Hundred Health Protocol: What My 100-Day Plan Recommended and What the Retest Showed

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Updated October 16, 2026

When I published my Hundred Health review back in March, I ended it with an open question. The biomarker panel impressed me, the medical records import surprised me and the app was clean even in beta. But I could not tell you whether the Hundred Health protocol would be built around me or whether it would read like generic wellness advice. That was the question that mattered most and I promised to answer it once the protocol arrived, whichever way it went.

It arrived. My protocol is dated July 1, 2026 and I followed the original version all the way to Hundred’s retest on September 21. An off-schedule draw five weeks in looked like a breakthrough, with my total cholesterol down 68 points and my ApoB at 129. The retest, with nothing else in my life changed, came back mixed. My non-HDL was 216, up slightly from August but still my second-lowest reading since late 2022. My ApoB was 157, back inside the range it has sat in for years.

So this article does two things. It shows you exactly what Hundred told me to do and checks every recommendation against the peer-reviewed research and it reports both blood draws, the one that looked like a breakthrough and the retest that only partly backed it up. Along the way I explain why I now think my genetics say more about my cholesterol than any capsule does.

That first part is revealing on its own. Some of what Hundred recommended is backed by more than 100 randomized controlled trials. One recommendation rests on five small studies. One is a statin in everything but name and I chose not to take it. If you are considering a membership and you want to know what you receive at the end of the process, this is it.

Disclaimer: Links may contain affiliate links, which means we may get paid a commission at no additional cost to you if you purchase through this page. Read our full disclosure here.

What Is the Hundred Health 100-Day Protocol?

The protocol is the whole reason Hundred exists. Plenty of companies will sell you a biomarker panel and hand you a dashboard. Hundred’s argument is that the dashboard is where most people get stuck, so the platform takes your labs, your wearable data, your intake questionnaire and your imported medical history, runs all of it past clinicians and produces a plan covering four areas: supplements, nutrition, exercise and recovery.

The 100-day window is deliberate. It is long enough for lipids, inflammation markers and body composition to shift and short enough that you are not signing up for an open-ended optimization project with no finish line. At the end you retest, and the protocol updates against the new numbers.

In the app it lives under the Protocol tab, split into Supplements, Nutrition, Exercise and Results. Each item opens into a detail screen with a plain-language explanation of what the thing is, a “Why we chose this for you” panel written against my specific results and a recommended dose.

That “Why we chose this for you” panel is where the personalization claim either holds up or falls apart. This is also the biggest structural difference between Hundred and the other panels I have run. Function Health gives you clinician notes and an AI coach against a dashboard, and Superpower gives you a plan plus chat, but neither hands you a fixed-length protocol with a defined end date and a retest built into it. If you want the full side by side, I compared Function Health and Superpower after running both.

My Retest Results: Non-HDL Mostly Held, ApoB Did Not

I wrote most of this article the week my protocol arrived, before I had anything to report. Then an off-schedule draw landed about five weeks in and the numbers were the best I had seen in years. I published them as a checkpoint rather than a result and said the retest would be the honest test. Hundred’s retest came back on September 21, about ten weeks in. Here is all of it.

The August numbers were the best I had recorded in years and I was pleased to see them. The retest is the one that counts, because it is the draw Hundred scheduled, it came after about ten weeks on the protocol instead of five and nothing else in my life changed between the two. Non-HDL rose 13 points from August to 216, which is still my second-lowest reading since late 2022 and 51 points below July. ApoB is the number that did not hold: 129 in August, 157 in September, which sits right inside the 141 to 167 range I have bounced around since 2023. All three draws were fasted.

Nobody Measured My LDL

Start with something almost nobody is told. My LDL was never measured on any of these panels. The lab measured total cholesterol, HDL and triglycerides, then calculated LDL from those three.

The classic way to do that is the Friedewald equation: total cholesterol, minus HDL, minus triglycerides divided by five. That divide-by-five step assumes a fixed ratio between triglycerides and VLDL cholesterol. Work published in JAMA covering more than 1.3 million lipid profiles checked that assumption against cholesterol measured by ultracentrifugation and found the real ratio is not fixed at all. It varies with your triglycerides and your non-HDL, with a median of 5.2 and a middle range running from 4.5 to 6.0. The same research group built a replacement, now called the Martin-Hopkins method, which picks the factor from a table based on your own numbers.

My lab uses Martin-Hopkins and says so right on the report. You can see the difference on my July panel. The old equation gives 331, minus 64, minus 214 divided by five, which is 224. The lab reported 227. Three points is small, but it is a reminder that the LDL on your report is an estimate and two labs can estimate it differently from the same blood.

That is why I now watch two numbers instead. Non-HDL is just total cholesterol minus HDL, both measured directly. ApoB is measured directly too. Neither depends on an estimating equation, which makes them the honest way to compare one draw against another. If you take one practical thing from this article, make it that: ask for ApoB and look at non-HDL on the panel you already have.

The Long Version of the Same Story

Here is my non-HDL going back to 2024. This is the chart I would want to see if someone were telling me their supplement worked.

Look at what that does to the headline. Measured from my July reading of 267, my non-HDL fell 51 points by the retest. Measured from February, which is where my trend sat before that July draw broke upward, it fell 12. Both numbers are true and describe the same result. The first is the one a supplement company would put on a graph. The second is close to ordinary test-to-test variation, which is why I am not calling it a result yet.

