This post discusses changes I made to my health in response to Bredesen’s The End of Alzheimer’s, with a much smaller influence from Gundry, and some changes that were incidental to Robert experimenting with the SCD diet.
My cholesterol has often been high, and when I’ve measured sdLDL or LDL-p, those have been too high. However, I measured my oxidized LDL once last fall, and it was fine.
I’m puzzled why Bredesen indicates that it’s ok to just measure one of these, since the oxidized LDL seems to measure a risk indication that is independent of the other two.
I’ve measured sdLDL and LDL-p enough to know that most forms of dietary saturated fat cause them to rise.
I had hoped that coconut fat was healthier than other saturated fats, and I used it increasingly in baking toward the end of last year. Then I measured my LDL-p, and found it way above Bredesen’s target. So I cut my coconut fat consumption to almost zero, and cut my chocolate consumption a bit (to maybe 10-20g per day). I also eliminated whey protein from my diet, for reasons that were somewhat aimed at cholesterol (based mainly on Gundry’s ApoE4 advice; I had been eating a fair amount of whey protein, and not much other diary products).
For SCD-related reasons, I made some changes to my diet for 5 or 6 weeks starting in early February. The biggest change was cutting my pastured chicken consumption by about half (to maybe an average of 2.5 oz/day?), replacing that with shrimp.
In mid-March I got one of my lowest LDL readings ever (I didn’t measure LDL-p or sdLDL then).
My chicken consumption went back to pre-February levels, and in mid-April I got an LDL reading that was 8% higher, and an LDL-p of 1286 (versus a target of <1000).
It’s possible that the March to April increase in LDL was due to a slight increase in saturated fat, but I think that any change in my saturated fat consumption was small enough for that to be unlikely. My intuition says it’s more than 50% likely that’s due to eating more chicken.
The other hypothesis that I find somewhat plausible is that pregnenolone (see below) better explains the changes. My next test should distinguish those hypotheses, as I’ve reduced my animal protein consumption a good deal, but only reduced my pregnenolone dose a modest amount.
My homocysteine levels have consistently been above Bredesen’s target of less than 7 (or is it 6? – he gives different numbers in different places). They often correlated with my saturated fat intake, and my LDL, when those were higher, but this year I’ve seen fluctuations that can’t be explained by saturated fat.
Bredesen convinced me to try different forms of B6 and B12 than I’d tried before, but I couldn’t see any effect from them. I stopped taking B6, because a blood test said I’d been getting enough B6 without supplements.
I’ve been taking megadoses of folate (3mg) for years, with little effect on my homocysteine.
Bredesen says when those fail, try TMG. I’ve tried it off and on this year, with inconclusive results.
The next step in Bredesen’s approach is reducing methionine in my diet (which mostly means less animal protein). I’m doing some of that, but I’m reluctant to add large new restrictions to my already quite restrictive diet.
I’ve noticed some correlation between my consumption of green coffee extract pills and higher homocysteine levels. Coffee and caffeine reportedly raise homocysteine, but green coffee extract seems to lower homocysteine a bit. The claimed benefits for green coffee extract are mostly for biomarkers that I’m not currently concerned about, so I’ve stopped taking them for now, but will probably try using them again someday.
My homocysteine levels have fluctuated in a range from 7.4 to 9.3 over the past year, and the factors I mentioned above can explain at most half of the variation. Maybe ashwagandha withdrawal (see below) caused some of the homocysteine spikes.
Either the changes that I’ve implemented will show results soon, or I’ll run out of ideas and decide it’s not worth worrying about.
[Warning: a long story that requires tracking lots of evidence if you want to understand it; many readers will want to skip to the next section.]
Bredesen convinced me to try ashwagandha – see my initial reactions here.
I started taking 25mg per day of DHEA in late December, doubling my blood levels to a still-low 200 mcg/dL, with probably not much effect on my thyroid levels.
