responding. And it means the thyroid in question is not working well. Which also means all the tissues downstream from the thyroid are going to be impacted.

The problem is called hypothyroidism, and it is a serious problem. But it’s treatment is beyond the scope of what we’re discussing today.

We want to know what the situation is when TSH is normal and T3 levels are low.

Since the levels of T3 feed info back to the hypothalamus and pituitary indicating thyroid hormone status, it would make sense that a low T3 would send a message to the gland to release TSH to stimulate the hormone to up the T3 level.

But that’s not what it does during a low-carb/ketogenic diet. The TSH remains normal, while the T3 is low.

The test for thyroid hormone was developed in the early 1970s. The test for TSH became available a couple of years later. When levels of hormones and other body chemicals such as cholesterol and insulin are first tested, the scientists developing the test typically run levels on as many “normal” subjects as they can get their hands on to see what the range of difference is between subjects. After testing, say, a thousand people, they do a Gaussian analysis and typically come up with a standard bell-shaped curve. They usually take two standard deviations from the mean and call anything within those limits as normal.

After a few years of experimenting with the lab values they begin to modify what may be high or low depending upon patient feedback. For instance, when I was in medical school, the upper limit of normal for total cholesterol was 350 mg/dl. That was just about the time that the lipid hypothesis of heart disease was really catching on, so those involved in determining the normal levels of lab samples decided that though 350 mg/dl might be within two standard deviations of the mean, it certainly wasn’t a healthy figure. So they backed it down, first to 300, then ultimately to 200 mg/dl where it remains today.

Back in the day when the testing of thyroid hormones was just coming on the market, people in the United States were eating a lot of carbohydrates. Most people had breakfast cereal in the morning along with toast, jelly, orange juice and coffee. Sandwiches of one kind or another were a standard at lunch. Dinner was a meat dish (casserole, maybe), mashed potatoes, bread, and some sort of sweet desert. (When I was working as an engineer, we all left the office in mid-morning and mid-afternoon for a donut run—I suspect we weren’t alone.)

I asked perplexity dot ai about the carb to fat to protein ratio in the US diet in 1970, and got back the following, which was close to what I was expecting.

Here are the three resources used. 1., 2., 3.

Since this was the diet of the average, ordinary American, it was used to determine the normal values of TSH and T3.

If you followed the 1970s diet mentioned above, a doctor noticing your T3 was low while your TSH was normal would be stumped. He might think you were hypothyroid, since your T3 was low and would probably ask you a number of questions about any symptoms of hypothyroidism you might have. If all checked out there, he might wonder what might be wrong with your hypothalamus: was it not sending thyrotropin releasing hormone (TRH) to your pituitary? Or was your pituitary not working properly and sending TSH to your thyroid?

Back in the early 1970s, there weren’t a lot of people on low-carb or ketogenic diets. I doubt that had you asked anyone back then what a ketogenic diet was, you could have gotten an accurate answer.

As it turns out, it requires a fair amount of T3 to deal with dietary carbohydrate. So those eating a lot of carbohydrate have elevated levels of T3 and normal levels of TSH to maintain their T3. Those on ketogenic diets have T3 levels that are sometimes half of what those on higher-carb diets would show, but without symptoms. It’s merely physiologic.

The significantly lowered T3 while THS stays normal tells me that TSH monitors a bit more than just T3 levels. TSH must also somehow monitor overall health levels to be unconcerned about a T3 that is half of what it would be with a larger carb intake.

So, if you decide to go from a diet with 45 -50 percent carbs, expect your T3 to fall. And likewise expect your THS, should you check that, to stay about the same.

An Austrian researcher named Wolfgang Kopp took a good look at this about 20 years ago and came up with some interesting ideas.

He describes the studies showing it is not starvation or the lack of another macronutrient that causes the fall in T3 on a ketogenic diet. It is definitely the lack of carbohydrate.

*This has been demonstrated first in studies on starvation: under total fasting conditions, serum T3 starts to decline within 24 h to reach a plateau approximately 50% below control levels within about 4–6 days, while reverse T3 (rT3) levels increase and thyroxin (T4) shows little or no effect .

* Further studies proved that this decline in serum T3 is not due to starvation, but results from a reduction in dietary carbohydrate: an isocaloric substitution of fat and/or protein for carbohydrate in a mixed diet was shown to decrease serum T3 concentrations similar to those induced by fasting.

• While refeeding (after starvation) with fat and/ or protein has no significant effect on decreased T3 levels, refeeding with carbohydrate leads to increasing T3 concentrations. The magnitude of this increase is dependent on the amount of carbohydrate, with 50 g of glucose partially and about 160 g of glucose fully re- storing T3 to control levels.

• Very low carbohydrate diets are associated with significantly lower T3 concentrations. In an norm-ocaloric diet containing less than 20 g of carbohydrate, T3 concentrations declined and reached a plateau approximately 50% below control levels, and stayed unchanged during a 4 week period until refeeding. In a study by Barrow and Snook, an amount of 30 g of carbohydrate in a calorie-reduced mixed diet was associated with T3 concentrations 36% below base line. T3 levels remained depressed throughout diet (12.9–22.4 weeks, with a mean of 18.1 weeks). [Minimally edited for clarity]

The paper is an easy one to read, and I suggest you do so. I stuck it in my Dropbox folder, so you can grab it here.