I should also say that the 239, 233 and 228 readings are not a downward trend at all. Non-HDL is built from two measured values that each carry ordinary lab and biological variation and on a total cholesterol near 300 that is worth roughly fifteen to twenty points on any single draw. What the chart shows is one large drop and then a plateau. The retest sits a little below that plateau but not clearly off it.

Four Things Changed Before I Took a Single Capsule

I share all of this to say no protocol is perfect and you can never know for certain what is moving numbers since you may be implementing other health strategies as you go. In early 2025 three things changed within weeks of each other. I started contest prep in January, which took me down to about 12 percent body fat by summer. In February I restarted thyroid medication after being off it for a while and changed my HRT delivery method, moving off pellets. Then from July 2025 to May 2026 I deliberately regained toward a healthier body fat. My non-HDL had already fallen from 290 to 228 before the Hundred protocol existed.

The thyroid change is the one I would bet on. Thyroid hormone drives how quickly your body clears LDL out of circulation and my worst reading in this whole record is the one taken while I was not medicated. A meta-analysis of thyroxine treatment trials found that total cholesterol, triglycerides and LDL all ran higher in people with subclinical hypothyroidism than in matched controls and dropped significantly once they were treated, with carotid artery wall thickness improving alongside. My own free T3 was below range through the first half of 2025 and normal from that autumn on, which lines up with the lipid picture.

Contest prep is the one most people would guess and my numbers argue against it. Prep ran from January to July 2025. Deep into it, my non-HDL went from 239 in April to 233 in June, which is flat. Then I ended prep and spent the next ten months deliberately regaining body fat, and my non-HDL did not climb back. It was 228 in February 2026. If the fat loss had driven the drop, putting the fat back on should have undone it. The one marker prep did move was triglycerides, 85 that April and the lowest in my record.

So: thyroid, hormone delivery, a 12 percent body fat cut, a deliberate regain and then a supplement protocol. None of the first four changed between my August draw and the retest, which makes the retest the cleanest comparison I have.

What the Retest Told Me

When I first published this I said the only honest test would be Hundred’s retest with nothing else changed in between. I held my training, my eating and my medications steady to protect it. I also stayed on the original protocol rather than switching to the updated one, so the retest measured the same supplements the August draw did.

It did not settle the question. After about ten weeks on plant sterols, amla and omega-3, my non-HDL sits 12 points below where it was before I started and my ApoB sits 9 points below my March reading. Both moved in the right direction and both are close to the range I would expect from two draws of the same blood a few weeks apart. Even a textbook response would have been hard to see. Plant sterols at 2 grams a day lower LDL by up to about 10 percent, as a randomized trial in the American Journal of Clinical Nutrition notes, which on my numbers is roughly 20 points.

The retest also showed something new. My triglycerides went back up to 195, my HDL dropped to 54 (the lowest on my record) and my particle test came back pattern B, meaning a higher share of small, dense LDL particles, where earlier particle tests had me at pattern A. Smaller particles each carry less cholesterol, so the same cholesterol number can travel in more of them. That, plus ordinary lab variation, is the most likely reason my ApoB rose far more between August and September than my non-HDL did. It is also why I ask for ApoB every time.

The one mistake in my own testing I want you to learn from rather than repeat: my July baseline panel did not include ApoB, so I have no true starting point for it. The initial draw had it back in March and the July one did not. I should have noticed. Ask for ApoB on every panel, especially the first one.

Why My Cholesterol Is Not a Diet Problem

Whenever someone posts numbers like mine, the first response is some version of “what are you eating?” It is a fair question. I happen to have an unusually complete answer to it and it is the reason I did not spend the last few years assuming I could fix this with a grocery list.

When I was in contest prep for an NPC physique show, I weighed and logged every single morsel that went into my body for six months. Not estimated. Not mostly. Every gram, for six months. My fat intake never went above 50 grams a day and most days sat closer to 30. I was in a deficit, losing weight, training hard and sleeping like it was my job.

My cholesterol barely moved. Deep into prep, my non-HDL went from 239 in April to 233 in June. The bigger drop from my December 2024 reading lines up with restarting thyroid medication rather than with the food, because when prep ended and I regained the body fat, my numbers stayed where they were. And this is not the first time I have done this kind of experiment, there have been other times where I tracked for months and checked cholesterol at the beginning and end with no significant change.

That is one person and one experiment, so I am not going to oversell it. But it is a cleaner experiment than most people ever run on themselves. The usual version of “I tried eating better and it did not work” involves guessing at portions for a few weeks. Mine involved six months of weighed food and a fat intake most people would find punishing, in a body that was getting leaner at the same time.

What the Research Says About Diet and LDL

The evidence here is more measured than either side of the internet argument suggests. A Cochrane review pooling 15 randomized trials and roughly 59,000 participants found that reducing saturated fat intake for at least two years cut combined cardiovascular events by 21 percent, which is a real and worthwhile effect. On the lipid numbers themselves, the same review describes small reductions in total cholesterol and LDL cholesterol. Small is the operative word, and that is the average across thousands of people. Some sit above the average and some sit below it. I appear to sit well below it.

What This Is Not

When people hear numbers in my range, familial hypercholesterolemia usually comes up. It has been raised with me before. It does not fit in my case though.