I slowly increased my ashwagandha dose through the end of February. I believed my thyroid levels remained a bit lower than optimal, due to a combination of heart rate measurements, subjective impressions, and a TSH reading of 2.18 on January 18.
In late February, I asked my doctor about getting medication to increase my thyroid levels. He had no experience with ashwagandha, and asked me to stop taking ashwagandha for two weeks, and then get a blood test after the ashwagandha effects had worn off.
I felt really bad most of those two weeks – a combination of depression, apathy, and muscle pain (some of it cramp-like, with one case of bad muscle cramps in one leg at bedtime after a hike). On day nine, it felt like a major struggle to do an unusually easy hike. That fit the description of declining thyroid levels pretty well.
The test results showed a TSH of 0.07 and a free T4 of 1.7. I.e. borderline hyperthyroid, and about as far from what I expected as I could imagine. Oops. My request for medication to increase my thyroid levels suddenly seemed foolish, and the surprise was big enough to leave me disoriented for days.
I had been overconfident in my ability to estimate my thyroid levels. Also, I had accidentally done something which caused an unexpectedly large increase in my thyroid levels.
My first guess involved DHEA: I had doubled my DHEA dose to 50mg, 4 days before the blood test. I started seeing signs of rising thyroid levels the day after the blood test. Maybe the DHEA had increased my T4 levels starting just at the time of the blood test, and slowness in converting T4 to T3 had delayed the symptoms? That hypothesis felt wrong, mainly because it strongly depended on two time delays that each seemed rather unlikely.
After about three days of feeling confused and worried (including an unhelpful talk with my doctor, then resuming ashwagandha, which improved my cognitive function, presumably due to thyroid changes), I decided to try abandoning my beliefs that I had usually been estimating my thyroid levels accurately and that the unexpected change had come shortly before the blood test.
Lo and behold, pregnenolone emerged as a possible cause: I started taking it in late January (10mg/day), and this was my first thyroid test since then. I had to accept the possibility that my thyroid levels soared in late January without me noticing any signs of the change. Once I accepted that unpleasant idea, the patterns started to fit somewhat well.
Apparently many of the symptoms that I had attributed to thyroid levels were actually symptoms of changes in thyroid levels. I now think I’m pretty good at noticing day to day changes in my thyroid levels, but I’m pretty poor at guessing whether the levels are too high, except via blood tests. I can tell something about the levels by my heart rate, anxiety levels, and the speed at which my digestive tract works, but the noise levels in those measures are several times the size of the signal.
In hindsight, it was foolish and costly to resume ashwagandha at the full standard dose. I was somewhat influenced by my doctor’s desire to make simple changes to supplement doses, and maintain fixed dosages for weeks, in order for the resulting tests to be maximally informative. I should have expected that the ashwagandha would push my thyroid levels too high, but I wasn’t thinking as clearly as usual when I decided on that dosage (presumably due to the continuing decline in thyroid levels due to ashwagandha withdrawal), and still somewhat attached to the belief that ashwagandha had good effects (since that was unmistakably true for the first month that I took it).
At any rate, my free T4 levels got up to at least 2.4 in early April (anything above about 1.8 has enough health risk to make me concerned). I then spent about 10 weeks lowering those levels, first by cutting my pregnenolone dose to 5 mg, then mostly by reducing my ashwagandha dose slowly to zero. For slightly more than 2 months, I kept expecting my thyroid levels to drop faster than they actually did, and yet the declines that did happen were enough to cause moderate discomfort and depression, so I was reluctant to reduce them faster.
Finally in mid June I got my free T4 level back into the range of acceptable values. My TSH is still suspiciously low. Bredesen seems unconcerned with low TSH, but other sources suggest I should be somewhat concerned. I’m unsure whether the low TSH is due to lingering effects of ashwagandha, or whether it means I should reduce my pregnenolone or TMG.