He goes on at length like one of my Paleolithic diet talks about how our ancient ancestors ate primarily meat they could kill or scavenge. For millennia that’s all we had to eat, so, he surmises, we evolved to have low T3 levels. It was normal given our diets at the time. But then came agriculture.

Beginning about 10,000 years ago agriculture began to develop. The agricultural revolution brought a sharp increase in the consumption of plant food, particularly of cereals which were high in starch. The industrial revolution, and especially the de- velopment of high-speed steel roller mills in the 19th century offered the possibility to grind cereals very finely, thereby removing almost all of the fibrous indigestible material, and increasing the yield and palatability. At the same time, potatoes and refined sugar were introduced into western diets. Since the end of 19th century, the consumption of sugar has increased steadily and has now reached 70 kg/150 lb per capita/per year in most western countries.

Thus, the carbohydrate content of human nutrition has increased during the millennia, with the current high-carbohydrate nutrition representing the culmination of dietary changes.

There can be no doubt that these increasing amounts of dietary carbohydrate must have significantly altered serum T3 levels during the past 10,000 years. From an evolutionary point of view, serum T3 levels may have increased by a factor of 1.5 since the introduction of starchy foods and of sugar into human nutrition. [Minimally edited for clarity]

Once all this sugar and refined grains became a large part of the human diet, another problem arose. The T3 levels went up accordingly, but that created a problem. Iodine is required for the proper synthesis and function of thyroid hormone.

Many areas of the world had soil containing plenty of iodine to prevent the development of disease, but not all areas had plentiful iodine. Those humans living in such areas developed iodine deficiency diseases (IDD), with hypothyroidism and goiter being the primary ones.

Adhering to your low-carb ketogenic diet will help prevent IDD.

There is another issue with thyroid hormone I want to discuss that I got caught up in ten or so years back that could have done me in.

I go to a lot of talks and conferences and know most of the docs there. Sometimes talks turn to health issues one of us might be dealing with. I had just had a thyroid panel done on myself along with a bunch of other labs. Everything looked pretty good except for my TSH, which was a little high.

I’ve been on a low-carb diet to some degree for the past 40-some years, so I was used to seeing a low T3 and a normal THS. The elevated TSH troubled me a bit, but I had no symptoms of hypothyroidism. I wasn’t chronically cold, I could think okay—at least as well as I ever had, and wasn’t gaining weight.

I asked one of the docs at the talk who often spoke about thyroid disease and asked what he thought I should do, given my thyroid labs. Had I not connected with him there, I would have probably done nothing and ignored it till I developed symptoms or got labs again.

My new doc told me I could probably use a little Armour thyroid, which he figured would fix me right up. He wrote me a script, and I started taking a low dose.

I didn’t really notice any change in anything. I didn’t suddenly become brilliant or start losing massive weight or anything.

I continued to take the Armour for a couple of years. Along the way, I didn’t think to test my thyroid again. But I did come across an article in the New England Journal of Medicine showing the many people who were aging developed mildly elevated TSH levels, which I think they categorized as idiopathic elevated TSH of the elderly. In order to qualify, one had to have mildly elevated TSH and no symptoms of hypothyroidism.

I qualified. And after several years on Armour thyroid, I quit taking them. I kept waiting to incur some sort of symptoms after going cold turkey, but nothing. I didn’t feel a thing.

So, I’ve never taken them since. I was kind of burned that I had taken the drugs for several years without actually needing them.

I continued to read about high THS in the elderly and recently came across a paper that gave me a real pause. It discussed a study on elderly people who were treated with thyroid for a mildly elevated TSH.

From the paper:

They found that among older adults, use of thyroid hormone increased risk of death 60% year over year (hazard ratio 1.6). They also limited the analysis to compare individuals with normal TSH levels, reflecting normal thyroid function, to those on thyroid hormone with normal TSH levels, who were therefore treated to target, and found those on treatment had almost double the risk of dying compared with untreated persons (hazard risk 1.9), Mammen reported.

Despite studies showing that hormone treatment of an isolated high TSH may not benefit older people, Mammen said, “we were surprised that we were able to demonstrate harm associated with thyroid hormone supplementation. Our work supports the growing calls to use age-specific TSH reference intervals to determine the threshold for thyroid hormone treatment.”

I’ve discovered a lot of doctors who think Armour thyroid is a wonderful medicine. I’m sure it is when it is needed. But I want to draw your attention to a mildly elevated TSH with a normal or low T3 (common in folks on low-carb diets). Be very careful about going on thyroid medication under these conditions. You really need to be hypothyroid with symptoms to do so, at least in my opinion.

Odds and Ends

Newsletter Recommendations

This is Dale Saran’s Substack, which I encourage you to read. I always find something worthwhile. Give it a try.

Video of the Week

For some reason today, I’ve had a hankering to hear Billy Strings sing and play “Don’t think twice it’s all right.” So I had to make a run through YouTube to find the right one. I listened to a bunch, but ended up choosing this one for whatever reason.

If you don’t know about Billy Strings, you should read up on him. Interesting story about a brilliant player.

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That’s about it for this week. Keep in good cheer, and I’ll be back next Thursday.

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This newsletter is for informational and educational purposes only. It is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.

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Finally, don’t forget to take a look at what our kind sponsors have to offer. Dry Farm WinesHLTH CodePrecision Health Reports, and Jaquish Biomedical.

And don’t forget my newest affiliate sponsor Lumen. Highly recommended to determine whether you’re burning fat or burning carbs.

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