Familial hypercholesterolemia is present from birth. A review of how lipids track across the life course in women and men in Atherosclerosis makes the point plainly: in hereditary lipid disorders, cholesterol runs high from birth onward. It is not something you acquire at 45.

My LDL used to be 110. That single fact does most of the work here. A number that sat in an ordinary range and then roughly doubled is not describing a condition I have carried since birth. It is describing something that changed. That does not mean genetics play no part, since plenty of common inherited variants nudge cholesterol without ever producing the picture familial hypercholesterolemia produces. I carry one of them and it deserves its own section.

ApoE 3/4: Part of Why My Numbers Do Not Move

I left this out the first time I published this article. My ApoE genotype is 3/4, which means I carry one copy of ApoE4. ApoE4 is better known for its link to Alzheimer’s risk, which is a separate conversation I am not getting into here. This section is about what it does to cholesterol.

ApoE is a protein that helps your liver recognize and clear cholesterol-carrying particles from your blood. It comes in three common versions, E2, E3 and E4. You inherit one from each parent. A JAMA meta-analysis of 82 studies and more than 86,000 people found LDL rises in a near straight line across the genotypes, lowest in E2 carriers and highest in E4 carriers, with about a 31 percent gap in LDL between the two extremes. My 3/4 sits second from the top. A study of healthy postmenopausal women aged 50 to 65 in Women and Health found the same thing in women my age, with higher LDL in E4 carriers than in women without it.

E4 carriers also absorb more of the cholesterol in their gut. An early study in The Journal of Clinical Investigation found people with E4 absorbed cholesterol more efficiently and made less of their own, while E2 carriers did the opposite.

Here is where I have to be careful, because the internet version of this story is that E4 carriers cannot move their cholesterol with diet. When it comes to diet, the research mostly says the reverse. In a randomized trial reported in Nutrients, E4 carriers saw bigger drops in total cholesterol and ApoB than people with E3/E3 when saturated fat was replaced with low glycemic carbohydrate on a lower fat diet. A systematic review in the American Journal of Clinical Nutrition found that genes including ApoE do shape how people respond to dietary change, but not consistently. Those trials changed the type of fat and not just the amount, so my contest prep and their experiments are not identical. Still, my genotype does not explain why six months of weighed, low fat eating left my numbers where they were. If anything it predicts I should have responded more.

It does not explain the bend in my forties either. I was born with this genotype and my LDL was 110 in 2013. A gene that never changed cannot by itself explain a number that doubled. My best reading of all of it is that ApoE 3/4 set my starting line higher than most women’s and menopause and thyroid moved it from there.

It also changes how I read the plant sterols. If E4 carriers absorb more cholesterol, a supplement that blocks absorption sounds like a perfect match. The best test of that idea I found recruited people by genotype in advance and found ApoE made no difference to how much 2 grams a day of plant sterols lowered LDL. Being E4 did not make me a guaranteed responder and my retest is consistent with that.

Finding the Year the Line Bent

So I went back and pulled every lab report I could find, some of them more than a decade old. Here is the long arc.

The bend happened somewhere between 2017 and 2019, in my mid forties. By March 2019 I was at 200 and by that August I was at 214, and I have been north of 200 far more often than not ever since.

That timing matters, because I did not start hormone therapy until October 2020. My cholesterol had already doubled and settled at its new level a year and a half before my first pellet, which rules HRT out as the cause of the original rise however tempting a culprit it makes. I would not have been able to say that without the old reports, which is the argument for testing regularly that nobody makes compellingly: not so you can optimize anything, but so that when something does change you have the resolution to work out when it happened and what else was going on.

So What Did Change in My Forties?

These are the candidates for the original rise, and they are things a lot of women reading this are living through at the same time I am. They are separate from the four changes in 2025 and 2026 I covered further up.

Menopause. The same Atherosclerosis review notes that women develop a more adverse lipid profile during the menopausal transition, and a review of dyslipidemia and cardiovascular disease in women describes menopause as associated with an increase in total and LDL cholesterol alongside a decrease in HDL. That is the exact shape of what happened to me, and the timing fits my mid forties. Because I had a hysterectomy in 2007 with my ovaries left in place, I have no periods to date the transition by, which is its own small frustration when you are trying to line a lab trend up against a hormonal one.

Thyroid. I manage hypothyroidism, and thyroid hormone governs how quickly your body clears LDL out of circulation. Studies of subclinical hypothyroidism have found higher total cholesterol, triglycerides and LDL with lower HDL compared with matched controls, and both papers I read ended with the same recommendation: screen the thyroid in anyone with dyslipidemia. I have not been consistently medicated across the whole of that period, and as I covered above, my worst panel on record is the one drawn while I was off it entirely.

The one that does not fit. I eat low carb and there is a described pattern where lean, metabolically healthy people on carbohydrate restriction develop large LDL increases. The phenotype has been defined as LDL at or above 190 together with HDL at or above 60 and triglycerides at or below 80. I meet the first two and fail the third, since my triglycerides have mostly run well above 80 although they have definitely been below 80 before as well. So the tidy explanation that would have flattered my diet does not apply to me. I will also note, since this research gets cited enthusiastically online, that a 2025 follow-up study from the same group has since been retracted, so anyone using that body of work to argue high LDL does not matter on a low-carb diet should take a closer look.