I can’t come close to explaining my free T4 measurements by a reasonable function of my ashwagandha and pregnenolone doses, so I’ve made some guesses about other causes. Here’s a list of my hypotheses, with a guess as to how much of my thyroid changes they caused, followed by a probability that they affected my thyroid levels:
Kelp is high in iodine, and excess iodine can depress thyroid levels. I believe I started adding kelp powder to my food in late 2012, and as of last year I was consuming somewhere between 1/4 and 1/2 teaspoon per day. I measured my thyroid levels about 5 months after starting to use kelp, and the free T4 level had dropped 0.2 from the prior year (and the TSH rose about 2 points). I paid little attention to that at the time, and didn’t detect any other changes that year which seem like symptoms of hypothyroidism.
I didn’t try to quantify my iodine intake until last month, relying instead on the heuristic that it’s safe to eat moderate amounts of natural food. I was apparently getting about 1mg/day of iodine, which is a level at which some sources say iodine starts to cause hypothyroidism.
For the month of February, I stopped taking kelp, for SCD-related reasons, and resumed taking it at somewhat lower levels in March. February is almost certainly when my thyroid levels became too high. I now suspect that high iodine levels made me somewhat hypothyroid from 2013 through 2017, and I accidentally stopped that shortly after starting pregnenolone and TMG.
So, beware of treating kelp as food. I’m guessing it cut my productivity by 5 to 10% for years.
It seems clear to me that the thyroid evolved mainly to signal how much energy an organism could afford to burn . So it seems clear that my body will increase my thyroid levels if my eating habits imply that there’s lots of food available.
As I mentioned in a prior post, calorie restriction probably contributed to my hypothyroidism up through last fall.
I increased my calorie consumption in response to the weight loss I sometimes experienced with the high thyroid levels. I stopped doing calorie restriction days for the month of May, and I’m slowing resuming those at less restrictive levels.
I’ve been trying to eat as much as I could for the past few months, subject only to the constraint that the food be healthy (more almonds, macadamias, sweet potatoes, and taro). My weight has stabilized at about 145, and it feels like I can’t gain weight unless I lower my thyroid levels further and/or eat food that’s less healthy. I’m uncertain whether the small additional declines in my thyroid levels that I’m planning will put me back into conditions where I could gain weight.
According to the Harris-Benedict Equation, I should need 1755 calories plus whatever I use while exercising (which I estimate at 200 calories last year, 240 now). My rough estimate is that I ate about 1900/day calories last year, and increased it to above 2400 calories briefly in April, and am now reducing it slowly.
That increase in calorie consumption is likely to have caused my body to decide calories are plentiful, so it can afford to burn more energy, and has caused my thyroid levels to be higher than they otherwise would be. Although that effect may only be changing my T3 levels, not my T4 levels, and I’ve mostly been trying to explain my T4 levels here.
This experience has convinced me that it’s a really bad idea to try to control my weight via calorie restriction. That approach is more effective at slowing my metabolism than at reducing weight. Slowing my metabolism is pretty similar to inducing depression.
Whereas it’s a good deal more effective to eat real food, not the food/drug hybrids (i.e. junk food) that most people are addicted to. The small decrease in pleasure from eliminating the taste of addictive foods has been compensated by the elimination of guilt/worry over how much I eat, and by my stomach feeling more comfortable.
There are a few reports of TMG raising thyroid levels. I see some weak evidence in my blood tests that it has moderately raised mine.
Thyroid concluding comments
I asked for my doctor’s help because ashwagandha didn’t seem to be enough by itself to raise my thyroid levels to optimal levels, and I despaired of finding other non-prescription methods. Yet it seems like I had already implemented between two and five other methods, and I now suspect that any two of the first 4 methods listed in that table would have been enough to get my thyroid levels where I wanted them.
I’m getting nearly 20% more exercise than last year, because it feels easier, and because I can hike about 10% faster. It’s time for me to resume regular hiking with a very ambitious hiking group.