Why This Changes How You Should Read My Results

If your cholesterol is driven mostly by what you eat, then eating differently should move it. Mine did not, across six months of tracked and weighed food. That is the reason I took a supplement protocol seriously enough to test it rather than dismissing it and also the reason I was unwilling to credit it after five weeks, which the retest supported.

The practical version, for anyone reading this with numbers that will not move: if you have done the dietary work properly and exercise regularly and your panel has not budged, the answer is probably not that you need to try harder. Pull your old lab reports and look for the year the line bent. Ask whether menopause, thyroid function or a medication change lines up with it. If you know your ApoE genotype, factor it into what you expect. Ask for ApoB rather than a standard lipid panel. I spent years assuming the next dietary change would be the one that worked. It was not and the useful step was working out why rather than repeating the attempt.

My Hundred Health Protocol at a Glance

Before I go through the recommendations one by one, here is the shape of the whole thing. This is what landed in my app.

Two things jump out immediately. First, almost every recommendation points at the same target: my lipids. Second, the iron goal is the one I want to flag, because it tells you something about how this system works.

In my original review I wrote about two out-of-range findings from my first draw: my iron and my iron saturation both came back elevated, with a normal TIBC, which is an iron overload picture rather than a deficiency one. I did not tell the app what to do with that. It built a nutrition goal around it on its own and titled it “Iron Saturation Management.” That is the software connecting a lab finding to a food strategy without me prompting it, and it is the moment I stopped wondering whether this thing was generic.

Rising iron in midlife is not a fluke, either. Once monthly blood loss stops, iron has room to climb, which is exactly why I care about seeing serum iron, saturation and TIBC together rather than a lone ferritin value. I dug into that pattern in my Superpower Health review, and it is also why I pay attention to iron leaching from cast iron cookware now in a way I did not a few years ago.

The rest of the protocol is aimed at my lipid panel. The app’s own language describes my LDL cholesterol, LDL particle number, ApoB and triglycerides as markedly elevated, references my personal and family history of high cholesterol, heart disease and stroke and mentions my hyperlipidemia diagnosis. Looking at a July total cholesterol of 331 and an LDL of 227, the app was not being dramatic. Those markers were high, they run in my family and they are the reason I started doing this kind of testing in the first place.

The Six Supplements, and the One I Declined

Hundred’s materials say each protocol includes the top six recommended supplements with timing and dosage guidance. Mine delivered exactly that: six, each with a dose. Plant sterols at 2,000 mg, omega-3 at 2,000 mg, amla at 1,000 mg, red yeast rice at 1,200 mg, plus creatine and magnesium.

I am taking five of them. The sixth is red yeast rice and I chose to leave it out, for a reason I will come back to at the end of this section, because it is the most interesting recommendation in the whole protocol.

One more app note: each supplement carries a small numbered badge on the protocol list screen. Nothing in the app explains what those numbers mean. In beta that is forgivable, but it is exactly the kind of unexplained data point that Hundred says it exists to eliminate and they have since removed.

Now the research. I looked up every one of these on PubMed and I am reporting what I found, including where the evidence is thinner than the app implies.

Plant Sterols for LDL Cholesterol: What 109 Trials Show

The app’s reasoning: my elevated LDL, LDL particle number and ApoB, combined with my family history, make plant sterols a non-pharmaceutical way to lower LDL by reducing cholesterol absorption in the gut. My recommended dose is 2,000 mg.

This is the best-supported recommendation in my protocol. A 2024 systematic review and meta-analysis of 109 randomized controlled trials in Phytotherapy Research found phytosterol intake significantly reduced total cholesterol, LDL cholesterol and triglycerides, with LDL falling by roughly 12.6 mg/dL on average. That is a large evidence base by supplement standards.

Here is the nuance the app does not give me. A review in Nutrition Reviews on why people respond so differently to plant sterols notes that while they lower LDL by about 5 to 15 percent in a dose-dependent way, they have no significant effect in a substantial number of individuals. Response depends heavily on whether you are a high cholesterol absorber or a high synthesizer and there appears to be a genetic component. So plant sterols work well on average, and “on average” is doing real work in that sentence.

There is also a trial that cuts the other way. The SPORT trial in the Journal of the American College of Cardiology randomized 190 adults to low-dose rosuvastatin, placebo or one of six supplements including plant sterols. After 28 days the statin lowered LDL by about 35 percent more than placebo, and none of the supplements, plant sterols included, produced a significant LDL reduction against placebo at all.

So how do I hold that against 109 trials pointing the other way? A few ways. SPORT ran 28 days, which sits right at the edge of how long plant sterols need to reach full effect. It had roughly 24 people per arm against a meta-analysis pooling more than a hundred studies. It was single-blind, single-center and tested one product at one dose in people with lower baseline risk than mine. None of that makes it wrong, and it is a well-run trial from a serious group. What it does is sharpen the same point the non-responder data already made: plant sterols are the best-supported supplement in my protocol and they still might do nothing for a given person. My own numbers happen to have landed on the other side of that question, at least so far.

The 2,000 mg dose sits inside the range used across this literature, so no complaints there.

Omega-3 Fatty Acids: Does Fish Oil Raise LDL?

The app’s reasoning: my elevated triglycerides, LDL and ApoB plus my family history of heart disease and stroke make EPA and DHA a strategic choice, with anti-inflammatory benefits supporting heart and brain health as I navigate menopause and manage hypothyroidism. My recommended dose is 2,000 mg.

This is the recommendation I have the most to say about and it is the one I am taking to my doctor.

The triglyceride case is strong. A 2025 systematic review and meta-analysis of 21 randomized controlled trials in Nutrients found marine omega-3s produce substantial triglyceride reductions, with the largest effects at doses above 2,000 mg per day sustained for eight weeks or more. Good. My triglycerides are elevated and that is a real target.

But the same analysis found something the app’s summary does not mention: LDL cholesterol may increase with omega-3 supplementation, particularly at lower doses, and the authors explicitly recommend monitoring LDL changes. That matters for me, since my LDL tends to be the biggest offender in my labs.

It gets more specific. A meta-analysis in Clinical Nutrition pooling 33 trials found that EPA and DHA are not interchangeable for someone in my position. Both lower triglycerides, but EPA decreased total cholesterol and LDL cholesterol, while DHA increased total cholesterol and LDL cholesterol. So for a person with markedly elevated LDL and elevated triglycerides, the EPA to DHA ratio is not a detail.

My protocol says omega-3 fatty acids, 2,000 mg. It does not specify an EPA to DHA split. Based on the research above, that split could pull my LDL in either direction. My LDL is lower at the retest than at my July baseline, so whatever I am taking does not appear to be working against me, but I would still rather know the ratio than infer it backward from a result. This is a good recommendation with a missing variable, and it is exactly the sort of thing I want a clinician looking at rather than a dose slider.

Does Amla Lower Cholesterol? The Evidence Is Thinner Than the App Suggests

The app’s reasoning: given my significantly elevated LDL, total cholesterol, triglycerides and ApoB, optimizing my lipid profile is a top priority, and the app states amla has demonstrated the ability to lower LDL and total cholesterol by 10 to 21 percent in clinical studies.

This is the recommendation where I want to slow down, because that 10 to 21 percent figure is stated with a confidence the literature has not earned.

Amla does have supportive data. A 2023 systematic review and meta-analysis of amla supplementation in Diabetes and Metabolic Syndrome found it significantly reduced LDL cholesterol, total cholesterol, triglycerides, fasting glucose and CRP while raising HDL. Those results are real and they point the right direction.

Now the caveats, all of which come from that same paper. The meta-analysis pooled five randomized controlled trials. Five. Interventions ran from three to 12 weeks. The authors themselves conclude that additional investigation is warranted to confirm the findings. Compare that to the 109 trials behind plant sterols and you can see the gap.

The individual trials are interesting though. A randomized, double-blind, placebo-controlled multicenter trial in BMC Complementary and Alternative Medicine gave 98 people with dyslipidemia 500 mg of amla extract twice daily for 12 weeks and found significant reductions in total cholesterol, triglycerides, LDL and VLDL against placebo, along with a 39 percent reduction in the atherogenic index of plasma. Notably for anyone weighing this against statins, cholesterol reduction happened without the drop in CoQ10 that statins can cause.

My protocol puts me at 1,000 mg. So my honest read: amla is a promising, low-risk addition with early evidence, tested mostly in small short trials. It is not in the same evidentiary tier as plant sterols and I do not think the app should present it as though it is. I am taking it. Given that my own LDL drop lands in the range you would expect from sterols and amla stacked together, I suspect it is contributing.

Magnesium for Sleep and Recovery

The app’s reasoning: supports sleep quality, muscle recovery and cardiovascular health.

This one made me laugh a little, because I have taken magnesium nightly for years. I have written at length about tolerability and interactions in my guide to magnesium glycinate side effects, and about which form to choose in magnesium for sleep. I use BIOptimizers Magnesium Breakthrough. Hundred had my medications and supplements from onboarding, so recommending something I already take is less a discovery than a confirmation. Still, confirmation has value. If the system had told me to stop, I would have wanted to know why.

The evidence here is real but modest, and I want to be careful not to oversell a supplement I personally like. A 2025 randomized, double-blind, placebo-controlled trial in Nature and Science of Sleep gave 155 adults 250 mg of elemental magnesium as bisglycinate or placebo. The magnesium group’s insomnia severity scores improved more than placebo, but the effect size was small at a Cohen’s d of 0.2, which the authors describe as a modest benefit. The more interesting finding: improvements were notably greater in participants with lower baseline dietary magnesium intake, suggesting the people who benefit most are the ones who were short to begin with.

A separate 2024 trial in Sleep Medicine: X is worth mentioning because of how it measured things. It tracked 80 adults aged 35 to 55 taking magnesium L-threonate or placebo for 21 days, with sleep measured both by questionnaire and objectively by Oura ring. The magnesium group showed improvements in deep sleep score, REM sleep score and readiness while the placebo group declined. I will note that several of that study’s authors are affiliated with an ingredient supplier, which is worth knowing when you read it.

Magnesium is a keeper for me. It is also not magic and the honest summary is a small effect that is largest in people who are deficient.

Creatine for Women in Midlife

The app’s reasoning: I exercise five or more times per week with a focus on strength and bodyweight training, which raises my need for recovery and energy support. It specifically notes creatine is beneficial for women in midlife to preserve lean muscle mass, enhance performance and support cognitive health.

That reasoning is sound and it is well matched to me. I lift five days a week and I compete in NPC physique competitions, so muscle retention is not a hypothetical interest.