When my thyroid levels were declining at a moderate pace this spring, I would typically get around 6 hours a day of good cognitive function, with the timing determined by when I took pregnenolone. Outside of that time, I had too little mental energy to do much.
Now that I’ve mostly stabilized my thyroid levels, I’m getting more like 10-12 hours a day when my mind works noticeably faster than it did last year. That has influenced how much I blog, so expect more blogging over the next month.
I was concerned that higher thyroid levels (than last year) would cause my body to be warmer in ways that would increase the impact of warm weather on my sleep and hiking. But I’ve experienced less heat-related discomfort this year while sleeping or hiking on warm days.
I’m sleeping better this month than is normal for June (the sun often woke me at sunrise in prior years). I can’t think of any changes that might explain it other than those I’ve described in this post, but I have no clue which of these changes did it.
I didn’t notice grass pollen allergies this spring. There was maybe a 30% chance this would happen by accident, so I’m uncertain whether to attribute it to a change I made.
I measured my reverse T3 twice, once before starting ashwagandha, and once shortly after starting ashwagandha. Both measurements showed it was higher than optimal.
I don’t think it’s causing problems, but it’s likely a symptom of some sort of problem. The higher of the two measurements was likely elevated by a calorie restriction day. I’ve given low priority to figuring out what else is elevating it, hoping that it’s something which will be fixed by the other issues that I’m working on.
My pregnenolone level was 29 last fall. 5mg/day of pregnenolone was enough to get that level above Bredesen’s minimum of 50, but I’ve since then decreased my dose to a bit less than 4mg due to the thyroid problems. The smallest dose that is sold seems to be 5mg, which is evidence that my reaction to pregnenolone is unusually strong. I’ve been buying Source Naturals 10mg lozenges, cutting them up, and weighing them with a scale that has milligram accuracy.
My potassium levels are lower than Bredesen recommends, and have been quite steady for 12 years, even though I know I’ve increased my potassium consumption a fair amount. I’ve postponed doing anything about this, hoping that some other change will improve it.
I’ve been taking 100 mcg of vitamin K2 mk7, and 100 mg of nicotinamide riboside. I think one of those has made my blood draws easier. Previously phlebotomists sometimes had trouble getting blood out of my arm. Now it seems trivial. K2 may also have decreased the calcium in my blood, but the current and prior calcium levels both seem healthy.
I’ve measured many of the other biomarkers that Bredesen recommends, and they’re all ok. I have not yet tested for vitamins C and E – I’m fairly sure I get enough of those in my diet. It’s been 6 years since I tested my omega-3 levels – that time a doctor who was consulting for WellnessFX told me my omega-3 levels were too high (and that my omega-6 levels were too low, even though my 6/3 ratio was 2.3!) – I was eating lots of salmon then, and I’ve cut back a lot on salmon, so I should measure it again before too long.
I’m avoiding some tests that are hard to get or unpleasant to take: leaky gut, sleep apnea, and the Cyrex Arrays. I have some reasons to doubt that I have the problems they’re designed for.
The book’s discussion of B6 enabled me to get someone I know to discover that he was suffering from dangerously high B6 levels. He stopped taking the multivitamin that was causing it, although it’s unclear whether that has made a difference.
The End of Alzheimer’s is a fairly good summary of how to optimize health in older people in developed societies, independent of whether it has a significant effect on Alzheimer’s. It is improving my quality of life, although it required a significant investment of time, attention, and money in order to achieve that. It appears to have somewhat reduced my risk of cardiovascular diseases. My risk of Alzheimer’s has probably been mostly influenced by the risk that cardiovascular problems would contribute to Alzheimer’s, so lowering my risk of cardiovascular disease probably yields a similar risk reduction for Alzheimer’s, but with more uncertainty.
He’s got many more suggestions about supplements to try, but I want to go slow about trying any more, and I’m uncertain how I would evaluate the effects of most of them.