The research supports the framing, and the female-specific angle is real rather than marketing. A review in Nutrients examining creatine across the female lifespan notes that women have roughly 70 to 80 percent lower endogenous creatine stores than men, that supplementation improves strength and exercise performance in premenopausal women and that postmenopausal women may see benefits in skeletal muscle size and function at higher doses, with favorable bone effects when combined with resistance training. It also points to positive effects on mood and cognition.

A 2025 review in the Journal of the International Society of Sports Nutrition on creatine and women’s health reaches similar conclusions and adds the caveat I appreciated most: data on perimenopausal women specifically remains limited, and the authors call for more work on dosing strategies in that group. Given that I am somewhere in the menopausal transition and cannot use cycles to pin down exactly where, that limitation lands close to home.

If you are new to this one, my full guide to creatine for women covers dosing, the creatinine question that shows up on blood panels and what to expect. Members can get creatine through Momentous or Thorne at a discount through the platform.

Red Yeast Rice: The Recommendation I Declined

This is the one I want you to pay attention to, because it is where the line between supplement and drug stops meaning anything.

My protocol recommended red yeast rice at 1,200 mg. Red yeast rice is fermented rice, sold on every supplement shelf in the country and it is the recommendation in my protocol with the most direct pharmacological effect on my cholesterol.

Here is why. A review in Nutrients explains that the cholesterol-lowering component of red yeast rice is a family of compounds called monacolins, and that monacolin K is structurally identical to lovastatin, targeting the same enzyme in cholesterol synthesis. Not similar to. Identical. The review reports LDL reductions of roughly 15 to 34 percent against placebo, comparable to a low-dose first-generation statin, and notes that at doses providing around 3 mg of monacolin K per day the adverse event profile also resembles a low-dose statin.

So the honest description is that red yeast rice is a statin that happens to be sold as a supplement. It works the same way, it lowers LDL by a similar amount and it carries a similar side effect profile.

I chose not to take it, because it is the same mechanism of action as a statin and I would rather make that decision deliberately with my doctor than arrive at it through a capsule I bought online. If I am going to take something that inhibits cholesterol synthesis, I want it prescribed, dosed and monitored, with my liver enzymes and my muscle symptoms being watched by someone whose job that is.

None of that is a criticism of red yeast rice, which has real evidence behind it and a legitimate role for people who cannot or will not take a statin. My criticism is of the framing. Nothing in the app told me that monacolin K and lovastatin are the same molecule, although I did happen to already know that having been deep into cholesterol research in the past. That is the single most important fact about this recommendation and a reader who did not go looking would never learn it. A platform whose entire pitch is turning data into clarity should have mentioned this in my opinion.

One more detail worth noticing and I will come back to it later. My updated protocol added CoQ10. Statins are known to deplete CoQ10, which is why people taking them are often told to supplement it. So pairing a statin-equivalent with CoQ10 is a coherent clinical move and it tells me the system knows exactly what red yeast rice is even though it never says so.

I am not taking the CoQ10 either, for the same reason. It was there to offset a supplement I declined. Take away the red yeast rice and the CoQ10 has no job to do in my protocol.

My Nutrition Protocol: 27 Foods and Four Goals

The nutrition tab organizes into four goals, listed as my top four out of a larger set, plus a browsable list of 27 foods to consume more of and a corresponding consume-less list.

My four goals: hormone and energy balance, iron saturation management, cholesterol and triglyceride reduction and avoiding heart risk and iron loading foods.

The 27 foods include almonds, arugula, avocado, black tea, broccoli, Brussels sprouts, cabbage, cauliflower, cheese, chia seeds, chicken breast, cocoa, coffee, cucumbers, extra virgin olive oil, flaxseeds, hazelnuts, herring, kale, mackerel, salmon, sardines, spinach, sunflower seeds, Swiss chard and walnuts.

Two observations. First, this list is remarkably compatible with how I already eat. It is whole foods, protein-forward and heavy on fatty fish, cruciferous vegetables, leafy greens, nuts and olive oil and the app describes the hormone goal as fiber-rich and keto-friendly. Nobody is telling me to give up cheese (thank goodness). For a platform that could easily have produced a low-fat lecture given my LDL, that restraint is notable. It also matters for interpreting my results, because I did not overhaul my diet between my baseline and the retest. The food list largely described what was already on my plate.

Second, and this is the detail I find clever: coffee and black tea are on the consume-more list, and coffee is the image the app uses for the iron saturation goal. Polyphenols and tannins in coffee and tea are well established as inhibitors of non-heme iron absorption. Read that way, the app is not telling me to drink coffee because coffee is healthy. It appears to be using coffee and tea as a dietary lever against my elevated iron saturation. That is a specific, mechanistic and slightly non-obvious move and it is the strongest evidence I have seen that something thoughtful is happening under the Hundred Health “hood”.

I will hold that read loosely, because the app does not spell out the reasoning on the food cards themselves. But the pairing of an iron goal with coffee and tea is not likely to be a coincidence.

My Exercise and Recovery Protocol

Five recommendations came through here: weight training, bodyweight exercises, Zone 2 cardio, hiking and yoga.

This is the section where the personalization is most obvious and the evidence is loosest, and I say that as someone who has been a yoga instructor for years and lifts five days a week. It’s not that these recommendations are bad for me. They are what I already do and I did not change any of it between my baseline and the retest, which is why the supplements were the only new variable.

But look at the pattern. Four of the five rationales lead with lowering LDL particle number or triglycerides. The protocol has clearly decided my lipids are the priority and routed everything toward them, which is defensible. The problem is that the specific claim attached to weight training, that it lowers LDL particle number, is stated more confidently than the trial evidence in women supports.

What I could find on exercise and LDL particle number specifically is thinner than you would expect. A randomized trial in Obesity put overweight and obese adults through 12 weeks of endurance training and measured lipoprotein subfractions, finding that in the women, training reduced LDL3 concentration and particle number and shifted HDL subfractions favorably. Useful, and it points the right way. But that was endurance training, not resistance training, in a population that does not look like me and it is a small study.

So the honest version is this: exercise improves lipid profiles, that much is not in dispute, and Zone 2 and hiking have a reasonable claim on the triglyceride and particle number effects the app describes. Attributing LDL particle number reduction specifically to weight training is a longer reach. I lift because it preserves muscle, supports bone and is the single best thing I do for my body composition in midlife, which is the case I make in my guide to strength training for weight loss. I would not sell it primarily as a lipid intervention.

The Protocol Updated Itself, and Here Is What Changed

When I started writing this I listed “whether the protocol updates” as an open question. Hundred’s whole premise is that this is dynamic rather than a PDF you receive once. I can now answer it, because my August draw went in and the protocol rewrote itself.

Read that table for a second, because a lot happened in it.

The two cholesterol absorption supplements came off. Plant sterols and amla, the two recommendations aimed squarely at pulling my LDL down, are both gone from the updated list. My LDL and non-HDL had just come in at their lowest in years, so a system that de-escalates when your numbers improve is behaving the way you would want it to rather than selling you more capsules.

My omega-3 doubled, from 2,000 mg to 4,000 mg. That is a meaningful change and it moves me from the bottom of the effective range into the middle of it. The Nutrients meta-analysis I cite above found the largest triglyceride reductions at doses above 2,000 mg per day sustained for eight weeks or more. At 4,000 mg I am solidly in that territory. The EPA to DHA ratio is still unspecified, which is still my main complaint.

Two things were added: vitamin D3 with K2, and CoQ10. The CoQ10 is the interesting one. Red yeast rice stayed on the list, red yeast rice works like a statin and statins deplete CoQ10. Adding CoQ10 alongside it is exactly what you would do if you knew that, and it is the most quietly competent decision in the whole protocol. It is also the clearest signal that the platform understands what it recommended, which makes the silence about it in the app harder to excuse rather than easier. I’ve been taking the D3 with K2.

I am skipping the CoQ10 as well as the red yeast rice, since the one was there to cover for the other. Of the six on the updated list I will be taking four.

Red yeast rice stayed. Which means the platform still thinks I should be inhibiting cholesterol synthesis and I still think that is a conversation for my doctor rather than a purchase.

So the dynamic claim holds up. This is the thing I was most skeptical of in March and it is the thing the platform delivered most convincingly. To be clear about what this article covers: both my August numbers and my retest came from the original protocol. I stayed on it through the retest so the two draws measured the same thing.

What the Protocol Gets Right

The question I asked in March was whether this would be built around me or generic advice dressed up in my numbers. The answer is that it was built around me, and I can point to why.

• It found the iron thing and built around it. A nutrition goal named for iron saturation, apparently supported by coffee and tea as absorption inhibitors, is not a template output. It traces directly to an out-of-range result from my first draw.
• It used my medical history, not just my labs. The rationales reference my family history of heart disease and stroke, my hyperlipidemia diagnosis and my hypothyroidism. That is the 21 years of imported records doing visible work.
• It used my training data. The creatine rationale cites my five-plus sessions per week and my strength focus. That came from my intake and my wearables, not a guess.
• It respected how I already eat. No low-fat sermon, no telling me to drop red meat entirely, no fighting my whole foods approach. Cheese and coffee stayed.
• Every supplement came with a dose. Six recommendations, six doses. That is what the marketing promised and it is what arrived.
• Five of six supplements have real evidence. Plant sterols, omega-3, creatine, magnesium and red yeast rice are all defensible on the research. Amla is the weak one.
• It updated itself when my new labs came in, and it de-escalated rather than adding more. That is the dynamic claim working.
• It scheduled the retest that kept me honest. My August numbers looked like a win and without a structured retest I might have believed them outright. The retest showed the non-HDL drop mostly held and the ApoB drop did not, which is far more useful to know.

What I Would Push Back On

Now the other side, because a review that only says nice things is not a review.

• It never tells you red yeast rice is a statin. Monacolin K and lovastatin are the same molecule. That is the most important fact about that recommendation and the app leaves you to find it yourself.
• The omega-3 EPA to DHA question. For someone with markedly elevated LDL, the split matters, and 2,000 mg of unspecified omega-3 leaves the most important variable open.
• The amla claim outruns its evidence. Ten to 21 percent stated flatly, resting on five short trials, sitting in the same visual format as a recommendation backed by 109 trials. The app gives the reader no way to tell those apart.
• The weight training and LDL-P claim is a reach. Right recommendation, shaky stated reason.
• Unexplained numbered badges. Small thing, but this is a platform whose pitch is turning data into clarity.

This is less a criticism of Hundred but more something to consider about doing your own labs without a doctor. My ApoB was 157 at the retest and optimal targets sit below 90, or below 80 given my family history of heart disease and stroke. Plant sterols, amla and omega-3 are legitimate adjuncts, but my retest showed at most a modest effect, with ApoB back in its usual range. They are also not the same order of magnitude as what a pharmaceutical conversation would offer someone with my risk profile, which is exactly what the SPORT trial’s statin arm demonstrated.

Hundred does not claim otherwise, and to its credit the platform is explicit that it does not prescribe and does not replace your physician. But if you are reading this with a lipid panel that looks like mine did in July, do not let a tidy supplement list substitute for the conversation you need to have with your doctor. I am having mine and I am having it with better numbers than I had six weeks ago rather than instead of having it at all.

Does the Wearable Integration Show Up?

Wearable integration is Hundred’s headline differentiator over Function Health and Superpower and I said in my full Hundred Health review that I would report back on whether it added real context or was just a badge feature.

Partial credit. My training frequency and focus clearly informed the creatine rationale and that information can only have come from my intake and my connected devices. The exercise protocol is calibrated to someone who already trains hard rather than someone starting from zero.

What I do not yet see is my Oura and Whoop data feeding the protocol dynamically. Magnesium is framed around sleep quality and I have years of continuous sleep data sitting right there. I would expect a platform built on wearable integration to reference my deep sleep trends or HRV when recommending a sleep supplement. It does not, at least not visibly. The integration informs the plan at the margins rather than driving it. However, I believe more is coming since I now have a screen in the app that says wearable insights coming soon.

That is still more than any competitor at this price does. If you are deciding which wearable to connect in the first place, my Whoop vs Oura comparison and my Oura Ring alternatives guide cover the tradeoffs.

What I Am Tracking Next

The retest answered the main question and sharpened several others. Here is what I am watching from here:

• My Function Health draw later this month. A second lab a few weeks after the retest. If it lands near 216 and 157, that is my real baseline on this protocol, with the caveat that switching labs adds its own variation.
• ApoB, every time. 166 in March, 129 in August, 157 in September. Three readings that bounce that much are the reason I will not read anything into a single one. My target is well below all three.
• Omega-3 and my triglycerides. On 2,000 mg a day my triglycerides went from 214 to 154 and back up to 195. The updated protocol doubles the dose to 4,000 mg, which is the range where trials see the larger triglyceride drops. I am also looking at the EPA to DHA ratio in the supplement I take.
• Iron and iron saturation. Both were out of range in March and came down after a blood donation. At the retest my iron was 129 and my saturation 39 percent, both inside the reference range.
• Adherence. Five of the six is manageable and I have taken magnesium nightly for years, so I know what sticks for me and what does not.
• What comes after the original protocol. I stayed on it through the retest. The updated version drops plant sterols and amla and whether I switch is a conversation I am having with my doctor, along with what comes next for my cholesterol.

I will also be tracking my biological age composite, which comes out of the same panel.

My Preliminary Verdict on the Hundred Health Protocol

I set a bar in March: would this be built around me, or generic wellness advice? It cleared that bar. The iron goal alone convinced me, because I did not ask for it and would not have thought to. The recommendations trace to my labs, my history, my family risk and my training. That is what Hundred said it would deliver and it delivered it.

At the retest, about ten weeks in with nothing else changed, my non-HDL had held most of its August drop and my ApoB had not. That is a mixed result. If the supplements are doing something for me, it is modest, which is what the trials behind them would predict for numbers like mine. I carry ApoE 3/4, my cholesterol did not move through six months of weighed low fat eating and the supplements Hundred chose have modest effects even in the trials that support them. What the platform did give me was a structured reason to retest on a schedule, which is the only reason I can tell you any of this.

Where the platform falls short is in presenting evidence of wildly different quality with identical confidence. A recommendation resting on 109 randomized trials and a recommendation resting on five short ones look exactly the same in the app. For a platform whose entire pitch is clinical rigor and turning data into clarity, that flattening is the thing I would most want fixed. Tell me how strong the evidence is, not just what to take.

The unspecified EPA to DHA ratio and the silence around what red yeast rice is are the two gaps I would most want closed. The 100-day structure remains the smartest thing about this platform, because it forces a retest and a reckoning instead of letting you take capsules on faith indefinitely, and my protocol did rewrite itself when the new numbers came in.

Would I recommend it? Yes, with the same framing I would give a coaching client. The Hundred Health protocol is a well-built, closely tailored starting point and a structured way to act on your labs instead of filing them. It is not medical care, and if your numbers look like mine did, it should send you to your doctor rather than away from one.

For the full breakdown of the panel, the pricing, the medical records import and how Hundred stacks up against the competition, read my complete Hundred Health review. If you are still choosing between platforms, I have also written up whether Function Health is worth it and an InsideTracker vs Function Health comparison. Check current Hundred Health pricing and availability here.

This article describes my personal experience with a health platform and my own lab results. It is not medical advice, and my results are one person’s data rather than a predictor of yours. Supplements can interact with medications and are not appropriate for everyone, and elevated cholesterol, ApoB or iron markers warrant evaluation by a qualified healthcare provider. Please talk to your physician before starting any supplement protocol or making changes based on biomarker testing.